Osteomyelitis is an infection of bone that can affect the jaws. It originates from Greek words meaning "bone marrow infection". The infection causes ischemia and necrosis of the infected bone. It can be acute or chronic, suppurative or nonsuppurative. Common causes are odontogenic infections, trauma, surgery, and hematogenous spread. Symptoms include swelling, pain, and draining sinus tracts. Treatment involves antibiotics, surgical drainage, debridement of necrotic bone, and hyperbaric oxygen therapy in some cases.
Temporomandibular joint and muscle disorders (TMJ) cause jaw pain and dysfunction. There are three main types: myofascial pain involving jaw muscles, internal derangement involving a displaced disc or joint injury, and arthritis. Causes include trauma, teeth grinding, hormones, genetics, and stress. Treatment involves heat/ice, soft diet, jaw exercises, relaxation techniques, and over-the-counter anti-inflammatory drugs. More severe cases may require physical therapy, splints, injections, or surgery like arthrocentesis, arthroscopy, or disc removal.
This document discusses osteomyelitis, an inflammatory condition of the bone and bone marrow. It defines osteomyelitis and outlines predisposing factors like immunocompromisation, hypovascularity, and microbial virulence. It also describes the pathogenesis, microbiology, classification systems, clinical presentation, investigations, and treatment approaches for osteomyelitis. Treatment involves both conservative measures like antibiotics and rest, as well as surgical interventions like incision and drainage, tooth extractions, sequestrectomy, and in severe cases, jaw resection and reconstruction.
Preauricular incision is commonly used for TMJ surgeries. Other approaches include endaural, post-auricular, submandibular, post-ramal, hemicoronal, and coronal incisions. The choice depends on extent of pathology and surgeon preference.
APPROACHES
This document discusses osteomyelitis, including its pathogenesis and management. It defines osteomyelitis as an infection of the bone marrow and describes how local and systemic predisposing factors can lead to decreased bone vitality and impaired host defense. The main types of osteomyelitis covered are suppurative, focal sclerosing, diffuse sclerosing, and proliferative perositis. For each type, the document discusses pathogenesis, clinical features, histology, radiology, and management. Key points include how acute suppurative osteomyelitis can progress to chronic form if inadequately treated, and how eliminating infection sources is important but bone changes may persist radiographically for some types.
Maxillary sinus diseases are presented by Dr. Vishal Modha. The maxillary sinus is the largest paranasal sinus located within the maxilla bone. It develops embryologically from the lateral nasal wall and grows postnatally. The maxillary sinus anatomy includes thin bony walls that are vulnerable to trauma and contain important structures. Mucociliary drainage flows from the maxillary sinus ostium to the nasal cavity. Common maxillary sinus diseases include acute or chronic sinusitis, which can result from dental infections, trauma, or nasal obstruction and cause symptoms like facial pain and nasal congestion. Radiographs and CT scans may reveal mucosal thickening or opacification in sinusitis. Treatment involves antibiotics,
Rene LeFort in 1901 classified midface fractures based on the level of injury into 3 types: Lefort I, II, and III fractures. Since then there have been modifications to the classification system. Lefort I fractures involve the maxilla above the teeth and nasal floor. Treatment involves either closed or open reduction with fixation methods like miniplates or wires. Potential complications include nerve damage, infection, malocclusion, and sinus issues. Contemporary approaches emphasize early open reduction and anatomical fixation with miniplates to achieve accurate reconstruction of the midface structural pillars.
Peripheral giant cell granuloma (giant cell epulisKhin Soe
The document discusses two types of giant cell lesions of the jaw: peripheral giant cell granuloma (PGG) and central giant cell granuloma (CGG). PGG is a reactive lesion caused by local irritation or trauma that occurs on the gingiva. CGG is a benign process that occurs within the jaw bones and can be non-aggressive or aggressive depending on symptoms and growth rate. Both lesions contain multinucleated giant cells and are treated with surgical excision, with CGG having a slightly higher recurrence rate. Key distinguishing features and histological characteristics are provided.
The document discusses osteomyelitis, which is an inflammatory condition of bone that begins as an infection of the medullary cavity and spreads to involve the periosteum. It can be acute or chronic, and is caused by bacteria or fungi entering via trauma or a blood-borne route. Symptoms include pain, swelling, and pus drainage. Diagnosis involves medical imaging and biopsy. Treatment involves antibiotics, drainage of pus, debridement of infected tissue, and sometimes surgery. Chronic osteomyelitis can be difficult to treat and may require repeated surgeries. Risk factors include reduced blood supply to bone from conditions like diabetes.
Temporomandibular joint and muscle disorders (TMJ) cause jaw pain and dysfunction. There are three main types: myofascial pain involving jaw muscles, internal derangement involving a displaced disc or joint injury, and arthritis. Causes include trauma, teeth grinding, hormones, genetics, and stress. Treatment involves heat/ice, soft diet, jaw exercises, relaxation techniques, and over-the-counter anti-inflammatory drugs. More severe cases may require physical therapy, splints, injections, or surgery like arthrocentesis, arthroscopy, or disc removal.
This document discusses osteomyelitis, an inflammatory condition of the bone and bone marrow. It defines osteomyelitis and outlines predisposing factors like immunocompromisation, hypovascularity, and microbial virulence. It also describes the pathogenesis, microbiology, classification systems, clinical presentation, investigations, and treatment approaches for osteomyelitis. Treatment involves both conservative measures like antibiotics and rest, as well as surgical interventions like incision and drainage, tooth extractions, sequestrectomy, and in severe cases, jaw resection and reconstruction.
Preauricular incision is commonly used for TMJ surgeries. Other approaches include endaural, post-auricular, submandibular, post-ramal, hemicoronal, and coronal incisions. The choice depends on extent of pathology and surgeon preference.
APPROACHES
This document discusses osteomyelitis, including its pathogenesis and management. It defines osteomyelitis as an infection of the bone marrow and describes how local and systemic predisposing factors can lead to decreased bone vitality and impaired host defense. The main types of osteomyelitis covered are suppurative, focal sclerosing, diffuse sclerosing, and proliferative perositis. For each type, the document discusses pathogenesis, clinical features, histology, radiology, and management. Key points include how acute suppurative osteomyelitis can progress to chronic form if inadequately treated, and how eliminating infection sources is important but bone changes may persist radiographically for some types.
