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    An atlas of_head_and_neck_images__part_ii__2002 An atlas of_head_and_neck_images__part_ii__2002 Document Transcript

    • Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) vii Preface An atlas of head and neck images, part II Richard H. Haug, DDS Charles Lee, MD Guest Editors Part I of An Atlas of Head and Neck Images reviewed imaging for the head and neck in trauma, chest pathology, and ultrasonography for the head and neck. It was offered both as an overview of technology and as a simple guide for the interpretation of images common to oral and maxillofacial surgeons, plastic and reconstructive surgeons, otorhinolaryngologists, and head and neck surgeons. It was also intended as a useful tool for radiologists, neurosurgeons, general surgeons, and the medical and dental communities at large. Part II of our series begins with an exhaustive compendium of panoramic images. These are provided not only as a quick review of common and uncommon pathoses of the mandible or maxilla, but also as a visual reference for how these lesions are most likely to appear on pano- ramic radiographs. The next article focuses on computed tomography of the head and neck, pro- viding representative images of the most common pathologic head and neck entities. An article on nuclear imaging provides a synopsis of the most frequently encountered vascular lesions of the head, face, and neck. Finally, an article on magnetic resonance imaging complements the two issues by providing one more additional imaging modality in the practitioner’s diagnostic armamentarium. Although this atlas series does provide an overview of signs, symptoms, etiology, and path- ophysiology of a vast array of head and neck problems, it is not meant to be a definitive treatise on injury and pathology. It is intended merely to quickly point practicing surgeons in the right direction when specific conditions and problems in head and neck surgery are encountered. It is highly visual in design so that it may serve as a quick and ready reference. Richard H. Haug, DDS Division of Oral and Maxillofacial Surgery University of Kentucky College of Dentistry D-509 Chandler Medical Center Lexington, KY 40536-0297, USA E-mail address: rhhaug@pop.uky.edu Charles Lee, MD Division of Diagnostic Radiology University of Kentucky College of Medicine Chandler Medical Center Lexington, KY 40536-0297, USA E-mail address: clee0@pop.uky.edu 1061-3315/03/$ - see front matter Ó 2003, Elsevier Science (USA). All rights reserved. doi:10.1016/S1061-3315(02)00027-6
    • Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Panoramic radiograph in pathology Dean K. White, DDS, MSD*, Chad C.Street, DMD, MD, William S.Jenkins, DMDAnthony R. Clark, DMD, Jason E. Ford, DMD Division of Oral and Maxillofacial Pathology, College of Dentistry, University of Kentucky, 800 Rose Street, Lexington, KY 40536-0298, USA The panoramic radiograph is an excellent extraoral radiograph to reveal abnormalities and pathologic conditions of the jaws and to show calcification of adjacent soft tissue. A single pan- oramic radiograph provides a significant image of the maxillofacial skeleton and dentition and often is used as a survey or screening film because of the area it covers. The panoramic radio- graph does not provide fine radiographic detail, however, and often is followed by intraoral radiographs that can provide sharper detail of an abnormal finding. Computed tomography (CT) and magnetic resonance imaging (MRI) often are utilized to further delineate the extent of a pathologic process found on panoramic radiograph. DEVELOPMENTAL DEFECTS Exostosis/torus Frequency/incidence The incidence of exostoses of the jaws is approximately 27% [1]. The prevalence and number of exostoses increase with age, and exostoses are more common in men than women. Palatal tori, however, are more common in women. Tori are large exostoses of the midline of the hard palate and the lingual surface of the mandible. Signs and symptoms Exostoses and tori are localized outgrowths or nodules on cortical bone, which usually are asymptomatic [2]. They may interfere with normal speech if excessively large and may become inflamed and painful if traumatized. Etiology/pathophysiology These outgrowths of bone are composed of dense cortical bone but may contain medullary bone. Several theories have been proposed concerning the development of exostoses that impli- cate genetic and environmental factors, including masticatory stress [3]. Image of choice for diagnosis Exostoses and tori may be depicted on panoramic and periapical radiographs depending on the size and density of the structures. The diagnosis of exostosis primarily is a clinical diagnosis, which may be confirmed by the radiograph. Image hallmark If an exostosis is of sufficient size and density, it may appear as a well-defined radiopacity on the radiograph in the area of clinical change (Fig. 1). * Corresponding author. E-mail address: dkwhite@pop.uky.edu (D.K. White). 1061-3315/03/$ - see front matter Ó 2003, Elsevier Science (USA). All rights reserved. PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 1 2 - 4
    • 2 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 1. Radiograph showing exostosis/torus. Management No treatment usually is necessary; however, exostoses and tori are removed when a prosthesis is placed on the involved mucosa, when they are chronically inflamed and painful, and when they interfere with normal speech. Condylar hyperplasia Frequency/incidence Condylar hyperplasia is a developmental abnormality that results in enlargement and occa- sionally deformity of the condylar head. This is an extremely rare condition with an incidence of less than 1% [4]. Signs and symptoms The clinical features include asymmetry of the lower third of the face, deviation of the man- dible and chin away from the affected side, and compensatory vertical growth of the maxilla on the affected side. Patients may also have significant temporomandibular joint symptoms, such as pain, joint noises, and diminished mouth opening. The mandibular midline also may be shifted, creating an anterior lateral crossbite with class III molar and canine occlusion on the affected side [5–7]. In addition, the height of the ramus will be increased on the affected side. Etiology/pathophysiology The cause of condylar hyperplasia is unknown but may result from circulatory abnormalities, previous trauma, hormonal disturbances, abnormal joint loading, genetic alterations, and as representing a cartilaginous exostosis [5–7]. Image of choice for diagnosis The panoramic radiograph is the initial screening film of choice. Further enhanced images include conventional CT and MRI.
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 3 Fig. 2. Condylar hyperplasia. Enlargement of the left mandibular condyle (arrow). (Courtesy of Dr. Gary Reinhart.) Image hallmarks The condyle may appear relatively normal in shape but enlarged (Fig. 2). It also may exhibit alteration in shape and be more radiopaque. The ramus and mandibular body on the affected side may also be enlarged, resulting in a characteristic depression of the inferior border of the mandible where the enlarged side joins with the contralateral normal side. In addition, the con- dylar neck is classically elongated on the ipsilateral side [8,9]. Management Treatment decisions are primarily based on the age of the patient [8]. Treatment consists of a combination of orthodontics and orthognathic surgery to correct the skeletal deformity and any dental malocclusion. Successful treatment has been reported with high condylectomy [7]. Calcified stylohyoid ligament Frequency/incidence Approximately 2% to 18% of the general population present radiographic evidence of ossifi- cation of the stylohyoid ligament [10]. There appears to be a slight predominance for women, and symptoms are more common in patients aged 40 and older. Signs and symptoms Most patients are asymptomatic; however, when symptoms occur, there is no correlation between the extent of the calcification and symptoms present. Eagle syndrome is a term used to describe the cluster of symptoms experienced. The symptoms include pain in the peritonsillar region and base of the tongue area posterior to the angle of the mandible, dysphagia and otal- gia. Eagle syndrome previously was reported only in patients post-tonsillectomy. Now it is applied to patients meeting the criteria of the previously described symptoms, with elongated, calcified stylohyoid ligaments [10–12]. Some patients may exhibit syncope when they quickly turn their heads because the rigid ligament compresses the carotid artery and cervical sympa- thetic chain (carotid artery syndrome) [12]. There also have been reports of cervical spine disease resulting in difficult intubations in patients with calcified stylohyoid ligaments [13]. Etiology/pathophysiology The stylohyoid ligament is a fibrous sheath that persists as a part of the ceratohyal element of the second branchial arch, extending from the base of the skull to the lesser horn of the hyoid bone and passing between the internal and external carotid arteries [14]. For unknown reasons, this ligamentous structure may undergo ossification, especially in the upper part of the ligament. Image of choice for diagnosis The panoramic radiograph is the image of choice for visualization. The ligament also may be seen on a routine skull series and cervical spine radiographs.
    • 4 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 3. Calcified stylohyoid ligament. Image hallmarks Calcified stylohyoid ligament presents as a radiopaque change along the course of the struc- ture in which the calcification may vary in density and length (Fig. 3). Management Treatment consists of surgical removal of the affected ligament as close to the cranial base as possible in patients with significant symptoms [11]. This can be accomplished through either an intraoral or extraoral approach, although the extraoral approach is preferred because of better access and visualization. Nasopalatine duct cyst Frequency/Incidence The nasopalatine duct cyst is the most common nonodontogenic cyst of the jaws with a pre- valence of approximately 1% [15,16]. It is most frequently found in patients between the ages of 40 and 60 years, with a slight male predilection [17]. Signs and symptoms Most patients are asymptomatic; however, pain, swelling, drainage, and movement of teeth may be noted. A large cyst may present with palatal swelling in which the cortical plate has been perforated and drainage of fluid or pus ensues. Etiology/pathophysiology The cause of the cyst is unknown, but some authors have attributed its development to trauma, infection, and spontaneous proliferation of residual embryonal epithelium as possible causes [15–18]. Image of choice for diagnosis The panoramic radiograph is the initial screening film of choice, followed by periapical radio- graphs for definitive visualization. Image hallmarks The classic presentation is a symmetrical, ovoid or heart-shaped radiolucency between the roots or at the apices of vital maxillary central incisors (Fig. 4) [19]. Management Thorough surgical curettage is the treatment of choice for symptomatic lesions or lesions measuring more than 6 mm in diameter. Recurrence after surgical removal is reported to
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 5 Fig. 4. Nasopalatine duct cyst. be approximately 2% [19]. Several other cystic lesions may mimic a nasopalatine duct cyst. Differential diagnosis includes an apical periodontal cyst, lateral periodontal cyst, and odonto- genic keratocyst [20]. INFLAMMATORY DISEASES Submandibular salivary gland cortical defect Frequency/incidence In 1942, Stafne first described 34 cases of this radiographic abnormality just anterior to the angle of the mandible [21]. The prevalence rate has been reported to be approximately 0.05%, with a slight male predominance [22].
    • 6 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 5. Submandibular salivary gland defect. Signs and symptoms This defect usually is asymptomatic and diagnosed on routine panoramic radiograph. When symptoms occur, they consist of pain and swelling in the area of the submandibular gland. There is no cortical expansion. Etiology/pathophysiology The cause of this cortical defect is unknown; however, various causes have been proposed, in- cluding stress alteration, pressure atrophy from an inflamed gland, and a congenital defect [22]. The contents of the defect contain submandibular salivary gland elements, fat, and connective tissue [23]. Image of choice for diagnosis The panoramic radiograph is the initial screening film of choice. A lateral jaw film also can detect the defect, and the diagnosis can be confirmed with CT, MRI, and a sialogram of the sub- mandibular gland that shows salivary gland contents in the cortical depression or defect. Image hallmarks The classic presentation is a well-defined radiolucency near the angle of the mandible below the inferior alveolar canal (Fig. 5). Most of these defects exhibit a hyperostotic border, and most cases are unilateral. A similar lingual cortical defect can be associated with the sublingual gland, although it is quite rare [24]. Management There is no treatment for the cortical defect; however, a symptomatic submandibular gland may require removal. Periapical inflammatory disease Frequency/incidence Inflammatory disease of pulp with periapical bone involvement is common, with incidence rates of 40% to 70% [25,26]. The most common location for periapical involvement is the max- illary anterior region, followed by posterior maxilla, the posterior mandible, and the anterior mandible [27]. Signs and symptoms Patients with periapical inflammatory disease may be asymptomatic or present with pain, swelling, drainage, and possibly fever and regional lymphadenopathy. The associated teeth also may be painful and tender to palpation and percussion. The involved teeth are nonvital. Etiology/pathophysiology Inflammatory periapical bone disease is initiated by the presence of micro-organisms in the apical portion of the root canal of the involved tooth [25]. The infection and resultant inflam-
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 7 Fig. 6. Periapical inflammatory disease. matory response may spread to periapical bone, producing a variety of pathologic conditions, including inflamed granulation tissue (periapical granuloma, chronic apical periodontitis), abscess, and apical periodontal cyst (radicular cyst). The development of inflamed granulation tissue or abscess depends on the virulence of the involved organisms and extent of the infection. Periapical granulation tissue may continue to destroy bone and ultimately destroy cortical bone. Fistula formation may occur. An abscess may perforate through cortical plates and create a soft tissue space infection, which may create significant morbidity. Activation of residual odonto- genic epithelium in the periodontal membrane may result in cyst formation. The cyst may ex- pand and destroy a significant amount of bone. The cyst may be asymptomatic, or the patient may complain of pain. In a review of 256 periapical lesions, Nair et al found that the majority (55%) were granulomas and the remaining lesions (45%) were periapical cysts or ab- scesses [25]. Image of choice for diagnosis The panoramic radiograph is the initial screening film of choice, followed by periapical radio- graphs for further delineation of the lesion. Image hallmarks The classic presentation is a radiolucency at the apex of a nonvital tooth (Fig. 6). The size and extent of the lesion varies considerably, with extension laterally and inferiorly from the apex. A periapical abscess may show only minimal widening of the periodontal membrane of the involved tooth. Management Treatment for periapical inflammatory disease involves either extraction of the involved tooth or root canal therapy with the appropriate use of antibiotics if the clinical situation war- rants it. In a follow-up study after root canal treatment, approximately 90% of the lesions resolved and were not detectable on radiographs [28]. The treatment for unresolved lesions is surgical removal of the involved tissue and submission of the tissue for microscopic examination. The distinction between periapical granuloma and apical periodontal cyst can only be made by microscopic examination [29].
    • 8 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 7. Periodontal disease. Periodontal disease Frequency/incidence Periodontal disease is the leading cause of tooth loss in patients over the age of 35 years. There is an increased prevalence associated with increased age, diabetes, smoking, and limited oral hygiene [30]. To some degree, periodontal disease affects most individuals at some point in their lifetime. Although periodontitis typically is a disease of adulthood, aggressive forms, termed early-onset periodontitis, may occur in children [31]. Signs and symptoms The typical sign of periodontal disease is erythematous and edematous gingiva that bleeds with tissue manipulation. The normal stippling is not present and the gingiva also may be blunted or apically positioned, depending on the degree of tissue involvement [32]. Patients may report bleeding with brushing and gingival pain, although these are not consistent symp- toms. Etiology/pathophysiology Periodontal disease primarily is caused by bacteria that colonize the gingival crevice. The re- sultant bacterial products and inflammation ultimately cause destruction of supporting alveolar bone, which leads to loss of bone support for the teeth. Gingival inflammation and periodontal bone loss may be localized to several teeth or generalized. Tissue pockets of more than 4 mm are indicative of an active disease process. Image of choice for diagnosis The panoramic radiograph is an excellent initial screening tool and is followed by periapical radiographs, which better define the amount of alveolar bone loss. Image hallmarks Gingival inflammation usually does not show alveolar bone loss. When the inflammatory response involves alveolar bone, gradual destruction of the interdental bone takes place. The amount of loss of bone that supports the teeth indicates the severity of the disease process (Fig. 7). Management Treatment depends on the severity of the symptoms and tissue destruction. It consists of a combination of oral hygiene procedures performed by the patient, mechanical debridement, sur- gical removal of diseased tissue, and topical antimicrobial agents.
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 9 Fig. 8. Osteomyelitis. (Courtesy of Dr. Jason Ford, Lexington, KY.) Osteomyelitis Frequency/incidence Osteomyelitis of the jaws was once a frequently encountered disease and was difficult to treat. Now it is much less common because of the improvement in dental and medical health care and the use of antibiotics [33]. Osteomyelitis is more common in the mandible because of its relative avascularity when compared with the maxilla. Signs and symptoms Patients often present with fever, malaise, edema of the overlying soft tissue, lymphadenop- athy, purulent discharge, pain, and leukocytosis [34]. Etiology/pathophysiology Osteomyelitis is an infectious process within the marrow spaces of bone. In the face, the angle and body of the mandible is the most commonly infected site. Most cases are the result of a bacterial dental infection. Infected mandibular fractures are the second most common cause of osteomyelitis [35]. Hematogenous spread also is responsible for cases of facial osteomyelitis. The cases may be acute or chronic and suppurative or nonsuppurative in nature. Diagnosis is based on clinical, histopathologic, and laboratory studies. Image of choice for diagnosis The panoramic radiograph serves as an initial screening tool. In many cases, CT bone scinto- grams and MRI are superior to conventional radiographs in delineating the extent of the infec- tious process. Bone scintography studies with technetium 99 are abnormal in 90% to 95% of patients with osteomyelitis [34]. Image hallmarks In the early stages, conventional radiographic images may fail to show any abnormalities; however, areas of ill-defined radiolucencies with or without radiopaque sequestrum and reactive bone soon develop. The radiographic changes may exhibit a mottled or ‘‘moth-eaten’’ pattern and mimic malignancy (Fig. 8). The diagnosis of osteomyelitis is based on clinical and radio- graphic findings.
    • 10 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Management Treatment consists of prompt aggressive surgical debridement of all infected bone down to healthy bleeding tissue, followed by long-term intravenous or oral antibiotics for 6 to 12 weeks with high-dose aqueous penicillin G (12–20 million U/day) or clindamycin (2700 mg/day) if the patient is allergic to penicillin [36]. The patient must be closely followed clinically and radio- graphically for resolution of the infection. Bony defects that result from the infection may require further surgical procedures. Proliferative periostitis (periostitis ossificans) Frequency/incidence Proliferative periostitis is a relatively rare, specific type of chronic osteomyelitis that occurs almost exclusively in children and young adults [37]. The average age of onset is 11 years with a male-to-female ratio of 1.4 to 1 [38]. Signs and symptoms Patients most commonly present with symptoms related to their primary infection and a painless swelling of bone of the affected area. The most common location is the posterior body of the mandible with an associated carious molar or premolar. The swelling may be of insidious onset with only minimal pain over the involved area [39]. Etiology/pathophysiology In most cases, the infected focus resulting in the periosteal hyperplasia represents a carious tooth, periodontal disease, or an infected extraction site. There have been reports of prolifera- tive periostitis resulting from an infected dentigerous cyst [40]. Image of choice for diagnosis Panoramic and lateral oblique radiographs are appropriate films to establish the diagnosis. If these images do not show the characteristic changes, occlusal and posteroanterior radiographs may be helpful. Fig. 9. Proliferative periostitis (periostitis ossificans). (Courtesy of Dr. Dean White, Lexington, KY.)
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 11 Image hallmarks The classic radiographic appearance shows reduplication of cortical bone with a lamellar or layering effect (‘‘onionskin’’ appearance) stimulated by the underlying inflammatory process (Fig. 9) [41]. Management Treatment involves elimination of the source of infection. The cortical enlargement usually undergoes resolution within 6 to 12 months. The presence of proliferative periostitis in the absence of an inflammatory process requires biopsy of the involved area because processes such as Ewing sarcoma, Langerhans cell histiocytosis, and metastatic disease can induce this reaction. Antral pseudocyst Frequency/incidence The antral pseudocyst is a relatively common finding on routine panoramic radiographs [42]. Reports indicate that 1.5% to 10% of the population have these on routine radiographic evaluation [43]. Signs and symptoms Patients are usually asymptomatic unless a localized infection is present [44]. These latter pa- tients exhibit symptoms of maxillary sinusitis including fever, nasal discharge, headache, and pain. Etiology/pathophysiology The antral pseudocyst represents an accumulation of fluid between antral mucosa and the floor of the sinus. The cause is unknown but some cases may represent the extension of an inflam- matory exudate from an infected maxillary tooth. The terms sinus mucocele and retention cyst have been used for this entity; however, there is no accumulation of mucous or true cyst lining in these lesions, and they should not be confused with the other, more aggressive lesions. Fig. 10. Antral pseudocyst. (Courtesy of Dr. Dan Trinler, Lexington, KY.)
    • 12 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Image of choice for diagnosis The panoramic radiograph is the diagnostic film of choice. A water’s view image and CT may be useful if the diagnosis is unclear on panoramic radiograph. Image hallmarks The classic radiographic presentation is a ‘‘domed-shaped,’’ finely radiopaque lesion with its base on the antral floor (Fig. 10). In rare instances, the entire sinus may be involved [45]; however, other space-occupying lesions of the sinus must be ruled out when it appears in this fashion. Management The lesion often regresses on its own and no treatment is necessary in most cases. If symptoms are present, either transantral or endoscopic techniques may be used for removal of the lesion [42]. Sialolith Frequency/incidence Salivary calculi (sialoliths) are a common cause of salivary gland dysfunction and may occur in any of the salivary glands and at almost any age. They occur most commonly in the submandibular gland duct (83%) and involve the parotid gland duct in 10% of cases. Minor salivary gland duct and sublingual gland involvement represents the remaining 7% of cases [46]. Occasionally, the salivary gland itself may be involved. The incidence of sialolithiasis is approximately 1% in the general population [47]. Signs and symptoms Some calculi remain asymptomatic; however, most calculi obstruct salivary flow to the point that the involved gland eventually becomes enlarged and painful. The gland often becomes tense and painful during or after a meal, which has stimulated the gland to produce and secrete saliva. A palpable mass may be present depending on the location of the stone within the duct, and at- tempts to express saliva from the involved duct may produce minimal or no flow. These symptoms are primarily related to the submandibular and parotid gland systems. Minor gland sialolithiasis usually manifests as a small nodular mass with possible localized tenderness. If the involved gland has become secondarily infected, purulent drainage may be seen at the meatus of the duct. Etiology/pathophysiology The mechanism behind the development of salivary calculi is not well understood but has been attributed to mucous stasis within a duct followed by the deposition of calcium salts in Fig. 11. Sialolith. (Courtesy of Dr. Denise Clarke, Port Angeles, WA.)
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 13 a nidus, leading to the development of a calcified mass. In most cases, the sialolith develops within the duct of the affected gland. Approximately 90% of submandibular stones are situated in the distal portion of the Wharton duct or at the hilum [48]. Image of choice for diagnosis The panoramic radiograph is an excellent screening film to detect submandibular and parotid calculi. This image may be coupled with an occlusal radiograph to determine the location of the sialolith in the involved duct. Image hallmarks Sialoliths appear as radiopaque, ovoid to linear structures often superimposed on normal radiographic anatomy (Fig. 11). They rarely develop in the gland itself. Management Treatment usually involves surgical removal of the sialolith from the duct; however, other mo- dalities of treatment include laser therapy, extracorporeal electromagnetic shock-wave lithotripsy and catheter retrieval under fluoroscopy [49]. If chronic sialadenitis is present, the entire gland usu- ally requires removal. Appropriate antibiotic therapy is indicated if purulent drainage is present. LOCALIZED METABOLIC DISORDERS Idiopathic osteosclerosis Frequency/incidence The incidence of osteosclerosis of the jaws is 4% to 31% [50]. Approximately 90% of osteo- sclerosis cases occur in the posterior mandible, with an age predilection between 20 to 40 years. Osteosclerosis shows equal sex distribution [50–52]. Fig. 12. Radiograph showing osteosclerosis.
    • 14 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Signs and symptoms Osteosclerosis is an asymptomatic, localized area of increased density of bone without expan- sion, which is discovered during routine radiographic examination. Etiology/pathophysiology The cause of idiopathic osteosclerosis is unknown. It is not associated with inflammatory and neoplastic processes [50–52]. It is distinguished from condensing osteitis, which has an inflam- matory origin. Image of choice for diagnosis Osteosclerosis is seen on panoramic and periapical radiographs. Image hallmarks Osteosclerosis usually is seen as a single, well-defined, homogeneous radiopacity that lacks a radiolucent rim (Fig. 12) [50,52,53]. It can be circular to ovoid to linear in shape, and the size ranges from several millimeters to actual diffuse areas of involvement. It typically is seen between teeth, at the apices of teeth, and below tooth-bearing areas. Root resorption occurs in approximately 10% of cases [51]. Management Once the diagnosis of idiopathic osteosclerosis is made, no treatment is required. Care should be taken to rule out soft tissue calcification, such as a sialolith, which is superimposed on the image, and an exostosis. Osseous dysplasia (cemeto-osseous dysplasia) Frequency/incidence Osseous dysplasia represents a reactive process of the jaws, which is subdivided into three, sometimes overlapping, categories [54–56]. Periapical cemental dysplasia overwhelmingly is seen in African American women aged 20 to 40 years and involves the periapical region of the ante- rior mandibular teeth [54,56,57]. Focal osseous dysplasia typically is recognized in women in their 20s and 40s and is found in the posterior mandibular region in tooth-bearing areas [56– 58]. Florid osseous dysplasia represents a process that usually involves the tooth-bearing areas of multiple quadrants of the jaws and primarily is seen in middle-aged to elderly African Amer- ican women [56,59]. Signs and symptoms Periapical cemental dysplasia and focal osseous dysplasia generally are asymptomatic [54,57,60]. Long-term lesions may exhibit mild cortical expansion. Florid osseous dysplasia usu- ally is asymptomatic but may show cortical expansion. In addition, some cases of florid osseous dysplasia will become secondarily inflamed and exhibit fistula formation, loose teeth, and pain. Etiology/pathophysiology The cause of osseous dysplasia is unknown [54,57]; however, it is theorized that it represents a reactive process in which normal bone is replaced by a poorly cellularized bonelike material and cellular fibrous connective tissue, which originate from periodontal membrane [54,57]. Image of choice for diagnosis This process is often identified first on periapical radiographs; however, the panoramic radio- graph is used to show the extent of the abnormality. Image hallmarks The radiographic changes depend on the subdivision of the process and the degree of miner- alization of the proliferation [57]. Periapical cemental dysplasia involves from one to all of the
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 15 Fig. 13. Florid osseous dysplasia. mandibular anterior teeth. Occasionally, it may also include other teeth. The initial changes are well-defined radiolucencies at the apices of the involved teeth. The area of bone remodeling may extend inferiorly and between teeth, and there usually is a progressive mineralization of the lesions. Thus, the changes range from radiolucent to radiolucent/radiopaque to radiopaque with a radiolucent rim in the final stage. Focal osseous dysplasia represents a solitary lesion associ- ated with the apex or lateral surface of the root of the involved tooth, and it will demonstrate the same maturation pattern [56,57]. The florid variant exhibits the same maturation pattern as the former two categories but will involve multiple teeth and usually multiple quadrants of the jaws (Fig. 13) [55,56]. The alterations may extend beyond tooth-bearing areas and persistent radio- lucencies may be present that represent idiopathic bone cavities [55]. Management Once the diagnosis of osseous dysplasia is made, the patient can be observed. Florid osseous dysplasia may require antibiotic therapy and surgical debridement if the process becomes secon- darily infected and undergoes sequestration. Patients with this process must practice sound oral hygiene to help prevent these complications. Focal osseous dysplasia can mimic central os- sifying fibroma of bone radiographically, and these two conditions may not even be separated by microscopic examination. Radiographic changes that support focal osseous dysplasia over ossifying fibroma include contact of the lesion with the apex and/or lateral aspect of the root and mineralization of the lesion without an increase in the dimensions of the lesion. If the two cannot be separated on a radiographic basis, biopsy usually is performed. The ossifying fibroma usually is a solid structure, whereas focal osseous dysplasia usually is friable and removed in pieces [54]. Simple bone cyst (idiopathic bone cavity, traumatic bone cyst) Frequency/incidence Simple bone cysts primarily occur in the mandible, with a predilection for the anterior man- dible between the mental foramina [61,62]. It usually affects individuals in their teens and 20s with near equal sex distribution [62–65].
    • 16 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 14. Idiopathic bone cavity. Signs and symptoms Simple bone cysts usually are asymptomatic [64], but expansion may occur. Some patients give a history of previous trauma to the area and may complain of mild pain and tenderness in the area [64]. Etiology/pathophysiology It is theorized that simple bone cysts occur secondarily to intraosseous hemorrhage in which the normal repair mechanism is disrupted, resulting in the defect [61]. The source of hemorrhage may be trauma, focal degeneration of connective tissue, or idiopathic [61,62,64]. Image of choice for diagnosis Simple bone cysts often are noted on routine panoramic radiographs, the film most utilized to identify odontogenic cysts and neoplasms of the jaws. Image hallmarks Simple bone cysts often appear as well-defined radiolucencies of the anterior and midbody of the mandible (Fig. 14) [61,62,64]. The border adjacent to teeth often extends between their roots, pro- ducing a scalloped border [61,63]. The radiographic image is not diagnostic for simple bone cyst alone, and other odontogenic lesions and neoplasms may exhibit a similar radiographic appearance. Management Management includes exploration and curettage of the bony walls to induce clot formation. Any soft tissue obtained during the procedure is examined microscopically to rule out a true odontogenic cyst [61,65]. Follow-up radiographic examinations are needed to ensure that bony fill takes place. SYSTEMIC METABOLIC DISORDERS Osteopetrosis Frequency/incidence Osteopetrosis is an extremely rare disorder related to a defect in normal bone remodeling. It is believed to occur in only 0.005% of the population [66,67]. It has three hereditary forms, which are variable in severity [68].
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 17 Fig. 15. Osteopetrosis. (Courtesy of Dr. Dan Sarasin.) Signs and symptoms Patients with the autosomal-recessive infantile form of the disease exhibit anemia and hepa- tosplenomegaly. They are susceptible to infections because of the granulocytopenia and exhibit enlargement of the jaws. A prominent sign is hypertrophy of the mandible, especially an in- creased width at the gonial angles [68]. Osteomyelitis is a common complication of tooth extrac- tion. Symptoms related to cranial nerve compression, such as blindness, facial paralysis and otologic disorders may develop [69,70]; and pathologic fractures are common. Patients with the autosomal-dominant adult form may exhibit few signs and symptoms. Etiology/pathophysiology Osteopetrosis represents a group of hereditary disorders characterized by a defect in osteo- clastic activity, which results in increased bone formation at the expense of normal marrow spaces [66,68]. The affected bone exhibits a decrease in vascularity and reduction or elimination of hematopoietic marrow. The bones become brittle and are susceptible to fracture and infection [66,68]. The severe type affects children who rarely survive past 2 years of age, whereas the milder forms primarily affect the skeleton and have a better prognosis [66,68]. Image of choice for diagnosis The jaw changes are best demonstrated on panoramic radiograph. Other conventional facial radiographs may also be useful in evaluating the extent of the disorder throughout the cranio- maxillofacial skeleton. Image hallmarks Radiographic images of the process show loss of normal medullary trabecular pattern with a generalized radiopacity of the affected bone resulting from increased bone density (Fig. 15). The distinction between cortical and medullary bone becomes nonexistent as the medullary spaces are obliterated [66,68,71]. Management Patients with osteopetrosis are highly susceptible to the development of osteomyelitis. Pre- vention plays an important role in managing a patient with this disease. Emphasis is placed on excellent oral hygiene and routine dental prophylaxis. Endodontic therapy is encouraged over dental extraction to avoid excessive trauma to bone. If debridement is necessary, conserva- tive bone removal is indicated, with minimal periosteal stripping after limited incisional access [66,69]. Although therapeutic levels of antibiotics are difficult to achieve in these patients, they are recommended [66].
    • 18 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Cleidocranial dysplasia Frequency/incidence Cleidocranial dysplasia is a rare hereditary disorder that affects the cranial bones and forma- tion of the clavicles [72,73]. It exhibits equal sex distribution. Signs and symptoms Affected individuals are usually short in stature and exhibit a spectrum of hypermobility of the shoulders, which results in a characteristic appearance of a long neck with a narrow, pigeon- shaped chest [73]. These patients also may be brachycephalic and exhibit ocular hypertelorism and altered tooth eruption [72,73]. Etiology/pathophysiology Cleidocranial dysplasia is a disorder of bone formation and ossification in which the cause is unknown. Most cases are autosomal dominant; however, 40% of cases represent mutations [72,73]. Image of choice for diagnosis The characteristic dental abnormalities are demonstrated on the panoramic radiograph. The anteroposterior (A-P) chest radiograph will show the degree to which the clavicles are affected. Image hallmarks The characteristic findings on panoramic radiograph are retained deciduous teeth, multiple impacted teeth, and supernumerary teeth, which may be impacted (Fig. 16). A nasoalveolar cleft also may be observed. A-P chest films may show the degree of malformation of the clavicles. Management Treatment of this disorder is challenging and complex, requiring a multidisciplinary ap- proach. The basic principles include removing any barriers to the eruption of permanent teeth [74–76]. This requires timely removal of deciduous teeth and bone with maintenance of space for future eruption [74,75]. Success is dependent on the formation of the teeth, which may be dam- Fig. 16. Cleidocranial dysplasia.
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 19 aged during surgical exposure, root development, and retention. These patients often require orthognathic surgery to correct skeletal malformation resulting from hypoplastic maxilla and hyperplastic mandible. Alternatives for tooth replacement if the permanent teeth are not positioned and retained include tooth transplantation, dental implants, and dental prostheses [74–76]. Paget disease Frequency/incidence Paget disease is a rare disorder of bone metabolism, which results in the alteration of normal bone deposition and resorption [77]. The disorder predominantly affects individuals in their 40s and 50s, with an increased prevalence in men [78–80]. Signs and symptoms The disease is associated with progressive enlargement of the affected bone. Enlargement of the jaws results in changes in occlusion, spacing of teeth, and facial deformity [81]. It may also cause pain in the affected bone, and multiple bones may be affected. Patients may exhibit neuro- logic complications, such as visual disturbances and hearing loss, when there is craniofacial bone involvement. Etiology/pathophysiology The cause of the alteration in bone remodeling is unknown [81]. Inflammation and endocrine and genetic factors have been considered but not substantiated. Image of choice for diagnosis The panoramic radiograph is an excellent imaging method to reveal involvement of the jaws with Paget disease. Image hallmarks The characteristic changes of the jaws in Paget disease are seen as areas of radiopacity sur- rounded by areas of radiolucency (Fig. 17). The areas tend to coalesce and become more radio- paque. They often exhibit a poorly defined hazy periphery, which is described as a ‘‘cotton wool’’ appearance. The teeth may exhibit hypercementosis, and there is an increase in interden- tal spacing [81]. Florid osseous dysplasia may appear in a similar fashion. Fig. 17. Paget disease. (Courtesy of Dr. Mark McIlwain, Sheffield, AL.)
    • 20 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Management Medical treatment consists of the alleviation of bone pain and the use of biphosphates to re- duce progression of the disease by inhibiting osteoclastic activity [77,82]. In patients with facial disfigurement, recontouring procedures may be performed [77,83]. Patients with advanced in- volvement of the jaws are susceptible to the development of osteomyelitis, giant cell tumor, and sarcomas [83]. Cherubism Frequency/incidence Cherubism is a rare familial disorder that affects children between the ages of 14 months to 20 years, with an increased prevalence in boys [84–86]. Isolated cases have been reported, indicating the possibility of a spontaneous mutation [85,86]. Signs and symptoms Cherubism is characterized by asymptomatic, bilateral expansion of the mandible, resulting in the classic picture of fullness of the cheeks. Involvement of the maxilla results in increased exposure of sclera, giving the appearance of an ‘‘upward gaze’’ to the eyes [84,86,87]. Etiology/pathophysiology Most cases (80%) are autosomal dominant, affecting 100% of boys and 50% to 70% of girls [84–86]. The remaining 20% of cases represent spontaneous mutations [84,85,88]. The enlargement of the jaws is secondary to space-occupying lesions, which microscopically resemble central giant cell granuloma. Image of choice for diagnosis The maxillofacial lesions associated with cherubism are best visualized by panoramic radio- graph. Image hallmarks The disorder is characterized by diffuse multilocular radiolucencies of the posterior mandible and maxilla, with the mandible being involved more frequently than the maxilla (Fig. 18) [84,87,89]. These lesions may alter tooth-eruption patterns, formation of teeth, and displace the inferior alveolar canal [85]. Fig. 18. Cherubism. (Courtesy of Dr. Denver Tackett, McDowell, KY.)
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 21 Management Cherubism is a self-limiting disorder after the second decade of life. Excess deformity may require recontouring but this is best postponed as long as possible because postsurgical regrowth has been reported [84,90]. Fibrous dysplasia of bone Frequency/incidence Fibrous dysplasia of bone is a rare proliferative condition that affects the craniofacial skele- ton and other bones of the body. There are two main patterns: monostotic, which represents single-bone involvement, and polyostotic, which involves multiple bones. The skull and the jaws represent the most commonly affected bones; however, the ribs and long bones also are involved [56,91]. This condition typically develops in the first two decades of life; the monostotic form is more common [56]. Fibrous dysplasia of bone is a component of McCune-Albright syndrome in which the affected individual exhibits polyostotic fibrous dysplasia, endocrine abnormalities, ´ and cafe-au-lait skin pigmentation [56]. Ninety-five percent of individuals with McCune- Albright syndrome are female [56,91]. Signs and symptoms Fibrous dysplasia of bone is an asymptomatic process that is characterized by expansion of the affected bone [56,92]. Etiology/pathophysiology This disorder is believed to result from a sporadic mutation in the GNAS1 gene postzygo- tically in a somatic cell [93]. The resulting clinical manifestations, whether McCune-Albright syndrome or fibrous dysplasia, depend on the size of the embryonic cell mass when the mutation occurs and where in the cell mass it develops. The earlier the mutation occurs within the embry- onic tissue, the more likely the chances of the multisystem disorder developing. Image of choice for diagnosis The changes of fibrous dysplasia of the jaws are best depicted on panoramic radiograph. Lat- eral skull and occlusal and periapical radiographs also are of help in demonstrating the charac- teristic findings. CT is helpful in determining the extent of the process, especially when multiple bones of the craniofacial complex are involved. Fig. 19. Fibrous dysplasia of bone. (Courtesy of Dr. Richard Lee, Findlay, OH.)
    • 22 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Image hallmarks The most characteristic change of fibrous dysplasia of the jaws is a finely radiopaque lesion that blends with normal surrounding bone (Fig. 19). On fine-grain films, such as periapical ra- diographs, the lesion exhibits a finely trabecular pattern, which has been termed ‘‘ground glass’’ in appearance [56,92]. Some cases, however, exhibit a multilocular or mottled appearance. Management The treatment of fibrous dysplasia of the jaws is variable. Most cases tend to stabilize as patients reach skeletal maturity [56], and mild cases may not require treatment. Patients with significant cosmetic and/or functional deformities may require one or more surgical reduc- tion procedures. In some patients, there may be continued enlargement of the affected bone in adulthood. Regrowth of the lesion after recontouring is variable, with 25% to 50% of patients exhibiting some postoperative expansion [56,94]. Gardner syndrome Frequency/incidence Gardner syndrome is a rare adenomatous polyposis syndrome that is characterized by familial polyposis, desmoid tumors, epidermoid cysts, and dental and skeletal abnormalities [95,96]. The mean age of diagnosis is 25 years; however, onset of symptoms may range from 2 to 70 years of age [95]. Gardner syndrome has been reported to occur in between 1 to 8300 and 1 to 16,000 births [95,97]. Signs and symptoms The extracolonic signs and symptoms are most often recognized first. These include multiple epidermoid cysts, impacted teeth, exophytic hard tissue masses of the mandible, and retinal pig- mented lesions [96]. Etiology/pathophysiology Gardner syndrome is an autosomal-dominant disorder with close to 100% penetrance [95,96,98]. The expression of the syndrome is variable. Nearly one third of cases occur sponta- neously [95,96]. A gene on chromosome 5 has been identified as being associated with the devel- opment of the disorder [99]. Fig. 20. Gardner syndrome. (Courtesy of Dr. Edyee Sturgill, Bowling Green, KY.)