Maxillary sinus diseases are presented by Dr. Vishal Modha. The maxillary sinus is the largest paranasal sinus located within the maxilla bone. It develops embryologically from the lateral nasal wall and grows postnatally. The maxillary sinus anatomy includes thin bony walls that are vulnerable to trauma and contain important structures. Mucociliary drainage flows from the maxillary sinus ostium to the nasal cavity. Common maxillary sinus diseases include acute or chronic sinusitis, which can result from dental infections, trauma, or nasal obstruction and cause symptoms like facial pain and nasal congestion. Radiographs and CT scans may reveal mucosal thickening or opacification in sinusitis. Treatment involves antibiotics,
Rene LeFort in 1901 classified midface fractures based on the level of injury into 3 types: Lefort I, II, and III fractures. Since then there have been modifications to the classification system. Lefort I fractures involve the maxilla above the teeth and nasal floor. Treatment involves either closed or open reduction with fixation methods like miniplates or wires. Potential complications include nerve damage, infection, malocclusion, and sinus issues. Contemporary approaches emphasize early open reduction and anatomical fixation with miniplates to achieve accurate reconstruction of the midface structural pillars.
Peripheral giant cell granuloma (giant cell epulisKhin Soe
The document discusses two types of giant cell lesions of the jaw: peripheral giant cell granuloma (PGG) and central giant cell granuloma (CGG). PGG is a reactive lesion caused by local irritation or trauma that occurs on the gingiva. CGG is a benign process that occurs within the jaw bones and can be non-aggressive or aggressive depending on symptoms and growth rate. Both lesions contain multinucleated giant cells and are treated with surgical excision, with CGG having a slightly higher recurrence rate. Key distinguishing features and histological characteristics are provided.
The document discusses osteomyelitis, which is an inflammatory condition of bone that begins as an infection of the medullary cavity and spreads to involve the periosteum. It can be acute or chronic, and is caused by bacteria or fungi entering via trauma or a blood-borne route. Symptoms include pain, swelling, and pus drainage. Diagnosis involves medical imaging and biopsy. Treatment involves antibiotics, drainage of pus, debridement of infected tissue, and sometimes surgery. Chronic osteomyelitis can be difficult to treat and may require repeated surgeries. Risk factors include reduced blood supply to bone from conditions like diabetes.
Central Giant Cell Granuloma :
WHO has defined it as an intraosseous lesion consisting of cellular and fibrous tissue that contains multiple foci of hemorrhage, aggregation of multinucleated giant cells and occasionally trabaculae of woven bone
Etiology JAFFE (1953): considered this lesion to be a local reparative reaction of bone, possibly to intramedullary hemorrhage or trauma, hence the term reparative giant cell granuloma was accepted.
Charles A Waldron & W G Shafer (1966) suggested trauma be an important etiological factor in the initiation of the CGCG of the jaws
Thoma K H (1986) suggested that the lesion may be due to capillary injury caused by defective wall due to some type of trauma
J V Soames and J C Southam (1997) suggested that it could be a reaction to some form of hemodynamic disturbance in bone marrow, perhaps associated with trauma and hemorrhage REGEZI AND SCIUBBA(1999) :
Suggested that
Response to previous traumatic or inflammatory episodes.
This lesion is charecterised by proliferation of fibroblasts and multinucleated giant cells, in a densely packed stromaThe CGCG is a benign process that occurs almost exclusively within the jaw bones
CLINICAL PRESENTATION
Found predominantly in children and young adult
It has a female predilection (2:1)
Most commonly affected site is the anterior portion of the jaws, with an increased frequency of occurrence in the mandible
Majority of the CGCG of jaws are painless, expansion of bone is detected on routine examination
Few cases may be associated with pain, paresthesia or perforation of a cortical bone plate, occasionally resulting in the ulceration of the mucosal surface by the underlying lesion
Radiographic featuresCentral giant cell lesions present as radiolucent defects. Which may be unilocular or multilocular.
The defect is usually well delineated
The lesion may vary from a 5×5mm incidental radiographic findings to a destructive lesion greater than 10cm in size.
radiographic findings
A small unilocular lesion may be confused with periapical granuloma or cysts.
multilocular giant cell lesions cannot be radiographically distinguished from ameloblastomas or other multilocular lesions. Based on clinical and radiological features CGCG may be divided into two categories
- Non-aggressive lesion
- Aggressive lesion
The non aggressive lesion makes up most cases and exhibit few or no symptoms, they demonstrate slow growth and do not show cortical perforation or root resorption of teeth involved in the lesion. The aggressive lesions are characterized by pain, rapid growth, cortical perforation and root resorption and show marked tendency to recur when compared with non aggressive typeSoft spongy, brownish to reddish friable tissue of various size.
A specimen is usually coated with fresh or coagulated blood. Giant cell lesions of the jaws show a variety of features. Common to all is the presence of few to many multinucleated
Peripheral and central giant cell granulomaRijuwana77
This document discusses two types of non-epithelial tumours of the oral cavity: peripheral giant cell granuloma and central giant cell granuloma. Peripheral giant cell granuloma originates from the periodontal membrane or alveolar bone and presents as a soft tissue nodule composed of multinucleated giant cells. Central giant cell granuloma is a rare, benign, intraosseous lesion most commonly found in the mandible of young people that causes expansion of the bone and resorption of tooth roots. Both lesions contain proliferation of multinucleated giant cells and other cells and may require surgical excision, with central giant cell granuloma having a higher rate of recurrence.
This document discusses impacted teeth, specifically focusing on impacted third molars. It begins with definitions of impacted teeth and provides the etymology and theories of tooth impaction. Local and systemic causes of impaction are described. Surgical anatomy of impacted third molars is reviewed, along with classifications of impacted mandibular third molars. Indications and contraindications for removal are outlined. Complications are briefly mentioned. The document is intended as a reference for oral and maxillofacial surgeons regarding the management of impacted third molars.
This document provides an overview of oral pigmentation and pigmented lesions. It begins by defining pigment and describing normal oral mucosal color. Melanin is identified as the primary pigment producing brown coloration in the body. Factors that can affect melanogenesis are discussed such as sun exposure, drugs, hormones and genetic constitution. The document then classifies pigmentation into endogenous (originating from within the body such as melanin pigmentation) and exogenous (from external sources). Specific endogenous and exogenous pigmented lesions are described. The document concludes by discussing malignant melanoma, describing its clinical presentation and treatment which primarily involves wide local excision surgery.
This document discusses red and white lesions of the oral cavity, focusing on oral candidiasis. It describes the various types of oral candidiasis including pseudomembranous, erythematous, chronic plaque-type, and median rhomboid glossitis. Predisposing factors, clinical findings, diagnosis, treatment with antifungal medications or surgery, and prognosis are summarized for each type. Chronic hyperplastic candidiasis may require long-term antifungal therapy or surgery due to risk of recurrence. Overall prognosis is generally good if predisposing factors can be addressed.
This document provides information about case histories in dentistry. It defines a case history as a planned conversation between patient and doctor to determine the nature of the patient's illness or mental state. The summary includes details about the contents, purpose, and components of a thorough case history, which establishes the patient's medical history, dental history, and other relevant details to allow for an accurate diagnosis and safe treatment plan. Physical examinations and potential investigations are also discussed.
This document discusses odontogenic keratocysts (OKCs), a type of jaw cyst. It covers the classification, causes, histopathology, clinical features, radiographic features, differential diagnosis, treatment principles, and surgical treatment options for OKCs. OKCs most commonly occur in the mandibular molar and ramus areas and are often radiolucent and multilocular in appearance on radiographs. Treatment options include wide surgical excision or marsupialization to prevent recurrence of these cysts which have a high rate of recurrence compared to other jaw cysts.
Cemento osseus dysplasia (Doctor Faris Alabeedi MSc, MMedSc, PgDip, BDS.)Doctor Faris Alabeedi
Cemento-osseous dysplasia is a non-neoplastic fibro-osseous lesion that commonly affects the tooth-bearing regions of the jaws in middle-aged black women. It has three variants defined by location: periapical cemento-osseous dysplasia near the tooth apex, focal cemento-osseous dysplasia associated with a single tooth, and florid cemento-osseous dysplasia with involvement of multiple jaw quadrants. Radiographically, lesions appear as well-defined radiolucencies early on and progress to mixed or diffuse radiopacities as they mature. Histologically, lesions contain mineralized bone and cementum-like
Indian Dental Academy is a leader in continuing dental education, providing both online and offline courses. The document discusses ameloblastoma, a type of odontogenic tumor. It defines ameloblastoma, provides its history and classifications including clinical, radiological, and histopathological. Treatment options discussed include medical therapy, radiotherapy, and various surgical treatments such as enucleation, marsupialization, and curettage. Radiographs, biopsy, CT, and MRI are investigated for ameloblastoma.
The document provides information on internal derangement of the temporomandibular joint (TMJ). It begins with definitions of internal derangement and Wilkes classification system for stages of derangement. It then discusses etiology, including trauma as a common cause. Physical findings and non-surgical and surgical treatment procedures are outlined. Non-surgical options include splint therapy, medications, acupuncture and others aimed at reducing pain and improving joint function.
This document discusses condylar fractures of the mandible. It begins by providing background on condylar fracture development, anatomy, surgical anatomy, blood supply, nerve supply and muscle attachments. It then covers the etiology, associated injuries, mechanisms of injury and various classification systems for condylar fractures. The document outlines the diagnosis process including history, clinical examination and radiographic imaging. It concludes by discussing treatment approaches, focusing on the aims of surgery and indications for conservative versus surgical management.
A cyst is an epithelium-lined sac containing fluid or semisolid material. In the formation of a cyst, the epithelial cells first proliferate and later undergo degeneration and liquefaction. The liquefied material exerts equal pressure on the walls of the cyst from within. Cysts grow by expansion and thus displace the adjacent teeth by pressure. May can produce expansion of the cortical bone. On a radiograph, the radiolucency of a cyst is usually bordered by a radiopaque periphery of dense sclerotic bone. The radiolucency may be unilocular or multilocular. Odontogenic cysts are those which arise from the epithelium associated with the development of teeth. The source of epithelium is from the enamel organ, the reduced enamel epithelium, the cell rests of Malassez or the remnants of the dental lamina.
This document provides an overview of fibro-osseous lesions and focuses on fibrous dysplasia. It discusses the classification, etiology, clinical features, radiographic features, histologic features, treatment and prognosis of fibrous dysplasia. Fibrous dysplasia is a benign bone lesion caused by a mutation in the GNAS1 gene. It can present as monostotic, polyostotic or craniofacial lesions. Radiographically, it appears as radiolucent or radiopaque areas with a "ground glass" appearance. Histologically, it is characterized by fibrous tissue and irregular woven bone trabeculae. Treatment involves surgery or bisphosphonates and the prognosis is generally good
This document discusses giant cell lesions of the jaws. It begins by defining giant cells and describing their origin from monocytes and macrophages. Giant cell lesions are then classified as inflammatory/reactive, metabolic, or neoplastic. Central giant cell granuloma, aneurysmal bone cyst, and traumatic bone cyst are discussed as examples of inflammatory/reactive lesions. Cherubism and brown tumor of hyperparathyroidism represent metabolic giant cell lesions. Osteoblastoma is provided as an example of a neoplastic giant cell lesion. Clinical, radiographic, histologic, and treatment details are outlined for many of the conditions.
This document discusses the history, definition, etiology, clinical characteristics, diagnostic methods, and treatment of myofascial pain dysfunction syndrome (MPDS). Some key points:
- MPDS is a pain disorder caused by trigger points in the muscles of mastication that refer pain to the head and neck. It is the most common cause of masticatory pain.
- Etiology may include occlusal factors, prosthetic problems, malocclusion, psychophysiologic factors, and trauma.
- Clinical characteristics include pain in the head/neck, limited jaw motion, joint noises, and tender muscles.
- Treatment involves a multidisciplinary approach including medications, trigger point injections, physical
Wisdom teeth are the third and last molars on each side of the upper and lower jaws. They are also the final teeth to erupt; they usually appear when a person is in their late teens or early twenties
The document discusses cysts of the jaws, including definitions, classifications, pathogenesis, diagnosis and treatment. Some key points:
- Cysts are epithelial or non-epithelial lined pathological cavities filled with fluid or semi-fluid. The jaws are a common site.
- Cysts are classified based on origin (odontogenic vs non-odontogenic), lining (epithelial vs non-epithelial), and other factors.
- Diagnosis involves clinical exam, radiography, aspiration of cyst fluid, and biopsy. Radiographs show a radiolucent area with defined borders.
- Treatment aims to remove the cyst lining and prevent recurrence. Common procedures include en
This document discusses osteomyelitis, an infection and inflammation of bone and bone marrow. It begins by describing the typical blood supply to long bones in infants, children, and adults. It then covers the causes, classification, clinical features, locations, and pathophysiology of osteomyelitis. The remainder of the document focuses on the diagnostic imaging findings including bone scans, MRI, CT, and radiographic signs seen during early and late stages of the disease. Treatment typically involves intravenous antibiotics and possibly surgical drainage or debridement. Complications can include sinus track formation, pathological fractures, or rare secondary cancers.
This document provides information on osteomyelitis of the jaw, including its classification, etiology, pathogenesis, microbiology, clinical findings, imaging, and treatment. It discusses the different types of osteomyelitis (acute suppurative, secondary chronic, primary chronic, non-suppurative). It also covers osteoradionecrosis of the jaw, its definition, clinical findings, radiological features, treatment with hyperbaric oxygen therapy, and prevention. Microorganisms commonly involved include viridans streptococci and anaerobes such as Peptostreptococcus and Fusobacterium. Imaging tools like radiography, CT, MRI, and radionuclide bone scanning can aid in diagnosis
Central Giant Cell Granuloma :
WHO has defined it as an intraosseous lesion consisting of cellular and fibrous tissue that contains multiple foci of hemorrhage, aggregation of multinucleated giant cells and occasionally trabaculae of woven bone
Etiology JAFFE (1953): considered this lesion to be a local reparative reaction of bone, possibly to intramedullary hemorrhage or trauma, hence the term reparative giant cell granuloma was accepted.