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 23 Image of choice for diagnosis The dental and jaw changes associated with the syndrome are best identified on a panoramic radiograph. Image hallmarks The changes seen on radiographs consist of multiple impacted supernumerary and regular teeth, osteosclerotic areas, and exophytic sclerotic masses of cortical bone, usually seen at the angles of the mandible and termed osteomas (Fig. 20). Management Gardner syndrome is a serious condition that requires early intervention because untreated patients will develop colorectal adenocarcinoma [95,96]. In women, there also is an increased risk of developing thyroid carcinoma [96]. The impacted teeth may have to be removed because of development of odontogenic cysts, and the exophytic osteomas may be removed for cosmetic and functional problems. Hyperparathyroidism Frequency/incidence Hyperparathyroidism ranks third among the incidence of endocrine disorders behind dia- betes mellitus and hyperthyroidism. It occurs in 30 of every 100,000 patients [100,101]. This disorder may occur at any age but it predominantly affects those in their 40s and 50s, with a female-to-male ratio of 3 to 1 [100,101]. Signs and symptoms Hyperparathyroidism often is asymptomatic [100]; however, some patients will complain of or exhibit a variety of symptoms including the following: mental depression, confusion, leth- argy, muscle weakness, nausea and vomiting, peptic ulceration, renal calculi, anorexia, and skel- etal demineralization [102,103]. The signs and symptoms may be vague and nonspecific, and the disease may elude diagnosis for some time. Etiology/pathophysiology Hyperparathyroidism classically is divided into primary and secondary forms. The most com- mon cause of the primary form is a parathyroid adenoma that secretes parathyroid hormone. The excess parathormone results in a derangement of calcium, phosphate, and bone metabol- ism. This process has been linked to rearrangements of segments of chromosome 11, thus allow- ing for overexpression of a regulatory protein [100]. Inactivation of tumor suppressor genes and mutations of calcium-sensing receptor genes also have been postulated [100]. The secondary form is caused by gland hyperplasia in response to low-serum calcium levels resulting from renal failure or intestinal malabsorption. This disorder may result in alterations of bone because of the increased levels of parathormone, which stimulates increased bone resorption [100]. Image of choice for diagnosis Panoramic and periapical radiographs are the ideal imaging methods to evaluate jaw changes that may occur with the disorder. Image hallmarks In primary hyperparathyroidism, the jaw changes may occur as unilocular or multilocular ra- diolucencies referred to as ‘‘brown tumors’’ [100]. Microscopically, they are identical to central giant cell granuloma. In addition, the changes may consist of a generalized alteration of medul- lary bone that exhibits a ‘‘ground glass’’ appearance; however, this change is more commonly seen in secondary hyperparathyroidism (Fig. 21). This change usually is accompanied by a loss of lamina dura. Distinct lytic lesions are less common in secondary hyperparathyroidism.
    • 24 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 21. Hyperparathyroidism. Management Primary hyperparathyroidism is treated with parathyroidectomy with a 90% success rate [100]. Those patients refractory to or not surgical candidates are managed medically with oral- phosphate supplements, estrogen therapy, and calmodulin to decrease serum calcium [100]. The secondary form is treated by correcting the underlying medical condition [100]. DEVELOPMENTAL ODONTOGENIC CYSTS Dentigerous cyst Frequency/incidence Dentigerous cysts are the second most common odontogenic cyst and account for 24% of true jaw cysts [104]. The frequency of dentigerous cysts is 1.44 per 100 unerupted teeth [105]. The mandibular third molars are the most commonly involved teeth. Signs and symptoms Most patients with dentigerous cysts are asymptomatic. Large cysts may cause expansion of bone in the involved area. Etiology/pathophysiology The dentigerous cyst represents a pathologic cystic cavity lined by follicular epithelium that develops around the crown of an impacted tooth [106]. It is capable of significant enlargement and destruction of bone. The cause of its development is unknown. Image of choice for diagnosis The panoramic radiograph is an ideal imaging method to detect dentigerous cysts. The cysts also may be detected with periapical radiographs. Image hallmarks The radiographic presentation of the dentigerous cyst is a well-circumscribed, unilocular ra- diolucency around the crown of an impacted tooth (Fig. 22). The cyst measures from 3 to 5 mm to many centimeters [107]. It typically affects permanent impacted teeth; but in rare incidences,
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 25 Fig. 22. Dentigerous cyst. deciduous teeth may be involved. The cyst is usually an isolated lesion, but several teeth may be affected. Multiple dentigerous cysts may occur without the characteristic features of the nevoid basal cell carcinoma syndrome [108]. Management The treatment of dentigerous cysts is complete enucleation of the cyst and removal of the in- volved impacted tooth. The cystic tissue is submitted for microscopic examination to rule out other aggressive odontogenic lesions. Odontogenic keratocyst Frequency/incidence Odontogenic keratocysts make up approximately 12% of odontogenic cysts [109]. The man- dible is involved in 65% of the cases, and the molar region is the most common location [109]. There is an equal sex distribution. A significant recurrence rate has been reported [110,111], and it has been reported that 8.8% to 12% of patients with odontogenic keratocysts have the nevoid basal cell carcinoma syndrome [110]. Signs and symptoms Most patients with odontogenic keratocysts are asymptomatic; however, some may exhibit pain and swelling of the involved area of the jaw. Etiology/pathophysiology Odontogenic keratocysts most likely develop from remnants of dental lamina. The cause is unknown. Image of choice for diagnosis The panoramic radiograph is an excellent imaging method to demonstrate the odontogenic keratocyst, especially in the posterior regions of the jaws. Periapical radiographs also are able to detect the cyst when it develops in tooth-bearing areas. Image hallmarks Odontogenic keratocysts typically present as unilocular radiolucencies; however, they also may be multilocular, especially large keratocysts (Fig. 23). Keratocysts are often associated
    • 26 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 23. Odontogenic keratocyst. with impacted teeth and resemble dentigerous cysts radiographically. They also can develop in between teeth (lateral periodontal cyst position) and in place of a tooth. In addition, keratocysts may mimic nasopalatine duct cysts [109] and apical periodontal cysts. In some cases, a curved scalloped border may be present [112]. Management Treatment of odontogenic keratocysts is complete removal, ranging from enucleation and curettage to en bloc resection. The treatment depends on many factors, including position and extent of the lesion and patient cooperation. No single treatment is applied to all patients. Recurrent lesions often require more aggressive therapy [113]. Nevoid basal cell carcinoma syndrome Frequency/incidence The incidence of the syndrome is 1 in 57,000 to 1 in 164,000 births [114]. Signs and symptoms Up to 75% of patients have odontogenic keratocysts of the jaws, and these often develop before the age of 20 [114]. These cysts are situated around the crowns of unerupted teeth and between teeth. The basal cell carcinomas usually develop during or after puberty; and by the age of 40, up to 97% of affected persons exhibit these changes. Most patients have palmar and/or plantar pits. Other potential abnormalities include frontal bossing, hypertelorism, stra- bismus, palate abnormalities, calcified falx cerebri, and macrocephaly [115]. Etiology/pathophysiology The nevoid basal cell carcinoma syndrome is an autosomal dominant disorder, and an abnor- mality of chromosome 9 has been identified in those patients who have the syndrome [116]. Its expression is thought to be caused by a modification of a tumor suppression gene. Image of choice for diagnosis The panoramic radiograph is the image of choice to identify the cystic lesions of the jaws.
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 27 Fig. 24. Nevoid basal cell carcinoma syndrome. (From Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 2nd edition. Philadelphia: WB Saunders; 2002.) Image hallmarks The jaw changes represent single or multiple unilocular radiolucencies, usually situated around the crowns of unerupted teeth and between the roots of teeth (Fig. 24). Management The radiolucent lesions microscopically represent odontogenic keratocysts, and treatment is the same for those in the non-syndrome patient. Lateral periodontal cyst Frequency/incidence Lateral periodontal cysts are relatively rare, comprising approximately 8% of cysts of the jaws [117]. The lesion typically is seen in adults and most commonly in the sixth decade of life. There is no sex predilection [118,119]. Signs and symptoms The lateral periodontal cyst is asymptomatic and usually discovered on routine radiographs. Etiology/pathophysiology Lateral periodontal cysts develop from rests of dental lamina found in the periodontal mem- brane and interradicular bone. The cause is unknown. The cysts are not associated with an in- flammatory process. Image of choice for diagnosis Lateral periodontal cysts are identified on panoramic and periapical radiographs. Image hallmarks The lesion typically is viewed as a small, well-circumscribed radiolucency between the roots of vital teeth (Fig. 25). It may have a sclerotic border [120]. Most lesions occur in the mandib- ular canine-premolar area and the maxillary incisor to first premolar region [121]. The odonto- genic keratocyst may give a similar radiographic appearance. Management Lateral periodontal cysts are treated by enucleation. Recurrence is rare [122].
    • 28 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 25. Lateral periodontal cyst. Calcifying odontogenic cyst Frequency/incidence Calcifying odontogenic cysts are rare and represent 1% to 2% of all odontogenic lesions [123]. They are found in patients of a broad age range, and there is equal sex distribution. The man- dible and maxilla are almost equally affected, and 65% of cysts occur in the anterior regions of the jaws [124]. Signs and symptoms Most calcifying odontogenic cysts are asymptomatic but enlargement of bone may occur. The cysts also may develop primarily in the gingiva with no bone involvement. Etiology/pathophysiology The cause of calcifying odontogenic cysts is unknown. The cysts most likely develop from dental lamina. Image of choice for diagnosis Calcifying odontogenic cysts are detected on panoramic and periapical radiographs. Image hallmarks The radiographic appearance of calcifying odontogenic cysts is variable (Fig. 26). They may be unilocular or multilocular. The cysts are usually well-outlined and may contain areas of calcification [125]. They may also develop in association with odontomas, and they are often associated with impacted or unerupted teeth and found in between teeth.
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 29 Fig. 26. Calcifying odontogenic cyst. (From Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 2nd edition. Philadelphia: WB Saunders; 2002.) Management Treatment of calcifying odontogenic cysts is enucleation but they may require more aggressive therapy depending on the extent of the lesion and the microscopic findings [126]. ODONTOGENIC NEOPLASMS Ameloblastoma Frequency/incidence Ameloblastomas represent 1% of all oral tumors, and 80% to 85% occur in the mandible. There is no sex predilection [127]. The average age at diagnosis is 33 years [128]. Signs and symptoms Ameloblastomas are infiltrating, locally aggressive neoplasms that can destroy bone, per- forate cortical plates, and cause considerable expansion. They are generally considered to be slowly growing, and there usually is no associated pain [127]. In rare instances, the ameloblas- toma has metastasized; and in 75% to 80% of cases, the lungs represented the metastatic focus [129]. Ameloblastomas also may develop outside of bone on the gingiva.
    • 30 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 27. Cropped radiograph of an ameloblastoma. (Courtesy of Dr. Arthur Gonty, Lexington, KY.) Etiology/pathophysiology Ameloblastomas arise from odontogenic epithelium, principally dental lamina, and possibly dentigerous cyst lining. Peripheral ameloblastomas also may develop from the basal cell layer of gingival surface epithelium. The cause is unknown. Image of choice for diagnosis The image of choice for the detection of ameloblastomas is the panoramic radiograph. The periapical radiograph may also be used to detect ameloblastomas and other jaw proliferations. CT also is used to determine the extent of the lesion. Image hallmarks Ameloblastomas have a variable radiographic appearance. The classic description is that of a multilocular, well-defined radiolucency of the posterior mandible in the molar-ramus region (Fig. 27) [130]. Ameloblastomas also may be unilocular, and they occur in the anterior mandible and maxilla. They may be associated with impacted teeth and may occur in between teeth. Management Complete surgical excision is the treatment for ameloblastomas. Reported treatment ranges from curettage to radical resection depending on the type of ameloblastoma, its location, and the extent of the lesion. More radical treatment may lower the recurrence rate [131], which varies greatly in published reports [127]. Fifty percent of all recurrences occur within 5 years of surgery [127]. Calcifying epithelial odontogenic tumor Frequency/incidence Calcifying epithelial odontogenic tumors are rare, representing 1% of all odontogenic tumors [132]. Most of the tumors occur in men and women from the ages of 20 to 40 years. There is equal sex distribution [133]. The tumors occur twice as often in the mandible than the maxilla. Many of the reported cases have developed in association with impacted teeth.
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 31 Fig. 28. Calcifying epithelial odontogenic tumor. (Courtesy of Dr. Samuel McKenna.) Signs and symptoms Most cases of calcifying epithelial odontogenic tumors are asymptomatic. They may cause cortical expansion, and may develop in the gingiva as an asymptomatic swelling. Etiology/pathophysiology The origin of calcifying epithelial odontogenic tumors is believed to be reduced enamel epi- thelium or stratum intermedium [134]. The cause is unknown. Image of choice for diagnosis The image of choice for the evaluation of jaw cysts and neoplasms is the panoramic radio- graph. CT is helpful to determine the extent of the lesion. Image hallmarks The radiographic appearance of a calcifying epithelial odontogenic tumor is variable. It may be unilocular or multilocular and associated with an impacted tooth (Fig. 28). The tumor’s out- line ranges from well circumscribed to irregular, and it may exhibit areas of radiopacity. Management The treatment of calcifying epithelial odontogenic tumors is surgical excision. Maxillary lesions may require more aggressive therapy if vital structures are involved [134]. Recurrences may develop up to several decades after initial therapy [134]. Adenomatoid odontogenic tumor Frequency/incidence Adenomatoid odontogenic tumors are the fifth most common odontogenic tumors, with an incidence of between 2.2% and 7.1% [135]. They occur most commonly in the second decade of life, primarily in women [136]. The tumors are most often seen in the anterior regions of the jaws, usually the maxilla. Signs and symptoms Most cases of adenomatoid odontogenic tumor are asymptomatic. The tumors may cause cortical expansion. They are often discovered on routine radiographic examination or when a patient is being evaluated for a delay in eruption of a permanent anterior tooth.
    • 32 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 29. Adenomatoid odontogenic tumor. (Courtesy of Dr. William Dobbin, Manchester, NH.) Etiology/pathophysiology The tumors most likely arise from dental lamina. The cause is unknown. The tumors have been described as occurring with other odontogenic neoplasms [137]. Image of choice for diagnosis The panoramic and periapical radiographs are the images used to detect this tumor. Image hallmarks Adenomatoid odontogenic tumors present as well-defined, unilocular radiolucencies (Fig. 29). Most cases are associated with the crown of an unerupted tooth, usually a maxillary cuspid. They also occur between the roots of anterior teeth. The radiolucency may show a flocculent pattern of discrete, noncoalescing radiopacities [138]. Management Treatment of adenomatoid odontogenic tumors is surgical enucleation. The lesion usually is well encapsulated, and recurrence, even after conservative therapy, is rare to nonexistent [135]. Odontogenic myxoma Frequency/incidence Odontogenic myxomas are rare, accounting for 3.1% to 11.8% of all odontogenic tumors [139]. They involve the mandible more than the maxilla and are most common in men and women in their teens and 20s. There is a slight female predilection [140]. Signs and symptoms Most cases of odontogenic myxoma are asymptomatic; however, enlargement of the involved bone may be present. Etiology/pathophysiology Odontogenic myxomas are benign but potentially locally aggressive neoplasms of odonto- genic ectomesenchyme. Their cause is unknown. Image of choice for diagnosis Odontogenic myxomas are best visualized on the panoramic radiograph. Small myxomas situated between teeth also may be seen on periapical radiographs. CT is helpful in determining the extent of the lesion.
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 33 Fig. 30. Odontogenic myxoma. (From Fonseca RJ. Oral and maxillofacial surgery. 1st edition. Philadelphia: WB Saunders; 2000.) Image hallmarks The radiographic appearance of odontogenic myxomas is variable. The classic description is a circumscribed, multilocular (‘‘soap bubble’’) radiolucency of the body and posterior mandible (Fig. 30) [141]. They can be unilocular, especially when they occur between teeth, and they may be associated with the crown of an unerupted tooth. Management The treatment of odontogenic myxomas varies from curettage to en bloc resection, depending on the location and extent of the lesion. Recurrence rates range from 10% to 33% [140]. Odontoma Frequency/incidence Odontomas are the most common odontogenic proliferations. Their frequency has been reported to be 46% to 74% of all odontogenic tumors [139,142]. Most odontomas, however, represent hamartomas rather than true neoplasms. They usually are found in the first to third decades of life, and there is an equal sex distribution. Signs and symptoms Odontomas usually are asymptomatic; they are found on routine dental radiographs and when a patient is being evaluated for a delay in eruption of a permanent tooth [143]. In rare instances, multiple odontomas have been described in systemic abnormalities, such as cleidoc- ranial dysostosis and Gardner syndrome [144]. Etiology/pathophysiology Most odontomas represent developmental anomalies and not true neoplasms [145]. The cause is unknown. Image of choice for diagnosis Odontomas are seen on both panoramic and periapical radiographs. Image hallmarks Odontomas exhibit a varying radiographic appearance. Compound odontomas are charac- terized by the formation of tooth-like structures. There may be a peripheral area of radio- lucency. Complex odontomas are radiopaque and represent a haphazard arrangement of dental hard and soft tissue (Fig. 31). A radiolucent rim also may be present. Odontomas usually are seen adjacent to the crown of an unerupted tooth and between the roots of teeth [146].
    • 34 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 31. Odontoma. Management Treatment of odontomas is conservative surgical removal (enucleation). Recurrences are rare to nonexistent [147]. Ameloblastic fibroma Frequency/incidence Ameloblastic fibromas are rare odontogenic neoplasms, representing 2.5% of all odontogenic tumors [148]. The average age at the time of diagnosis is 15 years. More than 80% of cases occur in mandible in the premolar-molar region. Fig. 32. Ameloblastic fibroma. (Courtesy of Dr. Douglas Damm, Lexington, KY.)
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 35 Signs and symptoms Most ameloblastic fibromas are asymptomatic. They may cause expansion of the involved bone. They are often discovered when a patient is being evaluated for a delay in eruption of a permanent tooth. Etiology/pathophysiology Ameloblastic fibromas are benign, encapsulated odontogenic neoplasms of both odontogenic epithelium and mesenchyme. Their cause is unknown. Image of choice for diagnosis The image of choice for detection is the panoramic radiograph. Periapical radiographs may also be used to detect the lesion. Image hallmarks The ameloblastic fibroma is usually seen as a unilocular radiolucency associated with the crown of an unerupted posterior mandibular tooth (Fig. 32) [149]. It often exhibits a sclerotic border and, at times, may be compartmentalized. Management Treatment is enucleation and curettage. Recurrences occasionally have been described and follow-up is important [150]. Ameloblastic fibro-odontoma Frequency/incidence The incidence of ameloblastic fibro-odontomas ranges from 1.7% to 3.1% of all odontogenic neoplasms [134,151]. They occur most commonly in the posterior regions of the jaws in the first two decades of life. Eighty-three percent are associated with unerupted teeth [151]. Signs and symptoms Most ameloblastic fibro-odontomas are asymptomatic. They may be associated with enlarge- ment of the involved bone, and they often are detected when the patient is evaluated for an un- erupted tooth. Fig. 33. Ameloblastic fibro-odontoma. (Courtesy of Dr. Samuel McKenna.)
    • 36 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Etiology/pathophysiology Ameloblastic fibro-odontomas are neoplasms of odontogenic epithelium and mesenchyme. They have the capacity to form dental hard tissue [152]. The cause is unknown. Image of choice for diagnosis The panoramic radiograph is the image of choice for the detection and evaluation of amelo- blastic fibro-odontomas. Image hallmarks Ameloblastic fibro-odontomas typically appear as mixed radiolucent-radiopaque lesions as- sociated with the crown of one or more unerupted posterior teeth (Fig. 33). They are more com- mon in the mandible. The affected teeth may be displaced away from the normal tooth-bearing area [153]. The radiopaque material has the radiodensity of tooth structure. Management Treatment is by conservative surgical enucleation or curettage with removal of the associated unerupted teeth. Maintenance of the teeth may lead to recurrence [151,153]. NONODONTOGENIC NEOPLASMS Central giant cell granuloma Frequency/incidence More than 60% of all central giant cell granulomas occur before the age of 30 years. Two thirds of all cases develop in women, and the mandible is affected approximately 70% of the time. The lesion affects the anterior portions of the jaws more frequently than the posterior seg- ments, and it is not uncommon for the lesion to cross the midline of the mandible [154]. Fig. 34. Central giant cell granuloma.