Charles A Waldron & W G Shafer (1966) suggested trauma be an important etiological factor in the initiation of the CGCG of the jaws
Thoma K H (1986) suggested that the lesion may be due to capillary injury caused by defective wall due to some type of trauma
J V Soames and J C Southam (1997) suggested that it could be a reaction to some form of hemodynamic disturbance in bone marrow, perhaps associated with trauma and hemorrhage REGEZI AND SCIUBBA(1999) :
Suggested that
Response to previous traumatic or inflammatory episodes.
This lesion is charecterised by proliferation of fibroblasts and multinucleated giant cells, in a densely packed stromaThe CGCG is a benign process that occurs almost exclusively within the jaw bones
CLINICAL PRESENTATION
Found predominantly in children and young adult
It has a female predilection (2:1)
Most commonly affected site is the anterior portion of the jaws, with an increased frequency of occurrence in the mandible
Majority of the CGCG of jaws are painless, expansion of bone is detected on routine examination
Few cases may be associated with pain, paresthesia or perforation of a cortical bone plate, occasionally resulting in the ulceration of the mucosal surface by the underlying lesion
Radiographic featuresCentral giant cell lesions present as radiolucent defects. Which may be unilocular or multilocular.
The defect is usually well delineated
The lesion may vary from a 5×5mm incidental radiographic findings to a destructive lesion greater than 10cm in size.
radiographic findings
A small unilocular lesion may be confused with periapical granuloma or cysts.
multilocular giant cell lesions cannot be radiographically distinguished from ameloblastomas or other multilocular lesions. Based on clinical and radiological features CGCG may be divided into two categories
- Non-aggressive lesion
- Aggressive lesion
The non aggressive lesion makes up most cases and exhibit few or no symptoms, they demonstrate slow growth and do not show cortical perforation or root resorption of teeth involved in the lesion. The aggressive lesions are characterized by pain, rapid growth, cortical perforation and root resorption and show marked tendency to recur when compared with non aggressive typeSoft spongy, brownish to reddish friable tissue of various size.
A specimen is usually coated with fresh or coagulated blood. Giant cell lesions of the jaws show a variety of features. Common to all is the presence of few to many multinucleated
Peripheral and central giant cell granulomaRijuwana77
This document discusses two types of non-epithelial tumours of the oral cavity: peripheral giant cell granuloma and central giant cell granuloma. Peripheral giant cell granuloma originates from the periodontal membrane or alveolar bone and presents as a soft tissue nodule composed of multinucleated giant cells. Central giant cell granuloma is a rare, benign, intraosseous lesion most commonly found in the mandible of young people that causes expansion of the bone and resorption of tooth roots. Both lesions contain proliferation of multinucleated giant cells and other cells and may require surgical excision, with central giant cell granuloma having a higher rate of recurrence.
This document discusses impacted teeth, specifically focusing on impacted third molars. It begins with definitions of impacted teeth and provides the etymology and theories of tooth impaction. Local and systemic causes of impaction are described. Surgical anatomy of impacted third molars is reviewed, along with classifications of impacted mandibular third molars. Indications and contraindications for removal are outlined. Complications are briefly mentioned. The document is intended as a reference for oral and maxillofacial surgeons regarding the management of impacted third molars.
This document provides an overview of oral pigmentation and pigmented lesions. It begins by defining pigment and describing normal oral mucosal color. Melanin is identified as the primary pigment producing brown coloration in the body. Factors that can affect melanogenesis are discussed such as sun exposure, drugs, hormones and genetic constitution. The document then classifies pigmentation into endogenous (originating from within the body such as melanin pigmentation) and exogenous (from external sources). Specific endogenous and exogenous pigmented lesions are described. The document concludes by discussing malignant melanoma, describing its clinical presentation and treatment which primarily involves wide local excision surgery.
This document discusses red and white lesions of the oral cavity, focusing on oral candidiasis. It describes the various types of oral candidiasis including pseudomembranous, erythematous, chronic plaque-type, and median rhomboid glossitis. Predisposing factors, clinical findings, diagnosis, treatment with antifungal medications or surgery, and prognosis are summarized for each type. Chronic hyperplastic candidiasis may require long-term antifungal therapy or surgery due to risk of recurrence. Overall prognosis is generally good if predisposing factors can be addressed.
This document provides information about case histories in dentistry. It defines a case history as a planned conversation between patient and doctor to determine the nature of the patient's illness or mental state. The summary includes details about the contents, purpose, and components of a thorough case history, which establishes the patient's medical history, dental history, and other relevant details to allow for an accurate diagnosis and safe treatment plan. Physical examinations and potential investigations are also discussed.
This document discusses odontogenic keratocysts (OKCs), a type of jaw cyst. It covers the classification, causes, histopathology, clinical features, radiographic features, differential diagnosis, treatment principles, and surgical treatment options for OKCs. OKCs most commonly occur in the mandibular molar and ramus areas and are often radiolucent and multilocular in appearance on radiographs. Treatment options include wide surgical excision or marsupialization to prevent recurrence of these cysts which have a high rate of recurrence compared to other jaw cysts.
Cemento osseus dysplasia (Doctor Faris Alabeedi MSc, MMedSc, PgDip, BDS.)Doctor Faris Alabeedi
Cemento-osseous dysplasia is a non-neoplastic fibro-osseous lesion that commonly affects the tooth-bearing regions of the jaws in middle-aged black women. It has three variants defined by location: periapical cemento-osseous dysplasia near the tooth apex, focal cemento-osseous dysplasia associated with a single tooth, and florid cemento-osseous dysplasia with involvement of multiple jaw quadrants. Radiographically, lesions appear as well-defined radiolucencies early on and progress to mixed or diffuse radiopacities as they mature. Histologically, lesions contain mineralized bone and cementum-like
Indian Dental Academy is a leader in continuing dental education, providing both online and offline courses. The document discusses ameloblastoma, a type of odontogenic tumor. It defines ameloblastoma, provides its history and classifications including clinical, radiological, and histopathological. Treatment options discussed include medical therapy, radiotherapy, and various surgical treatments such as enucleation, marsupialization, and curettage. Radiographs, biopsy, CT, and MRI are investigated for ameloblastoma.