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 37 Signs and symptoms Most central giant cell granulomas are asymptomatic. They may cause expansion and perfo- ration of bone, and a minority of cases may be associated with pain and paresthesia [155]. Etiology/pathophysiology The cause of central giant cell granuloma is unknown. There is no consensus that this process represents a true neoplasm; however, the lesion may exhibit aggressive growth and destroy sig- nificant bone. The microscopic features are the same as seen in the brown tumor of hyperpar- athyroidism [154]. Image of choice for diagnosis The image of choice is the panoramic radiograph. Periapical radiographs may also be used to detect these lesions, especially those that develop in tooth-bearing areas of the jaws. Image hallmarks Most central giant cell granulomas appear as well-defined multilocular radiolucencies (60%) of the anterior mandible below the apices of involved teeth (Fig. 34). Root resorption and tooth displacement may occur. The granulomas also may appear unilocular (39%) [154]. They may develop between teeth and be associated with unerupted teeth. Management The usual treatment of central giant cell granuloma is aggressive curettage; the recurrence rate with this treatment ranges from 15% to 20%. More aggressive lesions may be treated by resection. Nonsurgical management has been considered recently and has included intralesional injection of corticosteroids and the systemic use of calcitonin [156]. Ossifying fibroma Frequency incidence Ossifying fibromas are most common during the third and fourth decades of life, primarily in women. Most cases develop in the mandible, but 20% develop in the maxilla [57,157]. Signs and symptoms Most ossifying fibromas are asymptomatic. Some will exhibit enlargement of the involved bone [57]. Fig. 35. Ossifying fibroma. (Courtesy of Dr. John Cramer, Corbin, KY.)
    • 38 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Etiology/pathophysiology Central ossifying fibromas represent true primary neoplasms of bone. The cause is un- known. Image of choice for diagnosis The panoramic radiograph is the image of choice for detecting the lesion. Periapical radio- graphs may also be used to identify ossifying fibroma. Image hallmarks Ossifying fibromas may be either unilocular or multilocular (Fig. 35). They usually are well defined and may have a sclerotic border. Depending on the degree of mineralization of the tumor’s connective tissue, the fibromas may appear radiolucent or radiolucent/radiopaque. Displacement of the roots of teeth also may be seen [157,158]. Management Conservative surgical treatment is the treatment of choice for most ossifying fibromas. Ag- gressive tumors may need more aggressive therapy. The tumor usually is separated from sur- rounding normal bone and typically can be removed in a single piece. This is in contrast to focal osseous dysplasia, a reactive process with a similar radiographic picture, which blends with surrounding normal bone and is removed in small fragments [57]. Osteoblastoma/cementoblastoma Frequency/incidence Osteoblastomas and cemetoblastomas are believed to represent the same neoplastic process. The main difference is that cementoblastomas are attached to the root of an involved tooth and originate from progenitor cells in the periodontal membrane rather than medullary bone as in osteoblastomas. Both are rare neoplasms of the jaws. Approximately 70% of osteoblastomas have been reported to occur in the mandible [159]. They show a mean age of occurrence of 20 years, with a range of 5 to 59 years [159]. Cementoblastomas typically occur before the age of 30 years, with a range of 6 to 75 years [159]. More than 90% of cases occur in the molar-premolar region of the jaws, and the mandible is more commonly affected [159]. Signs and symptoms Most osteoblastomas and cementoblastomas exhibit enlargement of the involved bone at the time of discovery. Most patients will complain of spontaneous pain. Displacement of teeth may occur [160,161]. Etiology/pathophysiology The lesions represent true neoplasms of osteoblasts and cementoblasts. The cause is unknown. Image of choice for diagnosis The panoramic radiograph is the image of choice for detection. Periapical radiographs are helpful in determining whether attachment to an involved tooth may exist, and CT is useful to determine the extent of the lesion. Image hallmarks The osteoblastoma usually appears as a well-circumscribed lesion that exhibits radiolucent and radiopaque areas (Fig. 36). In some cases, it will not be well delineated from surrounding bone. It is not continuous with the root surface of involved teeth. The cementoblastoma has a distinct radiographic appearance. It typically is well defined from surrounding bone, and it ap- pears attached to the root of a tooth. The cementoblastoma usually is a mixed radiolucent/ radiopaque lesion or one that is mostly radiopaque. The periodontal membrane space of the involved tooth characteristically is continuous with a radiolucent rim that surrounds the lesion [159,161,162].
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 39 Fig. 36. Osteoblastoma/cementoblastoma. (Courtesy of Dr. Robert Hastings, Campbellsville, KY.) Management Osteoblastomas of the jaws are treated by complete surgical removal, often by curettage. Re- currence is uncommon. Cementoblastomas are treated by the surgical removal of the affected tooth and tumor mass. Removal of the mass and only the root portion of the tooth that is involved also has been utilized [161,162]. Follow-up information on this technique is not well established. Osteosarcoma Frequency/incidence Osteosarcomas of all bones in the skeleton affect only 1 in 100,000 persons each year. Osteo- sarcomas of the jaws account for approximately 5% of all osteosarcomas. Lesions generally oc- cur in the third decade of the life in the jaws, but osteosarcomas of long bones usually occur in the second decade of life. Men have a slightly increased incidence, and the mandible and maxilla are equally affected [163,164]. Signs and symptoms Cortical expansion and pain are the most common symptoms of an osteosarcoma. Depend- ing on the location within the jaws, paresthesia and tooth mobility may be present [165,166]. Etiology/pathophysiology An osteosarcoma is a malignancy of bone-forming cells. The cause is unknown, but there is an increased incidence in the growth plates of long bones. There also is an association of the disease with other pathologic processes that involve increased bone remodeling and growth and previous radiation therapy [163,164]. Image of choice for diagnosis The panoramic radiograph is the image of choice for visualizing the disease. CT is helpful in determining the extent of the process.
    • 40 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 37. Osteosarcoma. (Courtesy of Dr. Joseph Finelli, Syracuse, NY.) Image hallmarks The lesion of osteosarcoma may be radiolucent, mixed radiolucent/radiopaque, or radiopaque (Fig. 37). It may exhibit a mottled appearance, and the borders are commonly ill defined. The peripheral borders may exhibit a radiating growth pattern of tumor bone referred to as a ‘‘sun- burst’’ pattern, which is present in approximately 25% of the cases. Those lesions that arise in tooth-bearing areas may involve periodontal membrane and produce a widened space. This is not an exclusive feature of osteosarcoma because it may be seen with other malignancies [163,166]. Management Surgical resection is the treatment of choice for osteosarcomas. Pre- and postoperative che- motherapy and postoperative radiation also are utilized. The survival rate does not appear to increase with the use of adjunctive chemotherapy as in long bones [163,165,166]. Up to 18% of the patients will exhibit metastasis, usually to lung. Uncontrolled local recurrence is the main cause of death in patients with osteoscarcoma of the jaws. Mardinger et al [163] reported a 3-year survival rate of 72% for their patients. Chondrosarcoma Frequency/incidence Chondrosarcomas are rare, malignant neoplasms. They are reported to account for less than 3% of all head and neck tumors. They occur most often in the third to sixth decades of life. Men show a very slight predilection. There is equal distribution in the mandible and maxilla [167]. Signs and symptoms The most common symptom of chondrosarcoma of the orofacial structures is a painless swel- ling or mass. Other symptoms include pain, loose teeth, epistaxis, nasal obstruction, and visual or ocular changes [168]. Etiology/pathophysiology Chondrosarcoma is a malignancy of cartilage-forming cells. The cause is unknown.
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 41 Fig. 38. Chondrosarcoma. (Courtesy of Dr. Robert Morris, Lexington, KY.) Image of choice for diagnosis The panoramic radiograph is the image of choice for detection. CT scan is used to evaluate the extent of the tumor. Image hallmarks Chondrosarcomas typically appear as ill-defined lesions that may be radiolucent or mixed radiolucent/radiopaque (Fig. 38). They may also induce widening of the periodontal membrane space [169]. Management Surgical resection is the treatment of choice for chondrosarcomas. Chemotherapy and radi- ation therapy normally are not effective against these neoplasms. The prognosis of chondrosar- coma of the jaws is poor [167,169]. Ewing sarcoma Frequency/incidence Ewing sarcomas are rare, malignant neoplasms that predominantly occur in the first two dec- ades of life. About two thirds of all reported Ewing sarcomas occur in the lower skeleton. Less than 1% of cases occur in the facial skeleton. The mandible is more commonly involved than the maxilla. Sixty-five percent of the tumors occur in males [170]. Signs and symptoms The most common symptoms are pain and swelling in the affected area. Loosening of teeth also may occur [170]. Etiology/pathophysiology Ewing sarcoma is a malignancy of primitive cells, thought to be derived from neuroectoderm [170]. The cause is unknown.
    • 42 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 39. Ewing sarcoma. (From Fonseca RJ. Oral and maxillofacial surgery. 1st edition. Philadelphia: WB Saunders; 2000.) Image of choice for diagnosis The image of choice for the identification of Ewing sarcoma is the panoramic radiograph. CT is helpful to determine the extent of the neoplasm. Image hallmarks The typical radiographic pattern is that of an ill-defined radiolucency (Fig. 39). The tumor may stimulate replication of cortical bone identical to that seen in proliferative periostitis [171,172]. Management Management of Ewing sarcoma consists of surgical resection and the use of radiation therapy and multiple chemotherapeutic agents. With the use of multiple modalities for treatment, the estimated 5-year survival rate for the tumor at a major treatment institution is 83% [170]. Metastatic neoplasms of the jaws Frequency/incidence Metastasis to the jaws is not rare. The most common location is the molar region of the man- dible [173]. The most common primary sites in women are breast, adrenal gland, colorectal sys- tem, genital organs, and thyroid gland. Breast is the most common organ, representing 30% of cases [174]. The most common primary sites in men are lung, prostate, kidney, bone, and adre- nal gland [173]. 30% of cases of jaw metastases represent the initial sign of the cancer. The male- to-female ratio is 1 to 2 [174]. Signs and symptoms Signs and symptoms range from mild soreness and pain to facial deformity and numb chin syndrome [174]. Loose teeth also are a sign. Etiology/pathophysiology Metastatic cancer to the oral cavity is believed to result from hematogenous spread from the primary site. Image of choice for diagnosis The panoramic radiograph and periapical films are the images of choice for detecting meta- stasis to the jaws.
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 43 Fig. 40. Metastatic neoplasms. Image hallmarks The typical radiographic presentation of jaw metastasis is that of a radiolucency that is either poorly defined or well outlined (Fig. 40). Certain cancers, such as breast and prostate, may in- duce new bone formation and create a mixed radiolucent/radiopaque lesion [175]. Management Metastasis to the jaws indicates that the therapy for the primary cancer has failed to control the disease. Treatment consists of modalities used for disseminated primary disease. Generally, patients diagnosed with metastatic disease of the jaws do not survive more than 1 year [173]. HEMATOLOGIC/LYMPHORETICULAR DISEASES Neutropenia Frequency/incidence Neutropenia is a rare, pathologic reduction of neutrophils that is subdivided into congenital (hereditary) and acquired forms. The congenital form commonly manifests in infants and ado- lescents. The acquired form more commonly occurs in later life [176]. Signs and symptoms Patients with neutropenia exhibit an increased incidence of bacterial infections. They exhibit fever, malaise, weakness, and symptoms of an infection at a specific anatomic site. In the oral cav- ity, patients typically develop aphthous-like ulcers, gingivitis, and periodontal bone loss [176,177]. Etiology/pathophysiology Neutropenia is defined as a circulating neutrophil count below 1500 mm3. Primary or con- genital neutropenia usually is the result of a genetic abnormality. Acquired neutropenia may
    • 44 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 Fig. 41. Neutropenia. (Courtesy of Dr. John Cramer, Corbin, KY.) result from a variety of causes, including chemical and drug exposure, radiation, and bacterial and viral infections. Because the neutrophil is the primary defense against bacterial infections, the patient experiences an increased incidence of infections from these agents [176,177]. The most common organisms are gram-negative bacteria and Staphylococcus aureus. Image of choice for diagnosis The image of choice for detection of the radiographic changes are panoramic and periapical radiographs. Image hallmarks The oral radiographic changes of neutropenia are areas of significant periodontal bone loss (Fig. 41) [177]. Management The infections that result from neutropenia are treated with appropriate antibiotics. Human granulocyte colony-stimulating factor has shown promise, and patients are encouraged to main- tain meticulous oral hygiene to decrease the effects of periodontal bacterial flora [176,177]. Langerhans cell histiocytosis Frequency/incidence This is an uncommon disorder of Langerhans histiocytes in which 10% to 20% of all cases affect the jaws. The mean age of diagnosis of the process in the jaws is reported as 18 years. The mandible is more often affected than the maxilla, and it is more common in men [178]. Signs and symptoms Bone lesions are the most common presenting symptoms of Langerhans cell disease [178]. Pa- tients may present with lymphadenopathy. Infants may exhibit a skin rash and necrotizing areas of the gingiva and alveolar ridge. Older children and adults also may exhibit changes, including pain, gingival swelling, tooth mobility, parasthesia, and facial swelling [178,179].
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 45 Fig. 42. Langerhans cell histiocytosis. (Courtesy of Dr. James White, Cinncinnati, OH.) Etiology/pathophysiology Langerhans cell histiocytosis represents a symptom complex characterized by the pathologic accumulation of histiocytic cells that normally populate epidermis, mucosa, lymph nodes, and bone marrow and are involved with the presentation of antigens to T lymphocytes. The cause is unknown. The process is subdivided into three categories but overlap of symptoms exists [180,181]. The categories include acute disseminated, chronic multifocal, and a process that affects one or multiple bones without soft tissue involvement (eosinophilic granuloma of bone). The acute disseminated form affects soft tissue, lymph nodes, and visceral organs and generally does not affect bone. The chronic multifocal form exhibits bone, skin, and visceral involvement. Image of choice for diagnosis The images of choice to detect the jaw lesions of Langerhans cell histiocytosis are panoramic and periapical radiographs. Image hallmarks The jaw lesions of Langerhans cell histiocytosis are characterized by a radiolucency that often is present in interradicular or periapical bone (Fig. 42). The histiocytosis often mimics an inflam- matory process [178] and may be poorly defined. Involved teeth may totally lack alveolar bone support and appear ‘‘floating in soft tissue.’’ Multiple lesions may be present. Management Once the microscopic diagnosis of Langerhans cell histiocytosis is established, the patient must be evaluated for multifocal involvement. Localized jaw lesions usually are treated by cur- ettage. Low-dose radiation may be used for less accessible bone lesions [178]. The other forms require systemic therapy, including chemotherapy. Eosinophilic granuloma of the jaws has a
    • 46 D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 good prognosis, with a reported recurrence rate of 1.6% to 25% [178,179]. Death is rare in the chronic disseminated form; the acute disseminated form has a poor prognosis [180,181]. Non-Hodgkin lymphoma Frequency/incidence Approximately 24% of non-Hodgkin lymphomas develop in extranodal sites. Primary intra- osseous lymphoma accounts for 5% of extranodal lymphomas, and jaw involvement is rare. When the oral cavity is involved, the jaws are affected approximately 30% of the time [182, 183,184]. Signs and symptoms Lymphomas of the head and neck and oral cavity primarily manifest as a soft tissue swelling. Those that involve the bone of the jaws often are associated with swelling of the involved area, pain, tooth mobility, and cervical lymphadenopathy [184,185]. Etiology/pathophysiology Most lymphomas of the jaws are B-cell lymphomas. The cause is unknown. The development of lymphomas has been associated with the Epstein-Barr virus and human T-cell lymphoma virus 1 [186]. Image of choice for diagnosis Panoramic and periapical radiographs are utilized to detect the change of the jaws associated with lymphoma. CT, MRI, and bone scintography also are helpful in evaluating the extent of involvement of the process. Image hallmarks Non-Hodgkin lymphoma of the jaws appears as single or multiple areas of ill-defined bone destruction, which may exhibit areas of reactive bone formation (Fig. 43) [185–187]. These areas may affect alveolar bone and mimic inflammation. Management Oral lymphoma is treated by radiation and/or chemotherapy in association with other site involvement. The survival time for patients with oral lymphoma is 11 to 38 months [185]. Fig. 43. Non-Hodgkin lymphoma. (Courtesy of Dr. William Schiro, Lansing, MI.)
    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 47 Fig. 44. Multiple myeloma. Multiple myeloma Frequency/incidence Multiple myeloma is a malignancy of plasma cells with variable systemic presentations. It is a rare disorder that is usually seen after the age of 40 years, with a mean age of occurrence of 60 years [188,189,190]. Signs and symptoms Multiple myeloma may be asymptomatic [191] or associated with the signs and symptoms of anemia, leukopenia, thrombocytopenia, hypercalcemia, and renal disease [188,192]. Oral in- volvement may be associated with jaw and tooth pain, tooth mobility, paresthesia, soft tissue swelling, and pathologic fracture [188,192]. Etiology/pathophysiology The cause of this plasma cell cancer is unknown. Image of choice for diagnosis The panoramic radiograph is the choice for detecting multiple lesions of myeloma. Periapical radiographs may also detect the changes in alveolar bone. Image hallmarks Multiple myeloma exhibits a varied radiographic appearance. The lesions are radiolucent and may exhibit a well-defined or poorly defined border (Fig. 44). They may be unilocular or multi- locular, and there may be multiple areas of bone destruction. The lesion may lack any reactive or defined border, which gives the lesion a ‘‘punched out’’ appearance [192]. Management Isolated lesions (plasmacytoma) are treated by radiation therapy [190,191]. Disseminated dis- ease is treated by chemotherapy [190]. References [1] Jainkittivong A, Langlais RP. Buccal and palatal exostoses: prevalence and concurrence with tori. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000 Jul;90(1):48–53. [2] Antoniades DZ, Belazi M, Papanayiotou P. Concurrence of Torus Palatinus with palatal and buccal exostoses. Case report and review of the literature. Oral Surg Oral Med Oral Path Oral Radiol Endod 1998;85:552–7.
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    • D.K. White et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 1–53 53 [179] Miyamoto H, Dance G, Wilson DF, Goss AN. Eosinophilic granuloma of the mandibular condyle. J Oral Maxillofac Surg 2000;58(5):560–562. [180] Neville B, Damm D, Allen C, Bouquot J. Oral and Maxillofacial Pathology. 1st ed. Philadelphia, Pennsylvannia: WB Saunders; 1995, 451–453. [181] Neville B, Damm D, White D. Color Atlas of Clinical Oral Pathology. 2nd ed. Philadelphia, Pennsylvannia: Lippincott Williams and Wilkins; 1999, 344–347. [182] Suryananrayan K, et al. Treatment of localized primary non-hodgkin’s lymphoma of bone in children: a Pediatric Oncology Group Study. J Clin Oncol 1999;17(2):456–459. [183] Kawasaki G, et al. Malignant lymphoma of the mandible: report of a case. Oral Surg Ora Med Oral Pathol Oral Radiol Endod 1997;83(3):345–349. [184] Piatelli A, Croce A, Tete S, Artese L. Primary non-Hodgkin’s lymphoma of the mandible: a case report. J Oral Maxillofac Surg 1997;55(10):1162–1166. [185] Kirita T, et al. Oral Surg Ora Med Oral Pathol Oral Radiol Endod 2000;90(4):450–455. [186] Neville B, Damm D, Allen C, Bouquot J. Oral and Maxillofacial Pathology. 1st ed. Philadelphia, Pennsylvannia: WB Saunders; 1995, 431–433. [187] Yamada T, et al. Enlargement of mandibular canal without hyperesthesia caused by extranodal non-Hodgkin’s lymphoma: a case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89(3):388–392. [188] Pisano JJ, Coupland R, Chen S, Miller AS. Plasmacytoma of the oral cavity and jaws-a clinicopathologic study of 113 cases. Oral Surg Ora Med Oral Pathol Oral Radiol Endod 1997;83:265–71. [189] Kyle RA. Multiple myeloma: review of 869 cases. Mayo Clin Proc 1975;50:8–30. [190] Ho CL, Chen CL, Yiang YT, Kao WY. Mandibular mass as the resenting manifestation of IgM myeloma in a 22 year-old man. Ann Hematol 1999;787:93–95. [191] Miller FR, Lavertu P, Wanamaker JR, Bonafede J, Wood BG. Plasmacytomas of the head and neck. Otolaryngol Head Neck Surg 1998 Dec;199(6):614–8. [192] Witt C, Borges AC, Klein K, Neumann H-J. Radiographic manifestations of multiple myeloma in the mandible: a retrospective study of 77 patients. J Oral Maxillofac Surg 1997;55:450–453.
    • Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 Neuroimaging of neck pathology Charles Lee, MDa,*, Tirbod Fattahi, DDS, MDb, Gregory Caldwell, DMD, MDc a Department of Diagnostic Radiology, University of Kentucky Chandler Medical Center, 800 Rose Street, Lexington, KY 40536-0293, USA b Private Practice, Maxillofacial and Facial Esthetic Surgery, 280 East Town Street, Suite C, Columbus, OH 43215, USA c Division of Oral and Maxillofacial Surgery, College of Dentistry, University of Kentucky, 800 Rose Street, Room D-508, Lexington, KY 40536-0297, USA Computed tomography (CT) scanning in the head and neck region has become an integral part of the preoperative evaluation of tumor in defining the full extent of anatomic involvement, and the relation of the tumor to vital vascular and neurologic structures. CT utilizes the same ionizing X rays as plain-film radiography, except the X-ray beam is a thin, collimated linear beam, single but more often multiple; in plain films, a single beam is used, which disperses outward. In CT, the beam attenuated by the object being studied then is detected by a crystal detector and converted to electric energy. In plain film, the attenuated beam then strikes a photoemulsion silver-based film, causing a photochemical reaction, which can then be processed into a photograph. Thus, the CT scan is not a real image of a real object, whereas the plain-film radiograph is. Basically, the object being studied casts a shadow (absorbs the X ray so that it does not penetrate to the film) of a real object. In CT, the final picture is a reconstructed computer simulation. Nevertheless, the simulation does accurately reflect the real anatomy. Unlike plain film, CT scanning takes thousands of small images and actual X-ray beam ex- posures compared with the one shot in plain film. Because the beam is so thin, however, the overall tissue absorption is about equal to, and sometimes less than, the amount of radiation exposure encountered in plain-film radiography. To generate a picture utilizing a matrix, there must be a way to spatially encode the thin X-ray beams of CT. This is accomplished in part by the rotating ring, with single, multiple, and radial beams, by incrementing in 1° intervals the X-ray tube and the crystal detectors around the object being studied, and taking pictures at each incremental rotation. In MR imaging, the spatial encoding is accomplished by applying small, linear, magnetic gradients, and thus frequency encoding, in the X direction, and phase encoding in the Y direction. The current CT technology then utilizes continual scanning but incrementing in a helical or spiral fashion to reduce further the CT scanning times, as opposed to the earlier scan utilizing one slice, stop, move table, and repeat. The latest technology places the crystal detectors in arrays or banks, rather than the linear-or circular-oriented single row of detectors. None of the new technologies increases anatomic resolution but instead reduces scanning times, which benefits CT angiography or cinefluoroscopic CT. The electric signal is then analyzed by Fourier transformation, which further adds informa- tion about spatial encoding. The spatially encoded electric signal, by means of back projection, can then be used to determine how bright or dark each pixel of the picture matrix should be. Resolution as high as a 1024 · 1024 matrix can then be created for temporal bone imaging. More often, a 512 · 512 matrix is used for most CT scanning of the head and neck. To generate a gray-scale image, a zero point needs to be established. CT intensity readings are assigned Hounsfield units (HUs), with the zero value representing water and cerebrospinal * Corresponding author. E-mail address: clee0@pop.uky.edu (C. Lee). 1061-3315/03/$ - see front matter Ó 2003, Elsevier Science (USA). All rights reserved. PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 0 7 - 0
    • 56 C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 fluid (CSF) because the original CT scanners only studied the head. Higher HUs indicate a denser material, which attenuates the CT beams, such as bone with a þ1000 HU, and blood (30– 100 HU) and muscle appear bright or white. Negative HUs include air with a ÿ1000 HU and fat (<ÿ100 HU), which appear to be dark or black. There are no exact HUs for each type of tis- sue because very small volumes of the tissue being analyzed may not be accurately measured due to the partial volume averaging of an adjacent tissue type. In addition, the HUs of water, using the same CT machine, vary each week, which is why they are routinely calibrated with a phantom disc of reference density. The main advantage of CT in head and neck imaging is the ability to capture entire slices in less than a second, which is advantageous in the uncooperative, moving patient. MR imaging requires at least a 3- to 4-minute scanning time without motion. The rapid MR scanning tech- niques do not provide the same high spatial resolution of the conventional MR pulse sequences. Rather, the fast MR techniques are better for MR angiography or cinescopic imaging, such as joint motion or cardiac imaging. The other advantage with CT compared with MR imaging is in determining whether there is bone destruction. Bone destruction can be implied on MR imaging by abnormal signal where bone should be. However, the CT often shows far more bony destruction than what was pre- dicted by MR imaging. Yet the two may actually be complementary. Because patients tolerate CT better than MR imaging, and CT does not have the many dangers and contraindications of MR imaging, CT probably is the best first study; however, if the soft tissue information is not answered by CT, MR imaging should also be obtained. This article focuses on CT scanning of various head and neck pathologies with occasional MR imaging, whenever it was the better method. The findings of both are discussed. Sialadenitis [1] Frequency/incidence The incidence of sialadenitis depends on the population at risk and whether the causative agent is viral, bacterial, or related to sialolithiasis (stones), autoimmune disorders, or iatrogenic. For instance, postoperative acute bacterial infections occur in 0.004% to 0.74% of patients after major oral surgical procedures, whereas the incidence would be much less in non-surgical patients. Viral causes are uncommon, with mumps being the most common. Sialadenitis is a common occurrence following oral cavity radiation therapy for carcinoma. Signs and symptoms The affected glands are swollen, tender, and painful, and may be enlarged. The face may be swollen, and the patient may have fever. If the causative agent is sialolithiasis, sharp pain may be present. In postradiation sialadenitis, the mouth is dry and painful and eating may not be tolerated. Etiology/pathophysiology The most common viral organisms producing sialadenitis are rubella and various staphylo- coccal and streptococcal bacterial agents. As the gland becomes swollen and enlarged, the ducts may become obstructed and begin to dilate. Eventually, the infection may rupture out of the gland to produce floor-of-the-mouth or upper neck abscesses. With chronic inflammation of the submandibular gland, the palpable mass, or stone, may be referred to as a Kuttner tumor. Of these stones, 80% to 90% occur in the Wharton duct because of its low gravity–dependent location, in addition to factors such as an alkaline pH level, which favors stone formation. Nearly all stones (85%) occurring within the Wharton duct appear toward the distal end, and not often within the gland itself. Only 10% to 20% of stones occur in the Stensen duct. The more superficial location of the Stensen duct makes the parotid gland more prone to infection than the submandibular gland.
    • C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 57 Image of choice for diagnosis CT demonstrates the calculi well in sialolithiasis. MR imaging, however, is much better for demonstrating dilation of the intraductal portions of the affected salivary gland. Therefore, the imaging method will depend on the clinical cause of the acute sialoadenitis. Sialography is contraindicated in acute suppurative sialoadenitis because it may exacerbate the infectious proc- ess and cannulation may further injure the already swollen duct opening. Image hallmarks The most common appearance on CT scan is a high-density stone seen in the floor of the mouth (Fig. 1). The affected gland may be enlarged and there may be secondary signs of inflam- mation, such as fat stranding. Intraductal dilatation is better seen on MR imaging as enlarged linear branching structures. Both modalities also demonstrate extensive reactive lymph nodes of which some may be enlarged by size into the adenopathic range (>1.0- or 1.5-cm diameter). With chronic dilatation, a ranula may develop as well (see section on ranulas). Fig. 1. Sialadenitis. Axial postcontrast CT shows enlarged bilateral submandibular glands with enlarged ducts (arrows) seen as branching low-density structures.
    • 58 C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 Management Surgical excision is the treatment of choice in acute suppurative bacterial sialoadenitis if a well-defined fluid pocket is seen representing abscess within the affected glands and if the gland ruptures into the adjacent soft tissues. Removal of the obstructing stone is also necessary. If there are no discrete abscess pockets, then appropriate antibiotic therapy should suffice. Retropharyngeal abscess [2,3] Frequency/incidence The incidence of occurrence for an abscess to occur as a direct extension of a pharyngeal/ tonsillar inflammatory process is rare. The majority of retropharyngeal abscesses represent an extension via the lymphatic system into the lateral retropharyngeal node of Rouviere, thus explaining the characteristic location. If this process ruptures out of the lymph node, the patient is at risk for mediastinitis as the infection accesses the danger space of Gradinsky and Holyoke, which communicates from the skull base down to the mediastinum (this is a potential space between the retropharyngeal and prevertebral space). Very rarely, the suppurative process may spread through the superior constrictor muscle to involve the parapharyngeal fat-filled space. Because of the involvement of the muscle, these patients will present with torticollis, severe neck pain, and a palpable laterally located neck mass. Signs and symptoms If the process directly suppurates through the muscle, the patient will present with torticollis, trismus, and a laterally located neck mass. If the process is confined to the lymph node of Rou- viere, then pain and dysphagia as well as fever will be the presenting symptoms. Etiology/pathophysiology The most common organisms producing pharyngitis/tonsillitis include b streptococci, staph- ylococcus aureus, and H. influenza. The most common abscess is in the lateral retropharyngeal space, caused by infection draining to the location node of Rouviere. The less common cause is direct erosion through the superficial mucosa, muscles, and then to the retropharyngeal space. Image of choice for diagnosis Because of the acuteness of symptoms, pain, and possibly difficulty with breathing, and the fact that the most common population involved is children, CT scan of the neck is the study of choice. MR images would be degraded by motion and breathing-motion artifacts. Image hallmarks The most common appearance on CT scan is a low-density, usually well-defined, and some- times irregularly margined area in the lateral neck region, medial to the carotid space and ante- rior to the prevertebral muscles (Fig. 2). The walls of the abscess may be faintly enhanced with usually well-defined margins when the abscess is contained within the lymph node. If the abscess has ruptured out of the node, the margins will be indistinct. The presence of a well-defined low- density fluid pocket is important for surgical planning. An ill-defined pocket without well-de- fined walls represents an early abscess in the phlegmon stage, and is thus not a well-defined pocket that can be surgically identified and drained. The more significant finding is if the bilateral fat-filled parapharyngeal spaces show irregular contrast enhancement and replacement of low-density fat with soft tissue density with a low- density fluid pocket, then the clinical prognosis is more severe, because infection is now within the space that contains branches of the vagus nerve.
    • C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 59 Fig. 2. Retropharyngeal abscess. Axial noncontrast CT scan in a child shows a low-density pocket of fluid in the right retropharyngeal space. This is the lateral retropharyngeal node of Rouviere, which drains the pharynx with the source of infection being a superficial mucosal pharyngitis. The classic retropharyngeal abscess occurs in this node, which normally can be seen in most children. Note the extensive reactive nodes in the posterior triangles on both sides. If the abscess pocket appears to be more lateral in location and at the angle of the jaw, there may be an infected second branchial cleft cyst (BCC). Management Surgical excision is the treatment of choice if a well-defined fluid pocket is seen. Thyroglossal duct cyst [2,4] Frequency/incidence The thyroglossal duct cyst (TDC) is the most common congenital anomaly of the neck and accounts for about 70% of all congenital lesions of the neck. This cyst occurs in the young pop- ulation (0–18 years old), with 70% of cysts encountered before the age of 30 years. In most cases (65%), TDC occurs in the infrahyoid location, followed by the suprahyoid region (20% of cases), and at the level of the hyoid bone (15% of cases). In 20%, the TDC may occur in the base of the
    • 60 C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 tongue at the foramen cecum. The suprahyoid TDCs are located in the midline, whereas the infrahyoid TDCs are off the midline. Although TDCs are benign lesions, less than 1% are associated with carcinomas, most commonly a papillary carcinoma of the thyroid gland. Signs and symptoms A soft tissue mass is the most common presentation. If these TDCs become infected, how- ever, then the usual findings of cellulitis/infection are present, including pain, redness, tender- ness, but rarely fever. Etiology/pathophysiology The thyroglossal duct is a remnant of tissue track from which the thyroid gland migrates down- ward from the base of the tongue (foramen cecum) to its anterior location in the lower neck. The course of the TDC is from the foramen cecum down to and in front of the hyoid bone, underneath the hyoid bone, and posterior to the hyoid bone, before taking a U-turn to head down the anterior neck to the thyroid gland. This remnant of the duct fails to involute and secretes fluid, which becomes the cyst. Often, these cysts are not detected until repeat infection of the anterior neck occurs. Image of choice for diagnosis Either CT or MR imaging can evaluate TDC well. The main imaging feature is a ‘‘cystic’’ fluid-filled sharply marginated mass, usually anterior to the hyoid bone. On CT, the TDC is of low or fluid density unless it is infected. There usually is no abnormal contrast enhancement unless the TDC is or has been infected in the past. On MR an image, the cyst has characteristic fluid signal, dark on the T1W and bright on the T2W images. If there has been infection, the fluid may be more proteinaceous and thus have a higher signal than water on the T1W images. Image hallmarks The key imaging feature for diagnosis is that the cyst is both in front of and behind the hyoid bone, thus encasing it (Fig. 3). Furthermore, the anterior portion of the cyst appears embedded into the overlying strap muscles, with the muscles in front of as well as behind the TDC. Care should be taken to examine the floor of the mouth as well, because a diving ranula may mimic a TDC. The ranula does not encase the hyoid bone, however, nor does it appear embedded within the overlying strap muscles. Management Surgery is the preferred treatment, particularly if there has been repeat bouts of infection. The TDC, along with the affected portion of the hyoid bone, is resected (Sistrunk procedure), and the tract is resected. If the hyoid bone and tract are not resected, the TDC will recur. Dermoid of the floor of the mouth [4] Frequency/incidence Dermoid cysts are the rarest of all cystic lesions of the head and neck. About 7% of all cystic lesions of the body occur in the head and neck region. About 80% of all dermoid cysts are found in the orbital, oral cavity, and nasal region. Dermoid cysts comprise about 22% of all midline neck lesions.
    • C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 61 Fig. 3. Thyroglossal duct cyst (TDC). Axial postcontrast CT scan shows a large, multilocular cystic structure at the level of the hyoid bone (black arrow), with the cyst both in front of and behind the hyoid bone, thus incorporating the hyoid. This cystic structure is also imbedded in the overlying strap muscles, which is classic for a TDC. The contents of the cyst are more dense than water, and the walls are slightly thick. These latter changes are related to past infection of the TDC. Signs and symptoms If the lesion is within the oral cavity, there may be compression of the Wharton duct and thus presentation with sialoadenitis of the submandibular gland. Otherwise, local mass effect is prob- ably the main clinical finding. Etiology/pathology The popular explanation is that ‘‘rests’’ of epithelial cells become trapped in the floor of the mouth as the first and second branchial clefts. These cysts may be epidermoid, dermoid, or ter- atoid cysts, depending on the germ cell layers found. Image of choice for diagnosis Either CT or MR imaging performs well in imaging this entity. The presence of fatty tissue, which is low signal on CT and high signal on MR imaging (with the added finding of chemical shift between fat and water), with other tissue density will help in the diagnosis. Measurements of the density, or HUs, will yield numbers in the minus range up to ÿ100 units. MR imaging, however, can better discriminate fatty from other soft tissues. Epidermoid cysts may resemble water or fluid, whereas dermoids will have fatty tissue rather than water signal. If calcification or a tooth is seen, the diagnosis of a teratoid cyst can be made.
    • 62 C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 Fig. 4. Dermoid of the floor of the mouth. Axial postcontrast CT scan shows a large, well-circumscribed low-density (fatty tissue by Hounsfield units) lesion, with a speckled appearance in the floor of the mouth located centrally (arrowhead). The speckled or bubbly appearance of the dermoid is characteristic. There are also many reactive level-I nodes, but not adenopathy. Image hallmarks The low-signal, sharply marginated lesion in the floor of the mouth has fatty signal character- istics (Fig. 4). There is also soft tissue mixed with the fatty tissue, and the appearance of multiple fat lobules resembling a collection of marbles is fairly characteristic of dermoid cysts. MR imag- ing, with its direct coronal view, can delineate the relationship of the cyst to the mylohyoid muscles for surgical approach. An external approach can be made if the cyst is below the muscle. Above the muscle, an intraoral approach is needed. Management Surgical resection is the preferred treatment.
    • C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 63 Cystic hygroma [4] Frequency/incidence Cystic hygromas occur most commonly in the head, neck, and axilla. They comprise about 5.6% of all benign lesions in infancy and childhood. The most common location of cystic hygromas is either the lateral neck in the posterior triangle or in the floor of the mouth. There is no sex or race predilection. About 50% to 60% of lesions are present at birth, with nearly 80% detected by the age of 2 years. Signs and symptoms If uncomplicated, cystic hygromas present as fluctuant, transilluminating, compressible, non- tender mass lesions of the neck, which may enlarge with time. Etiology/pathophysiology This disease process is related to abnormalities of the lymphatic system, allowing large, loculated fluid collections to occur in the lateral neck region. There are four distinct pathologic types of which the cystic hygroma is the most common. Other types include cavernous lymph- angioma, capillary or simple lymphangioma, and vascular/lymphatic malformation or the so- called lymphangioma/hemangioma. With the malformations that contain venous structures, there may be calcified phleobliths, which help to identify this malformation. There are several etiologic theories in which either primitive lymphatic sacs fail to drain into the jugular vein or there is abnormal sequestration or abnormal budding of the lymphatics. Failure to drain lymphatic fluid results in fluid collections occurring most characteristically (90% of cases) in the posterior triangle region (whereas BCCs most often are related to the an- terior triangle). Image of choice for diagnosis Either CT or MR imaging demonstrate these lesions well. The main advantage of MR imag- ing is the ability to obtain directly information from other imaging planes besides the usual axial projection. Image hallmarks The most common appearance on CT scan are low-density, usually well defined fluid pockets in the posterior triangle, and which are typically seen in fetal cystic hygroma (frequently in Turner syndrome) (Fig. 5). The cyst may be unilocular or, more likely, multilocular. The cyst is low signal on T1W and high signal on T2W images. The location in the posterior triangle is classic and may help to separate this lesion from a BCC. The multilocular appearance is also typical. The floor-of-mouth cystic hygroma may be somewhat difficult to separate from a ranula, but the latter does not occur in newborn infants. Separation of the cystic hygroma from a venous/capillary lymphangioma can be made with the presence of phleboliths, whereas the hemangiomatous type will display contrast enhancement. Management Surgical excision is the treatment of choice if the fluid collection is large. If there has been infection of the cystic hygroma, surgery should be performed.
    • 64 C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 Fig. 5. Cystic hygroma. Axial T2W images through the floor of the mouth show a multiseptated fluid collection in the floor of the mouth on both sides. Fluid is very bright or white on this pulse sequence. The floor of the mouth is a typical location, but the classic location is the posterior neck in the posterior triangle. Second branchial cleft cyst [5] Frequency/incidence Cysts, fistulas, and sinus tracts can occur related to the four branchial clefts. The following lists the four types of BCCs in descending order of frequency of occurrence: Second BCC: Most common form; 92% to 99% of all BC anomalies First BCC: Second most common form; 68% cysts, 16% sinuses, 16% fistulas  Third BCC very rare; no well documented incidences of occurrence. Fourth BCC Signs and symptoms Although this is a fluid-filled cyst, it usually is not noticed until after an upper respiratory infection with secondary infection of the BCC. With sinus tracts, there may be chronic drainage from the neck. Etiology/pathophysiology There are five mesodermal arches separated by clefts. Remnants of the cleft or pouch are trapped; thus a cyst is formed and named after the cleft from which it arose. Image of choice for diagnosis Either CT or MR imaging can diagnose this well. If the cyst occurs in a child, the fast scan- ning times of the CT scan may work better. On the CT scan, body settings (level 30, window
    • C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 65 340) work well for the neck and for demonstrating these cysts. Uncomplicated BCCs will have fluid signal characteristics on CT (low density) with sharp margins, unless there has been super- imposed infection. The BCC is also low signal on T1W and high signal on T2W images. If the cyst is infected, on the T1W images the signal may be higher than that of water. There is no enhancement of the BCC unless there has been prior infection, in which case only the margins are enhanced. Image hallmarks The most common of these cysts is the second BCC; this cyst is characteristically located at the angle of the jaw, and is superficial to the carotid artery and jugular vein and posterior to the submandibular gland, which may be displaced forward and—along the anterior margin of the sternocleidomastoid muscle. Thus, BCCs tend to occur in the anterior triangle of the neck, instead of the posterior triangle where cystic hygromas/lymphangiomas tend to occur. There should be no abnormal contrast enhancement unless the BCC is secondarily infected. In Fig. 6, the second BCC is in a characteristic location; however, there is a ‘‘dirty’’-appearing fat (so-called fat stranding), which indicates an inflammatory process—in this case, a cellulitis as well as the infected second BCC—which is why the margins are not discrete. There is no ab- normal contrast enhancement. There is marked enlargement of level-5 posterior triangle nodes on both sides but the enlargement is greater on the right. Fig. 6. Infected second branchial cleft cyst. Axial CT scan with contrast in a child shows cystic structure at the angle of the mandible with irregular margins. The cyst is anterior to the sternocleidomastoid muscle and thus is in the anterior triangle. The cyst is displacing the left submandibular gland in an anterior direction as well as compressing the right jugular vein. There is also retropharyngeal edema, but not an abscess (arrow).
    • 66 C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 In addition, there is edema in the danger space of Gradinsky and Holyoke, which communi- cates freely with the mediastinum. This potential space exists between the retropharyngeal space in front and the posterior prevertebral space. If untreated, the infectious process can track down to the lung and produce a mediastinitis. First BCCs are the next most common BCC, and may occur within the external auditory ca- nal, at the angle of the jaw, and parotid gland. Third and fourth BCCs are more complicated and beyond the scope of this article. The following sections list characteristics and locations of BCCs and sinus tracts: First BCC Possible sites of BCCs are around pinna of ear and external auditory canal and around the angle of the jaw. Second BCC Second BCC type I lies beneath the platysma and cervical fascia and anterior to the sterno- cleidomastoid (SCM) muscle. It arises from the remnant of tract joining the cervical sinus of HIS to skin. Type II is the most common and is adjacent to and adherent to the carotid/jugular. Type III courses between the internal carotid artery (ICA) and external carotid artery (XCA) to the lateral wall of the pharynx. Type IV is a columnar lined cyst, adjacent to wall of the pharynx. Sinuses and fistulas Sinuses and fistulas are more are common in children. Cysts are more common in adults. Classic sinuses and fistulas are superficial to the CCA and IJV in the anterior triangle, displacing the SMG anterior at the angle of the mandible. CT shows a thin smooth ring with slightly higher than cerebrospinal fluid signal (mucoid). If the cyst is infected, CT shows a thick enhanced rim. There may be a sinus tract extending from the cyst up to lateral pharynx wall, between the ICA and XCA, with the fistula extending up to the palatine tonsils. Third branchial sinus tract The third branchial sinus tract arises from the apex of the pyriform sinus and extends between the CCA and vagus nerve to the lower lateral neck, ICA, and vagus nerve, and down to the thyroid cartilage. Fourth branchial sinus tract The fourth branchial sinus tract arises from the apex of pyriform sinus and extends down to and loops under the left aortic arch and right subclavian artery, back up to and between the XCA and ICA to lateral neck. Management Surgical excision is the treatment of choice. If there is a third and fourth BCC, the anatomy is much more complicated and may require opening of the chest to get to these latter cysts or sinuses. Ranula [4,6] The term ranula comes from the Latin derivative for frog, because this entity causes fullness of the floor of the mouth like a bullfrog. Frequency/incidence Ranula is very rare. There is a reported incidence of 3% in a series of 1303 salivary gland cysts. Signs and symptoms Signs include an expanding mass in the floor of the mouth, but may also involve the anterior upper neck. There may be a history of repeat bouts of sialadenitis, but most often there is a his- tory of recent surgery in the oral cavity with injury of the Wharton duct.
    • C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 67 Etiology/pathophysiology Ranulas are also known as mucoceles or retention cysts of the Wharton duct. Either a stone or surgical injury occludes the Wharton duct. The submandibular gland continues to produce secretions, which then cause the duct to dilate (simple ranula). With increased pressure, the duct may rupture, spilling the mucinous contents into the soft tissues. Thus, the simple ranula becomes a diving or a plunging ranula if it passes through the floor of the mouth/mylohyoid muscles and presents as a soft tissue mass in the upper and anterior neck region. If the ranula crosses the midline, it becomes a dissecting ranula. Fig. 7. Diving ranula. Axial T2W MR of the floor of the mouth shows a large fluid collection (large bright, white structure) centered on the sublingual space that contains the Wharton duct. The small white arrow marks the normal midline fat-filled lingual septum, which is bowed to the left side by the ranula. The ranula has also herniated across the midline to the left side. The ranula has herniated through the mylohyoid muscles to become a diving ranula, which is now lateral to the mandible.
    • 68 C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 Image of choice for diagnosis This entity can be studied well by either CT or MR imaging. The ability to obtain direct sagittal and coronal images using MR imaging makes it more useful in assessing complicated ranulas. Image hallmarks Because a ranula is a fluid-like cavity, it will behave as fluid does on CT and MR imaging. On CT, the ranula is low density, which may not be exactly the density of water if infected. On MR imaging, the ranula is low signal on T1W and high signal on T2W images (Fig. 7). The key to the diagnosis is that the dilated fluid sac is in the sublingual space where the Wharton duct lies. On the coronal views, if the ranula is above the floor of the mouth or mylohyoid muscle, then it is considered simple, unless it crosses the midline to the other side (dissecting ranula). If the ranula is below the floor of the mouth or mylohyoid muscle, then it becomes a diving ranula; if it makes it down the anterior neck, it becomes a plunging ranula. Usually, the soft tissue mass/ fluid cavity occurs in the submental region or angle of the jaw region. Management Surgical excision is the preferred treatment. Floor-of-the-mouth abscess [4] Frequency/incidence The frequency of occurrence of this abscess depends on its location, the health of the patient, and whether a surgical procedure is being performed. Development of infection following dental extraction is not common, but is the most common cause for infection in the floor-of-the-mouth region. Signs and symptoms Symptoms include facial swelling with redness and tenderness, and if severe, the patient may be febrile with other systemic findings of infection. Etiology/pathophysiology Fig. 8 shows a case where the abscess was a result of dental extraction. Usually following dental extraction, the infectious process arises within the masticator space and thus involves the pterygoid muscles or the overlying masseter muscles. The infection can spread down from the gingival ridge into the floor of the mouth and below if the infection squeezes through the mylohyoid muscles. Image of choice for diagnosis Because the patient is in discomfort and can not hold still for a prolonged time, CT is the preferred imaging method. Furthermore, CT may identify an unsuspected calculus within the salivary gland ducts, which may be the cause of the infection; bony involvement or osteomyelitis may be also be detected by CT. Image hallmarks The most characteristic appearance on either CT or MR imaging is a contrast enhancement in a ringlike fashion with a central area of fluid signal. This represents the abscess capsule that is enhancing and may be regular or irregular shaped. Usually, there is extensive reactive
    • C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 69 Fig. 8. Floor-of-mouth abscess. Axial CT of the neck with contrast shows a large low-density collection of fluid with abnormal ringlike contrast enhancement (arrow). Just posterior to this is the compressed submandibular gland, which is now enhancing because it is also infected. The contrast-enhanced proximal portion of the Wharton duct can be seen (arrowhead). There are multiple, bilateral, reactive nodes. The normal right submandibular gland is also seen. adenopathy as well as fat stranding and skin thickening—all secondary signs of an inflammatory process. Squamous cell carcinoma of the neck usually does not show significant contrast enhancement. Management Surgical excision is the preferred treatment if there is a well-defined fluid pocket. Chondrosarcoma [7] Frequency/incidence The incidence of chondrosarcoma of the cartilage in the neck is very low. The overall inci- dence of all sarcomas is 0.3% to 1.0% of all laryngeal malignant tumors.
    • 70 C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 Signs and symptoms Symptoms probably occur late and are related to mass effect, producing difficulty breathing or difficulty in swallowing. Etiology/pathophysiology The cause of chondrosarcoma is probably spontaneous genetic mutation and is usually not a transmitted disease process. Image of choice for diagnosis CT demonstrates the calcific and characteristic chondroid pattern of calcification. MR-imag- ing findings are nonspecific, particularly because the bony nature and calcific pattern is not seen on MR images. Image hallmarks The most characteristic appearance on CT scan is an expansile lesion of the thyroid or cricoid cartilage with chondroid pattern of calcification without frank bony destruction or soft tissue mass (Fig. 9). Thus, a squamous cell carcinoma that destroys cartilage but does not expand it Fig. 9. Chondrosarcoma. Axial CT with contrast shows an expansile tumor of the cricoid cartilage with internal amorphous type of calcification typical of cartilaginous tumors. There is no soft tissue mass, but the expanded cricoid cartilage is narrowing the airway.
    • C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 71 can be differentiated. A hemangioma of the cartilage may have a similar appearance, but because of its vascular nature, it will enhance, whereas a chondrosarcoma will not. Another pos- sibility would be a Kaposi sarcoma in an HIV-positive patient, but which would have a more destructive nature and may be difficult to differentiate from squamous cell carcinoma, which comprises nearly 95% of all head and neck malignant tumors. Management Surgical excision may be the treatment of choice if the chondrosarcoma is lower grade and totally confined to the cartilage. If the cricoid is involved, a total laryngectomy may be needed. Venous lymphangioma [5,8] Frequency/incidence Please refer to the discussion on cystic hygromas. Signs and symptoms Venous lymphangiomas present as large, cutaneous lesions, which may have a dark bluish or purplish appearance and also appear to be enlarged or varicoid veins. Fig. 10. Venous lymphangioma/hemangioma. Axial CT of the neck with contrast shows a serpiginous collection of enhancing vessels in the left posterior triangle region but with extension through the muscle to the superficial skin. The more common cystic hygroma (lymphangioma) would not enhance but also is located commonly in the posterior triangle (behind the sternocleidomastoid muscle).
    • 72 C. Lee et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 55–72 Etiology/pathophysiology Please refer to the discussion on cystic hygromas. Image of choice for diagnosis Either CT or MR imaging demonstrate this lesion well. Image hallmarks The most characteristic appearance on either CT or MR images is a contrast-enhancing mass, which, despite its size, does not have significant mass effect, and is located superficially (Fig. 10). Management The size of the lesion and cosmetic deformity determine whether surgical intervention is required. References [1] Som P, Brandwein M. Salivary glands. In: Som P, Curtin H, editors. Head and neck imaging. St. Louis: Mosby; 1996. p. 846–66. [2] Hudgins P, Jacobs I, Castillo M. Pediatric airway disease. In: Som P, Curtin H, editors. Head and neck imaging. St. Louis: Mosby; 1996. p. 573–4. 585–6. [3] Som P, Curtin H. Fasciae and spaces. In: Som P, Curtin H, editors. Head and neck imaging. St. Louis: Mosby; 1996. p. 744. [4] Smoker W. Oral cavity. In: Som P, Curtin H, editors. Head and neck imaging. St. Louis: Mosby; 1996. p. 501–2, 506–10. [5] Weissman J. Nonnodal masses of the neck. In: Som P, Curtin H, editors. Head and neck imaging. St. Louis: Mosby; 1996. p. 794–8, 802–6. [6] DeGraff RV. Ranulas and plunging ranulas. Emedecine.com 2:7. [7] Curtin H. Larynx. In: Som P, Curtin H, editors. Head and neck imaging. St. Louis: Mosby; 1996. p. 658–62. [8] Benson M, Zadvinskis D, Som P, et al. Embryology and congenital cystic lesions. In: Som P, Curtin H, editors. Head and neck imaging. St. Louis: Mosby; 1996. p. 763–9.
    • Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 Angiographic evaluation of the head and neck Larry L. Cunningham, Jr, DDS, MD*, Joseph Van Sickels, DDS, M. Todd Brandt, DDS Division of Oral and Maxillofacial Surgery, College of Dentistry, University of Kentucky, 800 Rose Street, Room D-508, Lexington, KY 40536-0297, USA Facial trauma, craniomaxillofacial surgery, and certain idiopathic events can cause a variety of vascular pathologies. Those of special interest to craniomaxillofacial surgeons include the following: superficial vascular malformations (hemangiomas), intraosseous vascular tumors (central hemangioma of bone), aneurysms (false or true), arteriovenous fistulas (including carotid-cavernous fistulae (CCFs)), fibrovascular tumors (including juvenile nasopharyngeal an- giofibromas), and carotid body tumors. These vascular injuries can lead to airway compromise, significant hemorrhage, irreversible neurologic damage, or death. Appropriate management be- gins with early diagnosis. Because vascular injuries can go unrecognized in the acute setting when a diagnosis is based solely on clinical history and physical examination, interventional ra- diology has become the standard for definitive diagnosis. Angiography, the diagnostic mainstay of interventional radiology, provides images of normal and abnormal anatomical structures. It is also used to diagnose a vascular injury whose presence is suggested by noninvasive radiographic and clinical examinations. Thus, it is a useful adjunct before any surgical identification and repair, ligation, or ablation of indicated vasculature. When combined with endovascular embolization, angiography can successfully manage vascu- lar injury, spontaneous vascular pathology, and congenital vascular anomalies. Complications of angiography combined with embolization are varied but infrequent. Ischemic tissue necrosis after artery occlusion can involve large areas of the maxillofacial region. More serious unpre- dictable sequelae range from permanent neurologic morbidity to death. A working knowledge of angiography will facilitate communication between craniomaxillo- facial surgeons and interventional radiologists or interventional neuroradiologists. The images and associated descriptions in this article are presented as examples of vascular abnormalities that can be diagnosed with angiography. Hemangioma Frequency/incidence Hemangiomas of soft tissue are benign vascular tumors. They are the most common tumor of infancy and childhood, constituting 7% of all benign soft tissue tumors [1–3]. Hemangiomas are found in 1.1% to 2.6% of neonates, and they eventually develop in 10% to 12% of children, more often in girls than in boys (5:1). Approximately one fourth to one third of these tumors occur in the head and neck region [1]. * Corresponding author. E-mail address: llcunn2@uky.edu (L.L. Cunningham, Jr.). 1061-3315/03/$ - see front matter Ó 2003, Elsevier Science (USA). All rights reserved. PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 0 8 - 2
    • 74 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 Signs and symptoms Hemangiomas may begin as a flat area of red pigmentation that rapidly progresses to become a red to purple raised mass. A thrill or bruit may be detectable in arteriovenous hemangiomas because of the abnormal connection between arterial and venous circulation [1,2]. Approxi- mately 20% of hemangiomas grow large enough to require intervention [2]. Indications for medical or surgical treatment are compression of vital structures, hemorrhage as the result of trauma, and cosmetic concerns [2]. Etiology/pathophysiology Hemangiomas are the result of a benign proliferation of vascular channels lined with endo- thelium [1,2]. Image of choice for diagnosis Computed tomography (CT), ultrasonography, magnetic resonance imaging (MRI), and Doppler studies are useful noninvasive diagnostic techniques [2,3]. Angiography is performed before embolization or to map the extent of a lesion if surgery is planned [2,3]. Image hallmark Angiography will show a hypervascular tumor with an intense capillary blush and early venous filling [2] (Fig. 1). Fig. 1. Angiogram of a peripheral hemangioma involving the skin and subcutaneous layer of the forehead of a 6-month- old infant. (From Burrows P. Diagnostic imaging in the evaluation of vascular birthmarks. Dermatol Clin 1998;16:462; with permission.)
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 75 Management Reported therapies include compression therapy for localized lesions, intralesional or sys- temic corticosteroids, argon laser therapy, cryotherapy, sclerosing agents, and embolization with or without surgical identification and removal [2]. Central hemangioma of bone Frequency/incidence Central hemangiomas of bone are rare intrabony lesions; some are caused by trauma, others are hamartomas, and still others are true neoplasms [1]. Hemangiomas of bone are more com- mon in female patients and occur most frequently in patients in the first and second decades of life [1,3]. Common sites include the skull, the vertebrae, and the jaws; lesions appear twice as often in the mandible as in the maxilla [1]. Signs and symptoms Clinical findings associated with central hemangiomas include the following: spontaneous bleeding from the gingival sulcus, mobility of teeth, gingival discoloration, facial swelling or asymmetry, and a detectable thrill or bruit [3]. Indications for medical or surgical therapy are compression of vital structures, hemorrhage as the result of trauma, and cosmetic concerns [2]. Etiology/pathophysiology Hemangiomas are the result of a benign proliferation of vascular channels lined with epithe- lium [1,2]. Image of choice for diagnosis CT, ultrasonography, MRI, and Doppler studies are useful noninvasive diagnostic tech- niques [2,3]. Angiography combined with embolization can effectively reduce intraoperative hemorrhage [3]. Image hallmark Angiography will show a hypervascular tumor with an intense capillary blush and early venous filling [2] (Fig. 2). Management Reported therapies include systemic corticosteroids, laser therapy, sclerosing agents, radia- tion therapy, and embolization with or without surgical identification and removal [2]. Aneurysm Frequency/incidence Intracranial and extracranial aneurysms rarely affect the head and neck [4]. They have been reported to occur after facial trauma, head trauma, orthognathic surgery, and other head and neck surgery. Seventy percent of aneurysms result from blunt trauma, whereas 25% result from penetrating trauma [5].
    • 76 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 Fig. 2. (Top) CT showing a hemangioma of the right maxilla. (Bottom) Angiographic image of the same maxillary lesion.
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 77 Signs and symptoms Aneurysms typically remain asymptomatic until they rupture, usually within 1 month of their development; rupture causes a thromboembolic event or hemorrhage [6]. Aneurysms are often unrecognized in the acute clinical setting because the onset of symptoms can be delayed for a few hours to a few weeks after the traumatic incident [7]. Symptoms can range from neck stiff- ness and pain to focal or severe neurologic defects resulting from showering emboli [8,9]. Dis- section or expansion of traumatic lesions in the neck can cause airway compromise, soft tissue deformity, asymmetry, or cranial nerve deficits, and can even mimic a tonsilar abscess [10]. Mas- sive posterior epistaxis may occur as the result of a post-traumatic pseudoaneurysm of the intra- cavernous portion of the internal carotid artery (ICA) and can be life threatening [11,12]. Etiology/pathophysiology Aneurysms are classified as either true or false (pseudoaneurysm). True aneurysms result from the partial tearing or rupture of only the muscularis and intimal layers of an artery; this rupture allows the adventitia to prevent blood extravasation [6]. Complete transection of one side of an arterial wall leads to the formation of a pseudoaneurysm or pulsating hematoma that is contained by contiguous tissues. The organizing clot forms a psuedofibrous capsule with a liquefied central matrix. Without an arterial coat, the pressure in the hematoma increases until the pressure in the periarterial zone equals the mean arterial pressure [4]. The endothelial lining frequently produces a pseudointima continuous with the arterial lumen [4]. Hematoma liquefac- tion leads to the formation of a pulsating mass that can either rupture or continue to enlarge [4]. The instability of the vessel wall in both true and false aneurysms poses the constant threat of hemorrhage or infarction as the result of a thromboembolic event [6]. Left untreated, these lesions can lead to stenosis, dissection, arteriovenous fistulas, or hemorrhage [9,13]. Fig. 3. (A) Anterior-posterior (A-P) image of an aneurysm of the right internal carotid artery-posterior wall at the junction with the posterior communicating artery (not shown). (B) Lateral view. This patient presented with transient ischemic attacks and weakness of the left arm and face. An A-P (C) and lateral (D) view of an aneurysm of the basilar artery with the dome pointing down and to the right.
    • 78 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 Fig. 3 (continued )
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 79 Fig. 3 (continued ) Image of choice for diagnosis Angiography is the preferred imaging method for diagnosis, surgical mapping, or definitive treatment through endovascular approaches. Image hallmark An aneurysm appears as a projection or out-pouching from the parent vessel and may extend with dissection through soft tissue [6] (Fig. 3). Management Medical treatment with anticoagulant therapy may allow time for spontaneous healing of a pseudoaneurysm. However, medical therapy alone rarely accomplishes complete resolution, and there is a continuous threat of thrombotic emboli or spontaneous and rapid dissection leading to airway compromise [1]. The traditional surgical approach includes excision of the aneurysmal pouch and either direct closure or placement of a patch graft (synthetic or autologous). More recently, the placement of stents and coils through a vascular approach has proved successful. In addition, detachable balloons placed proximal and distal to the pseudoaneurysm have been shown to be effective [11,13,14]. Early treatment is imperative if detrimental sequelae are to be prevented [14]. Carotid body tumors Frequency/incidence Carotid body tumors are very rare, and their exact incidence is unknown. Signs and symptoms The presenting problem is usually a pulsatile and expansile mass at the angle of the mandible. Cranial nerve dysfunction can involve the vagus, hypoglossal, and cervical sympathetic nerves. More commonly, patients have vague complaints such as headache, neck and ear pain, hoarse- ness, syncope, tinnitus, and dysphagia [15].