The document provides information on internal derangement of the temporomandibular joint (TMJ). It begins with definitions of internal derangement and Wilkes classification system for stages of derangement. It then discusses etiology, including trauma as a common cause. Physical findings and non-surgical and surgical treatment procedures are outlined. Non-surgical options include splint therapy, medications, acupuncture and others aimed at reducing pain and improving joint function.
This document discusses condylar fractures of the mandible. It begins by providing background on condylar fracture development, anatomy, surgical anatomy, blood supply, nerve supply and muscle attachments. It then covers the etiology, associated injuries, mechanisms of injury and various classification systems for condylar fractures. The document outlines the diagnosis process including history, clinical examination and radiographic imaging. It concludes by discussing treatment approaches, focusing on the aims of surgery and indications for conservative versus surgical management.
A cyst is an epithelium-lined sac containing fluid or semisolid material. In the formation of a cyst, the epithelial cells first proliferate and later undergo degeneration and liquefaction. The liquefied material exerts equal pressure on the walls of the cyst from within. Cysts grow by expansion and thus displace the adjacent teeth by pressure. May can produce expansion of the cortical bone. On a radiograph, the radiolucency of a cyst is usually bordered by a radiopaque periphery of dense sclerotic bone. The radiolucency may be unilocular or multilocular. Odontogenic cysts are those which arise from the epithelium associated with the development of teeth. The source of epithelium is from the enamel organ, the reduced enamel epithelium, the cell rests of Malassez or the remnants of the dental lamina.
This document provides an overview of fibro-osseous lesions and focuses on fibrous dysplasia. It discusses the classification, etiology, clinical features, radiographic features, histologic features, treatment and prognosis of fibrous dysplasia. Fibrous dysplasia is a benign bone lesion caused by a mutation in the GNAS1 gene. It can present as monostotic, polyostotic or craniofacial lesions. Radiographically, it appears as radiolucent or radiopaque areas with a "ground glass" appearance. Histologically, it is characterized by fibrous tissue and irregular woven bone trabeculae. Treatment involves surgery or bisphosphonates and the prognosis is generally good
This document discusses giant cell lesions of the jaws. It begins by defining giant cells and describing their origin from monocytes and macrophages. Giant cell lesions are then classified as inflammatory/reactive, metabolic, or neoplastic. Central giant cell granuloma, aneurysmal bone cyst, and traumatic bone cyst are discussed as examples of inflammatory/reactive lesions. Cherubism and brown tumor of hyperparathyroidism represent metabolic giant cell lesions. Osteoblastoma is provided as an example of a neoplastic giant cell lesion. Clinical, radiographic, histologic, and treatment details are outlined for many of the conditions.
This document discusses the history, definition, etiology, clinical characteristics, diagnostic methods, and treatment of myofascial pain dysfunction syndrome (MPDS). Some key points:
- MPDS is a pain disorder caused by trigger points in the muscles of mastication that refer pain to the head and neck. It is the most common cause of masticatory pain.
- Etiology may include occlusal factors, prosthetic problems, malocclusion, psychophysiologic factors, and trauma.
- Clinical characteristics include pain in the head/neck, limited jaw motion, joint noises, and tender muscles.
- Treatment involves a multidisciplinary approach including medications, trigger point injections, physical
Wisdom teeth are the third and last molars on each side of the upper and lower jaws. They are also the final teeth to erupt; they usually appear when a person is in their late teens or early twenties
The document discusses cysts of the jaws, including definitions, classifications, pathogenesis, diagnosis and treatment. Some key points:
- Cysts are epithelial or non-epithelial lined pathological cavities filled with fluid or semi-fluid. The jaws are a common site.
- Cysts are classified based on origin (odontogenic vs non-odontogenic), lining (epithelial vs non-epithelial), and other factors.
- Diagnosis involves clinical exam, radiography, aspiration of cyst fluid, and biopsy. Radiographs show a radiolucent area with defined borders.
- Treatment aims to remove the cyst lining and prevent recurrence. Common procedures include en
This document discusses osteomyelitis, an infection and inflammation of bone and bone marrow. It begins by describing the typical blood supply to long bones in infants, children, and adults. It then covers the causes, classification, clinical features, locations, and pathophysiology of osteomyelitis. The remainder of the document focuses on the diagnostic imaging findings including bone scans, MRI, CT, and radiographic signs seen during early and late stages of the disease. Treatment typically involves intravenous antibiotics and possibly surgical drainage or debridement. Complications can include sinus track formation, pathological fractures, or rare secondary cancers.
This document provides information on osteomyelitis of the jaw, including its classification, etiology, pathogenesis, microbiology, clinical findings, imaging, and treatment. It discusses the different types of osteomyelitis (acute suppurative, secondary chronic, primary chronic, non-suppurative). It also covers osteoradionecrosis of the jaw, its definition, clinical findings, radiological features, treatment with hyperbaric oxygen therapy, and prevention. Microorganisms commonly involved include viridans streptococci and anaerobes such as Peptostreptococcus and Fusobacterium. Imaging tools like radiography, CT, MRI, and radionuclide bone scanning can aid in diagnosis
1) Osteomyelitis and osteoradionecrosis of the jaw bones are inflammatory conditions that can develop due to infections, trauma, radiation therapy or bisphosphonate use.
2) They are characterized by necrosis of bone tissue which fails to heal properly and can lead to exposed bone, pain, swelling and draining fistulas.
3) Treatment involves controlling infections, relieving pain, removing devitalized bone tissue surgically if needed, and reconstructing the affected area with grafts or flaps. Preventing these conditions involves minimizing invasive dental procedures for those at high risk.
This document summarizes fibro-osseous lesions (FOLs), which are characterized by the replacement of bone by a benign connective tissue matrix displaying varying degrees of mineralization. FOLs include fibrotic dysplasia, cemental lesions arising from the periodontal ligament, and fibro-osseous neoplasms. Fibrotic dysplasia is caused by a GNAS1 gene mutation and can be monostotic (single bone) or polyostotic (multiple bones). Polyostotic fibrotic dysplasia can occur with skin pigmentation and endocrine disorders. Treatment depends on symptoms and may include observation, medication such as bisphosphonates, surgical remodeling, or radical excision.
This document discusses osteomyelitis, an inflammation of bone tissue. It begins with definitions of osteomyelitis and classifications based on course, suppuration, and anatomical location. Etiology and pathogenesis are then reviewed, noting that osteomyelitis can arise from contiguous infections, hematogenous spread, or underlying bone diseases. Clinical features include pain, swelling and sinus tract formation. Investigations include imaging modalities like CT, MRI and scintigraphy to identify bone changes. Treatment involves antibiotics, surgery and supportive care to eliminate pathogens and promote healing.
Osteomyelitis is an inflammatory condition of bone that involves the medullary cavity and has a tendency to progress along this space and involve the adjacent cortex, periosteum, and soft tissue. It is commonly caused by odontogenic infections or trauma. Staphylococcus aureus accounts for 80% of jaw osteomyelitis cases. The infection initiates from a contiguous focus or hematogenous spread and causes inflammation, tissue necrosis, pus formation, and bone destruction if not properly treated. Without treatment, it can progress to chronic stages involving bone lysis, sequestrum formation, and involucrum development.
This document discusses TMJ ankylosis, including classifications, causes, diagnosis, and surgical treatment. It begins by classifying TMJ disorders into organic, non-organic functional, and non-organic with secondary organic changes. Ankylosis is discussed as an organic articular disturbance that can be fibrous, bony, unilateral, or bilateral. Common causes are trauma, infection, and inflammation. Diagnosis involves limited or no mouth opening and radiographic findings. Surgical treatment aims to create a gap, improve function and nutrition, and sometimes uses costochondral grafts or temporalis fascia. The Popowich modification of preauricular surgical approach is described as advantageous for reducing facial nerve injury and improving visibility
Osteomyelitis may be a very dreadful condition for both the suffering patient & the treating orthopaedic surgeon.Here is the brief presentation on it deeply focused on its standard management.
Introduction to radiological diagnosis of osteomyelitis for undergraduatesGirendra Shankar
This document discusses different types of bone infections seen in musculoskeletal radiology. It describes osteomyelitis as bacterial infection of bone that most commonly affects the long bones of children. Pott's disease refers to tuberculosis infection of the spine that causes vertebral body destruction. Congenital infections like rubella and syphilis can result in characteristic radiographic findings in newborns such as celery stalking of the metaphysis.
The document discusses infection of bone and joint, including osteomyelitis, septic arthritis, and tuberculosis. It provides details on the mechanisms, symptoms, investigations, and treatments for acute and chronic osteomyelitis. It describes how septic arthritis can infect joints via the bloodstream or skin. Tuberculosis is caused by Mycobacterium tuberculosis and can infect synovial joints, tendon sheaths, and vertebrae, leading to granuloma formation, joint destruction, and abscesses. Treatment involves chemotherapy with rifampicin and isoniazid.
Osteomyelitis is an infection of bone that has been described since ancient times. It is commonly caused by Staphylococcus aureus bacteria entering the bone hematogenously. Acute osteomyelitis typically affects the metaphysis of long bones in children. Chronic osteomyelitis results from untreated acute infection and is characterized by sequestered necrotic bone. Treatment involves antibiotics, drainage of pus, and surgical debridement or removal of infected bone.
This document provides an overview of chronic osteomyelitis. It begins with definitions and describes the pathogenesis as bacteria reaching the metaphysis, causing inflammation and tissue necrosis. Imaging can detect bone changes like lytic lesions. Diagnosis involves biopsy for culture and histology. Chronic osteomyelitis is characterized by infected dead bone (sequestrum) surrounded by sclerotic bone (involucrum) that forms draining sinus tracts. Multiple organisms are often present and biofilm formation complicates treatment. Differential diagnosis includes tuberculosis, soft tissue infection, and tumors.
1) Osteoarticular tuberculosis is a chronic infection that can affect bones and joints, most commonly the spine.
2) It is caused by hematogenous spread of Mycobacterium tuberculosis from a primary pulmonary or extrapulmonary focus of infection.
3) Diagnosis requires biopsy and culture of infected tissue, as clinical features can be nonspecific. Treatment involves a prolonged course of antitubercular drugs, sometimes with surgical intervention.
1. Chronic osteomyelitis in children can result from untreated acute hematogenous osteomyelitis or spread of infection from neighboring tissues. Common causes include open fractures and puncture wounds.
2. Clinical findings include fever, bone pain, local tenderness, sinus discharge, and bone deformities. Pathological features include bone necrosis, new bone formation, and prostaglandin-induced bone resorption.
3. Treatment involves antibiotics, surgical debridement to remove dead tissue, and reconstruction if significant bone loss. The goal is to eradicate infection while preserving bone stock.
This document discusses subacute osteomyelitis, which is a distinct type of osteomyelitis with milder symptoms than acute osteomyelitis. It most commonly affects the distal femur and proximal/distal tibia. Staphylococcus aureus is the most common causative organism. Clinical features include pain over several weeks/months, limping, swelling, and tenderness without fever. Radiological findings include Brodie's abscess appearing as an oval cavity surrounded by sclerosis. Treatment involves antibiotics, biopsy, and surgery if diagnosis is uncertain or conservative treatment fails.
This document provides information on aggressive periodontitis, including its historical background, classification, clinical presentation, epidemiology, etiology, and pathogenesis. Some key points include:
- Aggressive periodontitis is a rare, severe form of periodontitis characterized by early onset and familial aggregation. It includes localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP).
- LAP typically affects first molars and incisors in adolescents/young adults and is associated with A. actinomycetemcomitans infection, while GAP has a more generalized pattern of attachment/bone loss.
- Screening involves measuring attachment loss via probing or radiographic assessment of alveolar bone levels
Osteomyelitis is an inflammation of bone caused by an infecting organism. Staphylococcus aureus is the most common cause. Acute hematogenous osteomyelitis usually involves the metaphysis of long bones in children. Diagnosis is based on clinical features like localized tenderness and lab tests showing elevated inflammatory markers. Plain X-rays may initially only show soft tissue swelling and osteopenia before lytic bone changes appear in subacute or chronic cases.
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The facial nerve, also known as cranial nerve VII, is one of the 12 cranial nerves originating from the brain. It's a mixed nerve, meaning it contains both sensory and motor fibres, and it plays a crucial role in controlling various facial muscles, as well as conveying sensory information from the taste buds on the anterior two-thirds of the tongue.
2. The word “osteomyelitis” originates from the
ancient Greek words osteon (bone) and
muelinos (marrow) and means infection of
medullary portion of the bone.
The infection- pus and edema in the
medullary cavity and beneath the periosteum
compromises or obstructs the local blood
supply.
3. Following ischemia, the infected bone
becomes necrotic and leads to sequester
formation, which is considered a classical
sign of osteomyelitis (Topazian 1994, 2002).
True infection of the bone induced by
pyogenic microorganisms (Marx1991).
4. In the preantibiotic era:
an acute onset secondary chronic
process (Wassmund 1935; Axhausen 1934).
After the introduction of antibiotics:
Subacute or chronic forms of osteomyelitis
(Becker 1973; Bünger 1984).
5. Suppurative osteomyelitis(acute & chronic)
Chronic sclerosing non-suppurative
osteomyelitis or Garre’s osteomyelitis
Osteomyelitis accompanying systemic disease
such as tuberculosis,actinomycosis & syphillis
6. Reference Classification Classification
criteria
Hudson JW
Osteomyelitis of the jaws: a 50-
year
perspective.