    • 80 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 Fig. 4. Angiogram of a carotid body tumor showing the high vascularity of the tumor: (A) lateral and (B) A-P views. This tumor receives vascular supply from three branches of the external carotid artery. Etiology/pathophysiology Tumors arising at the bifurcation of the internal and external carotid arteries are called carotid body tumors. Because of their rarity and interesting histologic appearance, they are also known by several other names: glomus tumors, paragangliomas, nonchromaffin paragangliomas, and chemodectomas. These tumors are derived from neural crest tissue; their malignant potential is low but definite [15,16]. Image of choice for diagnosis Duplex scanning with color flow images can help to determine the dimensions of the tumor and can display the vascular flow. CT scans are useful for evaluating neck masses in general, and MRI techniques can readily differentiate the carotid body tumor from other soft tissues in the
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 81 neck. Angiography is the definitive diagnostic test for these lesions and is helpful in surgical planning. Image hallmark Carotid body tumors are extremely vascular and may appear as an angiomatous tumor [15]. Findings include early tumor blush and splaying of the internal and external carotid arteries at the carotid bifurcation [16] (Fig. 4). Management When the differential diagnosis includes carotid body tumor, needle aspiration or biopsy is contraindicated because of the vascularity of the tumor. In the presence of severe hyper- tension, screening for elevated serum catecholamine concentration may be warranted, as may other laboratory studies to rule out the presence of other functioning paraganglionic tumors (eg, pheochromocytomas). Surgical removal of these masses is indicated. Selective preopera- tive embolization of the tumor’s blood supply is helpful in decreasing intraoperative blood loss. Carotid-cavernous fistula Frequency/incidence Carotid-cavernous fistulas (CCFs) are vascular connections between the carotid artery and the cavernous sinus and are associated most frequently with trauma to the base of the skull [15]. Signs and symptoms Pulsating exophthalmus, edema of the preseptal orbital tissues, enlargement and restriction of motion of the extraocular muscles, and eventual ocular ischemia are caused by the reverse flow through the venous system. Patients with these symptoms should undergo frequent oph- thalmologic examinations with checks of visual acuity and ocular pressure. Changes in visual acuity necessitate immediate treatment [17]. Etiology/pathophysiology CCFs are classified as indirect or direct. Indirect CCFs occur by spontaneous dural arterio- venous communications supplied by the ICA or the external carotid artery. Multiple lesions can exist within the cavernous sinus wall. The exact causes of indirect CCFs are unknown. Direct (traumatic) CCFs most often demonstrate a single communication between the ICA and the cavernous sinus. Causes other than blunt or penetrating trauma include direct surgical trauma, ruptured aneurysm, collagen deficiency syndromes, fibromuscular dysplasia, or arterial dissec- tion [17,18]. Image of choice for diagnosis Selective cerebral angiography is the diagnostic standard. CT scanning and MRI can be help- ful in determining whether brain damage exists or in identifying fractures. Image hallmark In the case of a traumatic transection of the ICA, the cavernous sinus will opacify, and there may be decreased filling of intracranial vasculature from ipsilateral angiography (Fig. 5). Vas- cular injuries and associated pseudoaneurysm may be seen. Venous outflow from the cavernous sinus will be seen through the ophthalmic venous system. This flow may continue to the facial
    • 82 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 Fig. 5. Angiogram of a cavernous-carotid fistula following a gunshot wound to the head. The fistula is demonstrated by the blush in the cavernous sinus and during angiography of the right internal carotid artery. vein and the external jugular vein. Some patients may exhibit outflow through posterior drain- age of the cavernous sinus and the superior and inferior petrosal sinuses. Superior drainage may be displayed as opacification of the sphenoparietal sinus, which places the patients at risk of intracerebral hemorrhage. Most often, a combined pattern will be seen [17]. Management Patients with severe proptosis, increasing intraoccular pressure, and severely declining vis- ual acuity may require lateral canthotomy as a temporary step for preventing loss of vision. Endovascular approaches with either balloon embolization or coil embolization are the pre- ferred means of treatment. Proximal suture ligation of the ICA has been shown to be ineffec- tive and may induce or increase steal syndrome. Thus, this intervention should be avoided [19]. Dissecting carotid aneurysm Frequency/incidence Aneurysms of the intracranial and extracranial portions of the carotid artery are rare and may be difficult to diagnose. Aneurysms of the extracranial carotid artery compose fewer than 5% of all extracranial arterial aneurysms [20]. Signs and symptoms The signs and symptoms can vary greatly depending on the location of these aneurysms. Cer- vical aneurysms can bulge into the lateral parapharyngeal wall, mimicking a neck mass [21,22]. The mass may or may not pulsate, depending on whether a thrombus has formed within the lumen [20]. Symptoms may include hemorrhage, either otorrhagia or epistaxis. Nerves immedi- ately adjacent to the expanding mass may be compressed, and Horner syndrome has been de- scribed in several cases of carotid aneurysm. Patients with extracranial aneurysm may exhibit paralysis of cranial nerves IX, X, XI, and XII. Patients with intracranial aneurysm may exhibit headaches, nausea, vomiting, drowsiness, transient ischemic attacks, and loss of vision and
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 83 hearing. Associated signs and symptoms such as fever and upper airway obstruction can be related to the underlying cause of the aneurysm (see Etiology/pathophysiology). Etiology/pathophysiology Dissecting carotid aneurysms may be congenital or caused by trauma or infection [23,24]. They have been reported to occur after blunt trauma to the head and after a tonsillectomy. Although trauma appears to be the most common cause of these aneurysms, they may develop for several reasons, which vary according to the age of the patient. These aneurysms have occurred in patients younger than 5 years and in patients older than 40 years. Dissecting carotid aneurysms may be caused by a deep space infection of bacterial or mycotic origin. When they occur as a complication of neck space infection, the diagnosis may be difficult. Patients with fibromuscular dysplasia, Marfan syndrome, or Ehlers-Danlos syndrome, and those who have undergone radiation therapy, appear to be at greater risk of carotid aneurysm. The lesion may be a true or false aneurysm. True aneurysms are usually congenital, whereas false aneu- rysms are usually the result of trauma or infection. Image of choice for diagnosis CT scanning, MRI, and magnetic resonance angiography have been used to image carotid aneurysms; however, arteriography is the method of choice. Image hallmark Arteriography reveals a large outpouching of contrast beyond the walls of the ICA (Fig. 6). Management The choice of treatment depends on the location of the lesion and on the patient’s condition. Surgical intervention is used most often for lesions in the neck; this treatment involves resection Fig. 6. Dissecting carotid aneurism following blunt head trauma. Note the saclike projection extending superiorly from the internal carotid artery.
    • 84 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 of the lesion with repair of the carotid artery. Balloons and coils are used most often to treat intracranial lesions. The use of balloons allows an assessment of the status of the contralateral cerebral blood flow. Arteriovenous malformations Frequency/incidence Arteriovenous malformations (AVMs) are rare lesions that may be congenital or may result from trauma. Congenital lesions grow as the patient ages and may increase in size dramatically during puberty or pregnancy [25]. Signs and symptoms The clinical presentation of AVMs depends on the characteristics of the lesion. Patients with lesions in the head and neck may exhibit increased intracranial pressure, mass effect, or steal syndrome. Symptoms may include disfigurement, pain, bruit, or hemorrhage. When they occur in the region of the maxilla and mandible, AVMs may cause facial swelling, loose teeth, tinnitus, and headaches. Etiology/pathophysiology The clinical behavior and prognosis associated with AVMs are determined by the presence and degree of shunting. Congenital lesions are presumed to have been present at birth and to have grown with age. Traumatic lesions usually result from penetrating injuries and can originate from the internal or external carotid arteries, the vertebral arteries, or a transected vessel. Fig. 7. Angiogram of an arteriovenous malformation that presented as a swelling in the patient’s oropharynx. (A) Lateral view of the right carotid angiogram. Note there is also a cavernous-carotid fistula with drainage in an anterior direction to an enlarged superior ophthalmic vein. (B) On the A-P view of the selected left vertebral angiogram, there is contribution to the arteriovenous malformation.
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 85 Fig. 7 (continued ) Image of choice for diagnosis A Doppler ultrasound probe may be used to examine the lesion and to determine the need for further tests. Angiography may be either diagnostic or therapeutic. When the lesions are very large and involve both bone and soft tissue, MRI may be used to determine the extent of soft tissue involvement [26]. Image hallmark The appearance of AVMs varies greatly depending on their location, size, and degree of shunting and collateral circulation (Fig. 7).
    • 86 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 73–86 Management Patients with a bruit or palpable shunting are candidates for treatment. AVMs resulting from trauma lend themselves more easily to surgical intervention. Endovascular embolization with various materials has been used alone or in combination with surgical intervention. Endo- vascular embolization can be combined with percutaneous embolization (micropuncture directly into the lesion with the placement of microcoils). Recent case reports [27–29] indicate that the use of histoacrylic glue for both endovascular and percutaneous embolization is a promising treatment. References [1] Waldron CA. Bone pathology. In: Neville BW, Bouquot J, Allen C, Damm D, editors. Oral and maxillofacial pathology. Philadelphia: WB Saunders; 1995. p. 443–92. [2] Herbreteau D, Aymard A, Jhaveri HS, et al. Current management of cervicofacial superficial vascular mal- formations and hemangiomas. In: Connors JJ, Wojak JC, editors. Interventional neuroradiology: strategies and practical techniques. Philadelphia: WB Saunders; 1999. p. 317–26. [3] Larsen PE. Diagnosis and management of vascular malformations. In: Williams TP, Stewart JC, editors. Surgical pathology. Vol. 5. Philadelphia: WB Saunders; 2000. p. 432–45. [4] Lanigan DT, Hey JH, West RA. Major vascular complications of orthognathic surgery: false aneurysms and arteriovenous fistulas following orthognathic surgery. J Oral Maxillofac Surg 1991;49:571–7. [5] Bula WI, Loes DJ. Trauma to the cerebrovascular system. Neuroimaging Clin N Am 1994;4:753–72. [6] Acosta C, Williams PE Jr, Clark K. Traumatic aneurysms of the cerebral vessels. J Neurosurg 1972;36:531. [7] Pretre R, Reverdin A, Kalonji T, et al. Blunt carotid artery injury: difficult therapeutic approaches for an underrecognized entity. Surgery 1994;115:375–81. [8] Laitt RD, Lewis TT, Bradshaw JJ. Blunt carotid arterial trauma. Clin Radiol 1996;51:117–22. [9] Simionato F, Righi C, Scotti G. Post-traumatic dissecting aneurysm of extracranial internal carotid artery: endovascular treatment with stenting. Neuroradiology 1999;41:543–7. [10] Liebman KM, Rosenwasser RH, Heinel LA. Endovascular management of aneurysm and carotid-cavernous fistulae from gunshot wounds to the skull base and oropharynx. J Craniomaxillofac trauma 1996;2:10–16. [11] Chae SW, Choi G, Lee HM, et al. Intrasaccular detachable platinum coil embolization for traumatic pseudoaneurysm treatment of a cavernous carotid artery. Otolaryngol Head Neck Surg 2001;124:230–1. [12] Ghorayeb BY, Kopaniky DR, Yeakley JW. Massive posterior epistaxis. A manifestation of internal carotid injury at the skull base. Arch Otolaryngol Head Neck Surg 1988;114:1033–7. [13] Crow WN, Scott BA, Guinto FC Jr, et al. Massive epistaxis due to pseudoaneurysm treated with detachable balloons. Arch Otolaryngol Head Neck Surg 1992;118:321–4. [14] Jean WC, Barrett MD, Rockswold G, et al. Gunshot wound to the head resulting in a vertebral artery pseudoaneurysm at the base of the skull. J Trauma 2001;50:126–8. [15] Moore WS, editor. Surgery for cerebrovascular disease. 2nd edition. Philadelphia: WB Saunders; 1996. p. 432–9. [16] Zierler RE. Diagnosis and management of cerebrovascular disease. New York: McGraw-Hill. 1995. p. 491–500. [17] Connors JJ, Wojak JC, editors. Interventional neuroradiology: strategies and practical techniques. Philadelphia: WB Saunders; 1999. p. 215–25. [18] Lasjuanias PL, Berenstein A, editors. Surgical neuroangiography New York: Springer; 1992. p. 317. [19] Fox AJ, Vinuela F, Pelz DM, et al. Use of detachable balloons for proximal artery occlusion in the treatment of unclippable cerebral aneurysms. J Neurosurg 1987;66:40–6. [20] Unal OF, Hepgul KT, Turantan MI, et al. Extracranial carotid artery aneurysm in a child misdiagnosed as a parapharyngeal abscess: a case report. J Otolaryngol 1992;21:108–11. [21] Haynes DS, Schwaaber MK, Netterville JL. Internal carotid artery aneurysms presenting as neck masses. Otolaryngol Head Neck Surg 1992;107:787–91. [22] Yoshizaki T, Teranishi S, Matsui O, et al. Internal carotid artery aneurysm presenting as a large pharyngeal mass. Ann Otol Rhinol Laryngol 2000;109:690–2. [23] Coley SC, Clifton A, Britton J. Giant aneurysm of the petrous internal carotid artery. Diagnosis and treatment. J Laryngol Otol 1998;112:196–8. [24] Halliday AW, Mansfield AO. Congenital arteriovenous malformations. Br J Surg 1993;80:2–3. [25] Zachariades N, Mezitis M, Rallis G, et al. Vascular malformations in a 3-1/2 year old child. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;91:271–3. [26] Warren DJ, Hoggard N, Walton L, et al. Cerebral arteriovenous malformations: comparison of novel magnetic resonance angiographic techniques and conventional catheter angiography. Neurosurgery 2001;48:973–82. [27] Corsten L, Bashir Q, Thornton J, et al. Treatment of a giant mandibular arteriovenous malformation with percutaneous embolization using histoacrylic glue: a case report. J Oral Maxillofac Surg 2001;59:828–32. [28] Kaneko R, Tohnai I, Ueda M, et al. Curative treatment of central hemangioma in the mandible by direct puncture and embolization with n-butyl-cyanoacrylate (NBCA). Oral Oncol 2001;37:605–8. [29] Siu WW, Weill A, Gariepy JL, et al. Arteriovenous malformation of the mandible: embolization and direct injection therapy. J Vasc Interv Radiol 2001;12:1095–8.
    • Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 Magnetic resonance imaging of the head and neck Larry L. Cunningham, Jr, DDS, MDa,*, David M. Nadler, DMD, MDa, Charles Lee, MDb a Division of Oral and Maxillofacial Surgery, College of Dentistry, University of Kentucky, 800 Rose Street, Room D-508, Lexington, KY 40536-0297, USA b Department of Radiology, University of Kentucky, 800 Rose Street, Room HX-315D, Lexington, KY 40536-0297, USA Computed tomography (CT) and magnetic resonance imaging (MRI) are used to detect pathology of the head and neck. Although CT still has a superior role in detecting calcifications, bony pathology, fractures, and acute hemorrhage [1], MRI is now the preferred imaging method for head and neck pathology. MRI allows superior tissue discrimination and fat- and water-sup- pression imaging. Fat-suppression imaging has greatly improved the ability to detect abnormal contrast enhancement in the head and neck region. Without this technique, abnormal contrast enhancement appearing as a bright area may be hidden by the very bright signal of fat. Very rapid MRI techniques now allow angiographic images and kinescopic (real-time) depiction of movement. Injectable contrast agents (gadopentetate) aid in the differentiation of certain tumor types and vascular lesions. Albumin-tagged agents which allow direct blood-volume calcula- tions have been developed and are now pending FDA approval. Injectable MR agents, specif- ically for head and neck imaging, are also currently under development. MRI, which uses nonionizing radiation from the radio-frequency (RF) band of the electro- magnetic spectrum, functions by taking advantage of the weak magnetic properties of human tissue. The patient is placed inside a large magnet with a uniform magnetic field. When the hydrogen nuclei in the patient’s body are exposed to this magnetic field, they align with the field. A sequence of RF pulses is then applied to the area of the body being evaluated; this signal must be at the resonant frequency so that the body’s proteins can absorb it. These pulses create a transient magnetic field that is perpendicular to the main field; when exposed to this field, the hydrogen nuclei in the body absorb energy and change the direction of their axis of rotation. When the RF pulse is terminated, the nuclei again realign themselves with the external magnetic field. Energy is released from the tissue as weak RF signals, which are received by coils in the MRI device. The signals are rendered detectable by the application of an RF pulse that tips the energized proton down by 90° to be detected as a current by the receiving coil [2–4]. Subject- ing these signals to a series of computer operations translates the signal into an image. The signals emitted from the excited proton have two components, which are referred to as T1 and T2 relaxation times. T1 is defined as the spin-lattice relaxation time, reflecting the lon- gitudinal axis, and decays at a faster rate than the T2 relaxation time. This is the energy ex- pended by the excited proton to the lattice that contains the proton. As the excited proton is deflected by the 90° RF pulse toward the receiving coil and partially recovers to its free steady state during the early phase of read-out, the signal is dominated by the T1 relaxation time. T2 is defined as the spin-spin relaxation time and reflects the vertical axis. This is the energy expended between the various protons that have been energized. * Corresponding author. E-mail address: llcunn2@uky.edu (L.L. Cunningham, Jr.). 1061-3315/03/$ - see front matter Ó 2003, Elsevier Science (USA). All rights reserved. PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 1 1 - 2
    • 88 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 Following the 90° pulse, the T2 signal decays faster than the predicted rate because of can- cellation of signal vector by protons out of phase with each other. This results in the T2* (star) signal, which forms the basis for gradient echo imaging. By applying another 180° pulse (refo- cusing pulse), the protons reverse their direction and eventually come back into phase, generat- ing a signal or echo that can be repeated with other 180° pulses with eventual total decay of signal. This echo or signal forms the basis of the standard spin-echo technique widely used for most conventional MRI. When the proton has nearly recovered, the T2 relaxation signal dominates. Thus, both T1-weighted and T2-weighted effects exist in all types of MR images, but one effect usually dominates [2–4]. A T1-weighted image is produced by a short repetition time (TR) between pulse sequences plus a short echo time (TE). Tissue with a short T1 decay produces an intense bright or white MR image. Tissue with a long T1 decay produces a low-intensity signal and appears dark on a T1- weighted image [5]. On T1-weighted images, fat is bright or white, cerebrospinal fluid (CSF) is dark or black, and gray matter is slightly hypointense to white matter. This level of contrast makes it possible for the MR image to render a high degree of anatomic detail. Thus, T1-weighted images are useful for depicting small anatomic regions such as the temporomandibular joint (TMJ). A T2-weighted image is acquired by using a long TR and a long TE. Tissue with a long T2 decay produces a high-intensity signal and appears as a bright area on the image. Tissue with a short T2 decay produces a low-intensity signal and appears as a dark area on the image. On T2- weighted images, fat becomes less bright compared with its appearance on T1 images. CSF is bright or white, and gray matter is slightly hyperintense (brighter) to white matter, which appears dark or gray. In general, the T2 time of abnormal tissue is longer than that of normal tissue. Thus, T2-weighted images are ideal for showing inflammatory changes and tumors. This article discusses several diseases of the head and neck for which MR imaging has signifi- cant advantages. Sample MR images accompany each description. Osteomyelitis Frequency/incidence Osteomyelitis is an infection of bone that begins in the medullary cavity and extends to in- volve the cortical bone and periosteum. It is rare in the jaw in the absence of predisposing risk factors such as an immunocompromised state, trauma, and radiation treatment for cancer [6,7]. Signs and symptoms Pain and fever are the primary symptoms of both acute and chronic osteomyelitis. Swelling, paresthesia, loose teeth, and sinus tracks can also be present. The white blood cell count, eryth- rocyte sedimentation rate, and C-reactive protein concentration may be elevated, and blood cul- tures may also be positive [6–8]. Etiology/pathophysiology Osteomyelitis can spread hematogenously, as is most common outside the mandible, or by direct spread from an adjoining structure. Odontogenic infections and trauma are the most common causes of osteomyelitis in the jaw [6,7,9]. Acute osteomyelitis most often results from infection with staphylococci or streptococci, although recent studies have shown positive cultures for anaerobic bacteria in these infections. Chronic osteomyelitis results from untreated or undertreated acute osteomyelitis [6,7]. Image of choice for diagnosis Bone scintigraphy (radionuclide scanning), plain films, and CT scans have been used to diag- nose and manage osteomyelitis. Although scintigraphy is still the preferred imaging method for
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 89 Fig. 1. Osteomyelitis. (A) T1 noncontrast image showing decreased signal in the marrow of the left mandibular angle, thickening of the masticatory muscles, and loss of fat planes caused by edema. (B) T1 image with contrast showing moderate increase in signal of the bone marrow of the left mandible and masticatory muscles. (C) T1 noncontrast image showing loss of bone marrow signal. (D) T1 image with contrast showing heterogenous enhancement of the bone marrow with enlargement of the mandible. (From Reinert, S, Widlitzek H, Venderink DJ. The value of magnetic resonance imaging in the diagnosis of mandibular osteomyelitis. Br J Oral Maxillofac Surg 1999;37:459–463; with permission.)