J Oral Maxillofac Surg 1993 Dec;
51(12):1294-301
I. Acute forms of osteomyelitis
(suppurative
or nonsuppurative)
A. Contagious focus
1. Trauma
2. Surgery
3. Odontogenic Infection
B. Progressive
1. Burns
2. Sinusitis
3. Vascular insufficiency
C. Hematogenous(metastatic)
1. Developing skeleton (children)
II. Chronic forms of osteomyelitis
A. Recurrent multifocal
1. Developing skeleton (children)
2. Escalated osteogenic (activity
< age 25 years)
B. Garre's
1. Unique proliferative
subperiosteal reaction
2. Developing skeleton (children
and young adults)
Classification based on clinical
picture and
radiology.
The two major groups (acute and
chronic osteomyelitis) are
differentiated
by the clinical course of the
disease after onset, relative to
surgical
and antimicrobial therapy. The
arbitrary time limit of 1 month is
used
to differentiate acute from chronic
osteomyelitis (Marx 1991;
Mercuri1991;
Koorbusch1992).
7. C. Suppurative or nonsuppurative
1. Inadequately treated forms
2. Systemically compromised
forms
3. Refractory forms (chronic
recurrent
multifocal osteomyelitis
CROM)
D. Diffuse sclerosing
1. Fastidious microorganisms
2. Compromised host/pathogen
interface
8. Reference Classification Classification
criteria
Topazian RG
Osteomyelitis of the Jaws. In
Topizan RG,
Goldberg MH (eds): Oral and
Maxillofacial
Infections.
Philadelphia, WB Saunders 1994,
Chapter 7, pp 251-88
I. Suppurative osteomyelitis
1. Acute suppurative osteomyelitis
2. Chronic suppurative
osteomyelitis
– Primary chronic suppurative
osteomyelitis
– Secondary chronic suppurative
osteomyelitis
3. Infantile osteomyelitis
II. Nonsuppurative osteomyelitis
1. Chronic sclerosing osteomyelitis
– Focal sclerosing osteomyelitis
– Diffuse sclerosing osteomyelitis
2. Garre's sclerosing osteomyelitis
3. Actinomycotic osteomyelitis
4. Radiation osteomyelitis and
necrosis
Classification based on clinical
picture,
radiology, and etiology
(specific forms such as syphilitic,
tuberculous, brucellar, viral,
chemical,
Escherichia coli and Salmonella
osteomyelitis not integrated in
classification)
9.
10. Fractures due to trauma and RTA
Gunshot wounds
Radiation damage
Paeget’s disease
Osteoporosis
Systemic disease
:Malnutrition,acute
leukemia,uncontrolled D.M.,Sickle
cell anemia,Chronic alcoholism
11. Wilensky 1932
Hitchin & Naylor(1957)- 4 cases maxillitis of
infancy
Staphylococcus aureus
Injuries through foreign objects
Ramon et al 1977 –infections from infant’s
nose
Haematogenous invasion – streptococci
12. Sudden onset ,acute course
High fever, rapid pulse, vomiting, delirium.
Signs-
Swelling of face,
Edema of eyelids
Subperioteal abscess
Sinus tracts draining pus
13. Minimal bone involment
Long standing case -Sequestra
15. Localised or widespread
Debilitating systemic disease
(a) Close-up view of the socket in the
left mandibular first molar region.
16. Odontogenic infections
Periapical disease
Periodontal disease
Pericororonal infection
Infection from odontogenic cyst or tumor
Infection from extraction wound
o Staphylococcus aureus, rarely albus
17.
18. Panoramic radiograph showing neither
abnormal consolidation nor ill-defined
trabecular bone structure around the
socket and clear running of the inferior
alveolar arteries.
CT scans at 14 days after the initial visit
showing remarkable absorption of the
cortical bone in the left mandibular molar
region. (a) Axial section. (b) Coronal
section.
19. Mandible or maxilla
Presence of unerupted tooth
Conservative treatment (antibiotics)
Condyle or TMJ –Severe deformities (Rowe &
Heslop 1957)
20. A proliferative rather than a lytic bony
response is usually seen due to attenuation
of the causative organisms and the improved
immunological status of children in Britain.
The importance of penicillin-resistant
organisms and anaerobes, early diagnosis by
scintigraphy and the use of hyperbaric
oxygen therapy are highlighted.
Br J Oral Maxillofac Surg. 1987 Jun;25(3):204-17.
Osteomyelitis of the mandible in children--clinical presentations
and review of management.
Ord RA, el-Attar A.
21. Mandible> Maxilla
Sequestation of condyle rare –Linsey 1953
Rbc and hb decreased
Leukocytosis
22. Enlargement of marrow spaces(early)
Cortex involved-sequestra
Larger radiolucent areas –active bone
destruction.
23. Complete bed rest
High protein ,high caloric diet
I.V. solutions
Blood transfusions
Analgesics
Antibiotics –penicillin
24. Immobilization-bartons bandage
Hot moist compresses –localization of
infection
Surgical drainage
Extactions-offending tooth
Edentulous jaws
Incision –along alveolar crest
Window is cut
Rubber dam inserted
26. Continued use of
Antibiotics
External hot moist packs
Analgesics
Hot saline mouth rinses
o Catheter –irrigate area with warm normal
saline
o Further sequestrectomies-acute symptoms
subside
27. Primary or secondary
Radiopaque bone –dead sequestra attracts
calcium
Subperiosteal bone deposition
28. Bone biopsies from the mandibles of 5 patients
with PCO were sampled with an extraoral sterile
approach. Cultivation and polymerase chain
reaction (PCR) were performed.
RESULTS:
Two of the biopsies yielded growth of
Propionebacterium acnes. One biopsy also
demonstrated Staphylococcus capitis. The
biopsies with bacterial growth were also positive
for the same bacteria by PCR analysis.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod.2009
May;107(5):641-7. doi: 10.1016/j.tripleo.2009.01.020.
Primary chronic osteomyelitis of the jaw--a microbial
investigation using cultivation and DNA analysis: a pilot
study.