    • 90 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 Fig. 1 (continued )
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 91 localizing osteomyelitis, MRI has the advantage of providing good contrast between normal and abnormal bone marrow, which aids in the early detection of osteomyelitis while offering a significant increase in the level of anatomic detail [10,11]. Image hallmarks On T1-weighted MR images produced with and without contrast enhancement, the normal hyperintense signal of bone marrow fat is altered by inflammatory edema, and the signal inten- sity of fatty tissue within the marrow is decreased (dark) when compared with a normal bone marrow signal (Fig. 1). In addition, MR images may also show nonossified periosteal reaction indicating bony response to the infection; this reaction appears as a thickened area of hypoin- tensity surrounding the marrow [10]. Management Appropriate antibiotic therapy, as indicated by culture and sensitivity, and surgical debride- ment with or without hyperbaric oxygen therapy are the treatments of choice. Head and neck abscess Frequency/incidence Head and neck abscesses are relatively common and are often odontogenic in origin. Other sources include the sinuses, salivary glands, tonsils, traumatic wounds, and skin infections. Signs and symptoms The first symptoms of head and neck infections are pain and swelling. All infections involving the fascial planes of the head and neck can become life threatening, and symptoms may include trismus, stridor or airway compromise, inability to handle secretions, fever, and leukocytosis [6,12]. Etiology/pathophysiology Most head and neck infections are of dental, tonsillar, or salivary gland origin. These infec- tions are most often caused by mixed flora indigenous to the oropharyngeal region. Image of choice for diagnosis Both CT images and MR images are of diagnostic benefit in the evaluation of infections of the head and neck. If the patient’s airway is compromised, as may be the case with odontogenic or pharyngeal infections, CT is generally used because of the discomfort and potential com- plications that patients might encounter during the time required to generate an MR image. MRI, however, is the preferred imaging method for delineating abscesses of the midface and brain. Image hallmarks The affected tissues may demonstrate hypointensity on T1-weighted MR images and hyper- intensity on T2-weighted images, but the images are not specific for any organism (Fig. 2).
    • 92 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 Likewise, abscess formation will be displayed as a hypointense area on T1-weighted images and hyperintense on T2-weighted images with an enhancing capsule or wall around the abscess or invasion of adjacent tissue [13]. Alternatively, fungal infections appear dark on the T2-weighted images because of their relative lack of water. Therefore, a fungal ball can be separated from normal sinusitis changes, which are very bright on the T2-weighted images. Fig. 2. Peritonsillar abscess. (A) Axial T1-weighted image through the tonsillar area demonstrates a low-intensity mass in the left tonsillar area with mass effect. (B) Axial T2-weighted image at the same level demonstrates increased signal intensity of the abscess. (C) Coronal T2-weighted image shows a high-intensity abscess with a medial bulge of the pharyngeal wall. (From Weber AL, Siciliano A. Radiologic evaluation of the neck: CT and MR imaging evaluation of neck infections with clinical correlations. Radiol Clin North Am 2000;38:941–68; with permission.) Midface abscess is seen in (D) an axial T1-weighted image of an orbital/sinus abscess from an aspergillosis infection and (E) a coronal view of the same patient. The fungus has low signal and appears to be gray in contrast to the normal mucosa and normal inflammatory changes, which are bright.
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 93 Fig. 2 (continued ) Management Abscess drainage and appropriate antibiotic management are required for treatment of head and neck infections. If the infection is life threatening, empiric antibiotic therapy should be given in conjunction with surgical drainage. As culture and sensitivity studies become available, the antibiotic spectrum should be narrowed. Olfactory neuroblastoma (esthesioneuroblastoma) Frequency/incidence Unlike usual neuroblastomas, which occur predominantly in young children, olfactory neu- roblastomas (ESTs) are rare lesions occurring in adults over a wide age range. Signs and symptoms The most common symptoms associated with ESTs are nasal obstruction, rhinorrhea, epis- taxis, and pain [14]. This tumor may first appear as a polyp in the nasal roof or as a naso- pharyngeal mass, but it is most commonly seen as an invasive lesion of the paranasal sinuses (especially the ethmoid) or of the anterior cranial fossa [14,15]. Etiology/pathophysiology An EST is a neuroectodermal neoplasm that is believed to arise from the olfactory epithe- lium, usually high in the nasal cavity close to the cribiform plate [14].
    • 94 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 Image of choice for diagnosis The most important aspect of MRI is its ability to accurately determine the extent of tumor and to distinguish it from normal mucosa and from other pathologic changes such as inflamma- tion and retained secretions. T2-weighted spin-echo sequences and gadolinium-enhanced T1- weighted MR images are best for demonstrating such distinctions [16] and are the images of choice for all paranasal sinus tumors. Image hallmarks Fig. 3 shows a paranasal sinus tumor with a presentation typical of tumors in this region [14]. The tumor appears as a hypointense mass on gadolinium-enhanced T1-weighted images. The degree of enhancement appears to correlate with the degree of vascularity of the tumor. The tumor is further discriminated from associated sinusitis by T2-weighted spin-echo sequences, on which the EST appears less intense than the highly intense changes associated with secondary sinusitis. Because ESTs tend to grow along the various tiny perforating olfactory nerves, the tumor commonly pierces the cribriform plate and becomes a subfrontal, extradural tumor. This Fig. 3. Olfactory neuroblastoma. (A) T1-weighted image showing tumor filling the superior nasal cavity and ethmoid sinus with extension into the anterior cranial fossa. (Courtesy of Pamela Van Tassel, MD, Philadelphia, PA) (B) T1- weighted image showing an anteroposterior view of a similar tumor.
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 95 Fig. 3 (continued ) involvement through the cribriform plate is characteristic of ESTs but not of other paranasal sinus tumors, such as squamous cell carcinoma [10]. Management Surgical excision with adjunctive radiation therapy is the preferred treatment for all para- nasal sinus tumors. Because the cribriform plate is often involved by olfactory neuroblastoma, this structure must be removed along with the tumor to prevent recurrence. Pleomorphic adenoma Frequency/incidence Benign pleomorphic adenoma (BPMA) is the most common neoplasm of major and minor salivary glands. BPMA accounts for 53% to 77% of parotid tumors, 44% to 68% of submandib- ular tumors, and 38% to 43% of minor gland tumors [17]. Eighty-five percent of pleomorphic adenomas occur in the parotid gland, which is by far the most common site of occurrence. Roughly 60% of intraoral lesions are located on the palate [17,18]. Signs and symptoms Regardless of the site of origin, pleomorphic adenomas are typically painless, slow-growing, firm masses.
    • Fig. 4. Pleomorphic adenoma. Gadolinium-enhanced T1-weighted (A) axial and (B) coronal MR images showing bilateral synchronous pleomorphic adenomas of the parotid glands. (Ahn M. Familial mixed tumors of the parotid gland. Head Neck 1999;21:773; with permission.)
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 97 Etiology/pathophysiology Pleomorphic adenomas are derived from a mixture of ductal and myoepithelial elements [17]. Image of choice for diagnosis CT images and MR images are the studies of choice for diagnosing pleomorphic adenomas. Image hallmarks On CT images, BPMA appears hyperdense in comparison with the parotid; the tumor is smoothly marginated with very little contrast enhancement (Fig. 4). If the tumor is small, BPMA appears homogeneous. Larger tumors may contain low-density areas related to central necrosis, hemorrhage, or cystic degeneration. Calcifications are indicative of BPMA. On T1- weighted MR images, the signal intensity is low to intermediate. On T2-weighted images, the signal intensity is intermediate to high. When BPMA is associated with significant hemorrhage, the image may be hyperintense on T1- and T2-weighted images. Management Surgical resection is the treatment of choice. Superficial tumors are best treated with super- ficial parotidectomy; deep parotid tumors should be treated with total parotidectomy. Every ef- fort should be made to spare the facial nerve, because the tumor does not invade the nerve. When BMPA is treated by conservative enucleation, it commonly recurs. If BMPA is left un- treated for an extended length of time, malignant transformation occurs in approximately 25% of cases [18]. Sinus mucocele Frequency/incidence Sinus mucoceles are relatively common lesions that occur most frequently in the frontal and anterior ethmoid sinuses of persons between the ages of 13 and 80 years. Mucoceles occur less frequently in the maxillary, posterior ethmoid, and sphenoid sinuses [18,19]. Signs and symptoms The presentation of sinus mucoceles varies depending on their location. Because they occur in the sinuses, they may grow to large dimensions before they become symptomatic, and may be seen as incidental findings on images taken for other reasons. When they become symptomatic, headache, rhinnorhea, and epistaxis may be seen. The classic frontal sinus mucocele may present with proptosis of the globe. Etiology/pathophysiology Sinus mucoceles are accumulations of mucin that are completely encased by epithelium (ie, they are true cysts). They generally occur after trauma, sinus surgery, or obstruction of the sinus ostium. Image of choice for diagnosis CT and MRI are the preferred diagnostic procedures. Because mucoceles expand bone, CT imaging is necessary to determine whether the bone is completely eroded. Also, CT imaging of the nasal cavity may detect an anatomic lesion that is causing sinus obstruction. MRI
    • 98 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 distinguishes inflammatory tissue from neoplastic tissue. MRI can also detect breakthrough into the cranial vault. Image hallmarks Recently formed mucoceles contain a high degree of water and protein and produce a hypointense signal on T1-weighted images and a hyperintense signal on T2-weighted images (Fig. 5). Inspissated mucoceles with very low water content, as in cases of superimposed fungal Fig. 5. Sinus mucocele. (A) Axial T1-weighted image through the ethmoid sinus demonstrates expansion on the right with low intensity in the sinus consistent with mucocele. (B) Coronal view.
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 99 infections, have been reported to produce hypointense signals on T1- and T2-weighted images [19]. Management Surgical treatment either by debridement and curettage or marsupialization is recommended [19]. Adenoid cystic carcinoma Frequency/incidence Adenoid cystic carcinoma (ACC) is a relatively common salivary gland tumor that occurs most frequently in the minor salivary glands (50%), the submandibular glands (25%), and the parotid gland (25%). The palate is the most common intraoral site. ACC occurs primarily in middle-aged adults and is relatively rare in persons younger than 20. The tumor occurs fairly evenly in men and women, although some studies have reported that it is slightly more likely to occur in women [17,18]. Signs and symptoms ACC usually occurs as a painful, slow-growing mass. The pain is often described as a dull ache that gradually increases in intensity, which usually occurs before the appearance of any noticeable swelling. Parotid tumors may cause facial nerve paralysis, and palatal tumors may cause ulceration. Etiology/pathophysiology ACC is a slow-growing tumor of salivary gland origin, composed of a mixture of ductal and myoepithelial cells. These cells can be arranged in a cribriform, tubular, or solid pattern, with the cribriform pattern being the most common [17]. Perineural invasion is common for ACC. This invasion is usually detected at the time of recurrence rather than at the time of initial diagnosis, and extension of the tumor is often beyond what can be detected radiographically. Though the tumors grow slowly, local recurrence is common, and prognosis is poor. Image of choice for diagnosis Either CT or MRI demonstrate the primary salivary gland tumor. These imaging methods play a complementary role in the evaluation of perineural tumor spread: MRI demonstrates tumor spread along nerves, and CT demonstrates bony erosion and expansion. Image hallmarks When the tumor involves the parotid gland, it may appear benign with sharp margins. When it involves the minor salivary glands, the tumor may appear to infiltrate the margins. CT and MR images show abnormal soft tissue in the gland (Fig. 6). ACC shows enhancement with contrast, whereas benign pleomorphic adenoma does not. The presence of adenopathy also indicates malignancy. The imaging characteristics of this tumor are not specific; the tumor’s appearance may resemble that of the more common mucoepidermoid carcinoma of the parotid gland. On MR images, abnormal contrast enhancement of the mandible indicates perineural tumor spread along the V3 branch within the mandible. CT images may show bony erosion of the canal and even widening of the foramen through which the nerve enters.
    • 100 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 Fig. 6. Adenoid cystic carcinoma. (A) T2 axial view. (B) A different patient’s postresection of tumor showing recurrence along inferior alveolar nerve.
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 101 Management The preferred treatment for ACC is surgical excision with or without adjunctive radiation therapy. ACC is a relentless tumor that is prone to local recurrence and eventual distant meta- stasis. Because metastasis to regional lymph nodes is uncommon, neck dissection is not recom- mended. Because the overall prognosis for patients with ACC is so poor, regardless of treatment, surgical morbidity should be carefully considered, especially when the tumor is large or evidence of distant metastasis already exists [17]. Internal derangement of the temporomandibular joint Frequency/incidence Temporomandibular joint (TMJ) disorders are relatively common; 35% to 72% of the general population display symptoms of this disorder. Epidemiologic studies have not shown a differ- ence in the sex and age distribution of TMJ disorders; however, most patients who seek treat- ment are young women between the ages of 20 and 35 years [20]. Signs and symptoms Symptoms of TMJ internal derangement include pain in the joint, joint sounds (popping, clicking, crepitus), and changes in mobility of the mandible (decreased incisal opening, open lock, closed lock). Etiology/pathophysiology Anterior disc displacement results from elongation of the capsular and discal ligaments and concomitant thinning of the articular disc. These changes may be associated with trauma to the joint, either macro- or microtrauma. Sources of macrotrauma are obvious (motor vehicle acci- dent, assault) and are often reported in the patient’s history. Sources of microtrauma are subtler and usually associated with parafunctional habits [21]. Image of choice for diagnosis Closed- and open-mouth MR images are the images of choice for evaluating the TMJ. Image hallmarks T1-weighted images of the TMJ disk display a hypodense biconcave structure, which should be interposed between the hyperintense condylar head and articular eminence in the closed- and open-mouth positions. Displaced disks will often be seen anterior to the condyle in the closed position. If there is reduction of the disk on opening, then the open-mouth position will show the disk in a more anatomic position. If there is no reduction of the disk, then it will continue to be displaced anterior to the condyle when the mouth is open. A cinematic view of the TMJ and disk can be seen using rapid gradient echo techniques incrementally imaging as the patient opens and closes the mouth (Fig. 7). Management Management of internal derangement of the TMJ is aimed at reducing pain and increasing range of motion to allow for normal function. Goals for function include interincisal opening
    • 102 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 Fig. 7. Temporomandibular joint (TMJ). A closed (A) and open (B) T1-image of a normal condylar-disk relationship. A closed (C) and open (D) image of the left TMJ of a patient with severe long-standing rheumatoid arthritis and with a degenerated disk, which is anteriorly displaced. A closed (E) and open (F) T2 image of a nonrheumatoid patient’s anteriorly displaced disk without reduction.
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 103 Fig. 7 (continued )
    • 104 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 Fig. 7 (continued )
    • L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 105 of 40 mm with lateral excursions of 5 to 7 mm. Physical therapy, a nonchew diet, occlusal splints, nonsteroidal anti-inflammatories, and muscle relaxers have all been used in the nonsur- gical therapy and management of symptomatic internal derangement. When these treatments fail to improve symptoms, surgical treatments usually follow and might include arthrocentesis, arthroscopy, or open arthrotomy. Obstructive sleep apnea Frequency/incidence Obstructive sleep apnea is one in a spectrum of entities known collectively as sleep-disordered breathing. Although patients must have a polysomnogram (sleep study) to be diagnosed with obstructive sleep apnea, it is one of the most common diagnoses given by sleep centers, and reportedly affects 2% of women and 4% of men older than 30 [22]. Signs and symptoms Snoring, apnea, and hypopnea during sleep are signs associated with obstructive sleep apnea and can be evaluated by polysomnogram. In addition, physical characteristics may include obesity, retrognathia, and a long, soft palate. Patients may complain of snoring and daytime sleepiness. They may report falling to sleep very quickly (in bed, watching TV, or during other activities) and may report never feeling rested after a full night’s sleep. Etiology/pathophysiology Obstructive sleep apnea is a complex disease process caused by collapse or obstruction of the airway at one or multiple various levels, including the nasal airway, nasopharynx, oropharynx, and hypopharynx. Image of choice for diagnosis Sagittal and axial MR images can depict an obstructed airway and help diagnose the level of obstruction. Although such images are not necessary for diagnosis, they can be helpful in decid- ing how to treat the patient with obstructive sleep apnea. Most practitioners use plain radiog- raphy, especially lateral cephalometric radiographs, in their evaluation and treatment planning. Image hallmarks The soft palate and the tongue of patients with sleep apnea are much larger than those of patients who do not have this condition (Fig. 8). The size of the nasopharyngeal airway is re- duced. The upper airway is narrowed because the tongue is almost in contact with the back wall of the oropharynx. Large tonsils may also narrow this upper airway. Management Management of obstructive sleep apnea is generally multidisciplinary. Treatments in- clude continuous positive airway pressure machines; weight loss; dental appliances; and various surgical options, including nasal reconstruction, uvulopalatopharyngoplasty, uvulopalatal flap, mandibular osteotomy with or without hyoid myotomy and suspension, base of ton- gue surgery, tonsillectomy, maxillomandibular osteotomy and advancement, and tracheostomy [23].
    • 106 L.L. Cunningham Jr. et al / Atlas Oral Maxillofacial Surg Clin N Am 11 (2003) 87–107 Fig. 8. An MRI comparing the airway of a normal patient (A) versus a patient with obstructive sleep apnea (B). Note the difference in size of the airways. (C) and (D) show a similar comparison in the axial view. (From Schwab RJ. Upper airway assessment. Otolaryngol Clin North Am 1998;31 948–9; with permission.) References [1] Som PM, Curtin HD, editors. Head and neck imaging. Vol 1, 3rd edition. St. Louis, MO: Mosby; 1996. [2] Council on Scientific Affairs . Magnetic resonance imaging [prologue]. JAMA 1987;258:3283–5. [3] Future improvements in magnetic resonance imaging. Health Technol 1988;2:12–9. [4] Council on Scientific Affairs. Fundamentals of magnetic resonance imaging. JAMA 1987;258:3417–23. [5] Goaz PW, White SC, Pharoah MJ, editors. Goaz and White’s oral radiology: principles and interpretation. 4th edition. St. Louis, MO: Mosby; 1999. [6] Neville BW, Damm DD, Allen CM, et al. Pulpal and periapical disease. In: Oral and maxillofacial pathology. 2nd edition. Philadelphia: WB Saunders; 2002. p. 107–36. [7] Regezi JA, Sciubba J. Inflammatory jaw lesions. In: Oral pathology: clinical pathologic correlations. 3rd edition. Philadelphia: WB Saunders; 1999. p. 381–96. [8] Carek PJ, Dickerson LM, Sack JLDiagnosis and management of osteomyelitis. Am Fam Physician 2001;63: 2413–20. [9] Delbalso AM, Hall RE. Diagnostic imaging of maxillofacial and fascial space infections. In: Topazian RG, Goldberg MH, editors. Oral and maxillofacial infections. 3rd edition. Philadelphia: WB Saunders; 1994. p. 148–50. [10] Reinert S, Widlitzek H, Venderink DJ. The value of magnetic resonance imaging in the diagnosis of mandibular osteomyelitis. Br J Oral Maxillofac Surg 1999;37:459–63.
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