Frid P,Tornes K, Nielsen Ø, Skaug N
29. Surgical removal of sequestra
Not affected by systemic antibiotics –no
circulation(Khosla 1970)
Sequestrectomy & Sucerization –acute phase
subsided
Saucerization –eliminate dead space
Obwegeser (1960)-decortication of bone-
shortens healing time
30. Preoperative radiographs –site of incision
Maxilla – intraoral incisions
Mandible
1.Alveolar part –intraoral incisions
Involved teeth –removed
Intraoral wounds packed –iodoform gauge
soaked in compound tincture of benzoin or
balsam of peru
31. 2.Inferior body of mandible
Skin incision –below angle of jaw
Masseter muscle detached
Sequestra removed
3. Condyle
Preauricular incision
4. Coronoid
Intraoral –along ramus (anterior border)
5. Mandibular notch
Retromandibular approach –incision at angle of
jaw
32. Sequestrum –surface of bone
Window –sharp currette
Granulation –blunt curette
Closure
Completely with sutures
Sutures with Penrose rubber drain
Indwelling catheter
Smith –Peterson ,Larson (1945)-aqueous
penicillin
33. Large cavity –combined with sequestrectomy
Periosteum –retracted
Sequestrectomy –done
Abditional cortex-saucerize the cavity
Margins –smothened with bone file or round
bur
Suture & drain
Wound packed with iodoform gauge
Systemic antibiotics -10 days to 2 weeks
34. Paresthesia of lip
Frature of weakened bone –air drill with
sharp cutting instruments
Splints and fracture appliance
35. Systemic antibiotics -10 days to 2 weeks
Dehydration –I.V. fluids with added vitamins
Blood transfusion
High protein diet
Immobization of jaw –maxillomandibular
fixation or a Barton bandage –for several
weeks
Rubber catheter-normal saline irrigation
every 3-4 hrs
41. Incision from midline to high
on Ascending ramus
Reflection of buccal and
lingual mucoperiosteal flaps
and sectioning of the
neurovascular bundle at its
exit from mental foramen
42. Use of gigli saw to make
anterior osteotomy
Osteotomies made with a
combination of bur cuts
43. Space left should be closed in
layers to eliminate dead space
A drain is placed for 24 hrs
to 48 hrs to prevent
hematoma formation
44. Incision parallel to and
1cm below the angle of
mandible
Mandilmandible exposed
,neurovascular bundle
cut and tied
,osteotomies are made
with gigli saw ,air drill .
45. Mainous 1975,Marx 1983
Pure oxygen –greater alveolar
partial pressure
Elevation of oxygen tension
Improved vascular supply
& increased oxygen perfusion
Fibroblast proliferation ,
new capillary (Hunt et al 1975)
Osteogenesis (Maekley et al 1967)
46. Protocol –Hart 1976,Marx 1983
2 ATA -60 sessions (120 hrs)
Mansfield et al 1981-alternating 100% oxygen
with intermittent oxygen followed by air
Marx 1983 – osteoradionecrosis
1.30 initial dives
2.Clinical improvement -60 dives
3.Resection –additional 20 dives 10 weeks after
resection
47. Dry osteomyelitis
Localized or diffuse (Bell 1959 ,Shafer 1957)
Older people ,black women
Sclerotic opacities & lytic areas
Bone –granite hard ,mandible
48. Six patients- particulate cancellous bone and marrow
grafting after saucerization
The partial resection of the mandible is associated
with disadvantages- including loss of mandibular
support, dysfunction, and problems related to
mandibular reconstruction.
Therefore, it would be reasonable to choose
saucerization combined with particulate cancellous
bone and marrow grafting, which is a relatively
conservative surgical treatment for chronic diffuse
sclerosing osteomyelitis of the mandible.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod.2001
Apr;91(4):390-4.
Treating chronic diffuse sclerosing osteomyelitis of the
mandible with saucerization and autogenous bone grafting.
Ogawa A Miyate H Nakamura YShimada M Seki S Kudo K
49. “Nonsuppurative process in which there is
peripheral sub-periosteal bone deposition
caused by infection and irritation.”
Carles garre 1893
In mandible –Pell et al (1955)
Children and young adults
Etiology –carious tooth ,soft tissue infection
(Ellis ,Winslow 1977)
50. Radiograph
1.Condensation of cortical bone
2.Overgrowth of osseous tissue beneath
periosteum
Differential Diagnosis –
-Infantile cortical hyperstosis /Caffey’s Disease
young infants ,no of bones,clavicle .
51. Removal of infected tooth
Curettage of socket
Surgical recontouring
Surgery – obvious facial asymmetry -6 month waiting
period
Garre's osteomyelitis in a 10-year-old boy -pulpoperiapical
infection in relation to permanent mandibular right first
molar.
The elimination of periapical infection was achieved by
endodontic therapy and the complete bone remodeling
was seen radiographically after three months follow-up.
J Indian Soc Pedod Prev Dent.2007;25 Suppl:S30-3.
Garre's sclerosing osteomyelitis.
Suma R Vinay C, Shashikanth MC, Subba Reddy VV
1.the classical presentation of jawbone osteomyelitis , was ,,,,,usually followed by a later transition to a
2. acute phases were often concealed by these antimicrobial drugs without fully eliminating the infection,,,,,,,,, have therefore become more prominent, lacking an actual acute phase
Constitutional rx,,,,,,,
SUBP AB on alveolar mucosa and palate followed by
Lower resistance ,infants may refuse nourishment
Radiographs are of less use,,,,,,,,
1.2.Pus from sinus tract
1.With extensive sequetration and pathologic fracture,,,,,,,,,,,
2.may predispose
2.Complicated by –
4. Involvement of ,,,,,, may cause during period of skeletal growth
Scintigraphy ("scint," Latin scintilla, spark) is a form of diagnostic test used in nuclear medicine, wherein radioisotopes (here called radiopharmaceuticals) are taken internally, and the emitted radiation is captured by external detectors (gamma cameras) to form two-dimensional[1] images. In contrast, SPECT andpositron emission tomography (PET) form 3-dimensional images, and are therefore classified as separate techniques to scintigraphy, although they also usegamma cameras to detect internal radiation. Scintigraphy is unlike a diagnostic X-ray where external radiation is passed through the body to form an image.
To administer dehydration
Erythromycin ,lincomycin
5o mg /kg upto 2g every 4 hrly
Window –sharp osteotome or air drill for evacuation of pus
Primary –infection from subvirulent organism,,,,,,sec –acute infection not eliminated by treatment
Extraoral fistula and scar formation ,,,,,large exposure of infected bone and sequestra
No specific bacterial etiology was demonstrated. However, the results of bacterial cultivation and PCR analysis were in agreement. Based on these findings, the molecular procedure used in this study can be considered to be suitable for identification of bacterial specimens in mandibular biopsies. Further studies are needed with larger patient populations to confirm these findings.
Removal of seqestrum leaves large cavity and it is desirable to eliminate dead space to avoid extensive areas of clot that may get reinfected…
Iod g –removes necrotic tissue by its fibrinolytic act
Additional cortex should be removed
In blood cultures,,,,,
Lab studies
Posterrior cut at condyle for disarticulation ,ramus anterior cut in premolar region ,,coronoidectomy
with chronic diffuse sclerosing osteomyelitis of the mandible were treated by ,,,,,,,,,,,,,,,,,,,,,,,,,, and were retrospectively evaluated.