Radiographic Interpretation of Inflammatory Lesions of the Jaws

1. Inflammatory Lesions of the Jaws
Dr. Hadi Munib
Oral and Maxillofacial Surgery Resident

2. General Clinical Features
▪ The four cardinal signs of inflammation:
▪ Redness
▪ Swelling
▪ Heat, and
▪ Pain
▪ Acute lesions are those of recent onset.
▪ The onset typically is rapid, and these lesions cause pronounced pain, often accompanied
by fever and swelling.
▪ Chronic lesions have a prolonged course with a longer insidious onset and pain that is less
intense.

3. General Radiographic Features
▪ LOCATION
▪ With periapical inflammatory lesions; the epicenter typically is located at the apex of a tooth
▪ Lesions of pulpal origin also may be located anywhere along the root surface because of
accessory canals or perforations
▪ Periodontal lesions have an epicenter that is located at the alveolar crest.
▪ If bone loss is severe, the inflammatory changes may extend to the root furcation level or
even to the root apex.
▪ Osteomyelitis, a diffuse, uncontained inflammation of the bone, most commonly is found in
the posterior mandible.
▪ PERIPHERY; ill-defined, with a gradual blending of normal trabecular pattern into a sclerotic
pattern, or the normal trabecular pattern may gradually fade into a radiolucent region of
bone loss.

4. General Radiographic Features
▪ INTERNAL STRUCTURE
▪ Cancellous bone may respond to an insult by tipping the bone metabolic balance either in
favor of resorption or towards bone formation.
▪ The radiolucent regions may show no evidence of previous trabeculation or a very faint
pattern of trabeculation.
▪ The increased radiopacity is caused by an increase in bone formation on existing trabeculae.
▪ Radiographically these trabeculae appear thicker and more numerous.
▪ In acute disease, resorption typically predominates;
▪ Chronic disease; excessive bone formation leads to an overall radiopaque appearance.
▪ In cases of osteomyelitis, X-Ray films may reveal Sequestra, which appears as ill-defined
areas of radiolucency containing a radiopaque island of non-vital bone.

5. General Radiographic Features
▪ EFFECTS ON SURROUNDING STRUCTURES
▪ Radiopacity
▪ Radiolucency
▪ The periodontal ligament space involved in the lesion will be widened; this widening is
greatest at the source of the inflammation.

6. Periapical Inflammatory Lesions
▪ Acute/ Chronic apical periodontitis
▪ Periapical abscess/ Granuloma
▪ Radiolucent presentations; Rarefying osteitis
▪ Radiopaque presentations; Sclerosing osteitis, condensing osteitis, and focal sclerosing
osteitis
▪ Local response of the bone around the apex of a tooth that occurs as a result of necrosis of
the pulp or through destruction of the periapical tissues by extensive periodontal disease
▪ Symptoms; range from being asymptomatic to an occasional toothache to severe pain with
or without facial swelling, fever, and lymphadenopathy.
▪ A periapical abscess usually manifests with severe pain, mobility and sometimes elevation of
the involved tooth, swelling, and tenderness to percussion.
▪ Palpation of the apical region elicits pain.

7. Periapical Inflammatory Lesions
▪ Radiographic features; More chronic lesions may show lytic (radiolucent) or sclerotic
(radiopaque) changes, or both.
▪ Location. In most cases the epicenter is found at the apex of the involved tooth
▪ The lesion usually starts within the apical portion of the periodontal ligament space.
▪ Periphery; ill defined, showing a gradual transition from the surrounding normal
trabecular pattern into the abnormal bone pattern of the lesion.
▪ Rarely the periphery may be well defined, with a sharp transition zone and an
appearance suggesting a cortical boundary.

8. Periapical Inflammatory Lesions
▪ Internal Structure.
▪ Early periapical inflammatory lesions may show no radiographic change in the normal
bone pattern.
▪ The earliest detectable change is loss of bone density, which usually results in widening of
the periodontal ligament space at the apex of the tooth
▪ Periapical SclerosingOsteitis
▪ Periapical Rarefying Osteitis
▪ These lesions are capable of producing an inflammatory periosteal reaction, most notably
in the adjacent floor of the maxillary antrum.
▪ This usually results in a thin layer of new bone produced by the inflamed periosteum
within the maxillary antrum, sometimes referred to as a “ halo shadow ”

9. Periapical Inflammatory Lesions
▪ Differential Diagnosis
▪ Periapical Cemental Dysplasia
▪ Enostosis (Dense Bone Island); PDL space is of uniform width
▪ RadicularCysts

16. DBI

17. Pericoronitis/ Operculitis
▪ Inflammation of the tissues surrounding the crown of a partially erupted tooth.
▪ Most often seen in association with the mandibular third molars in young adults.
▪ The gingiva surrounding the erupted portion of the crown becomes inflamed when food or
microbial debris becomes trapped under the soft tissue.
▪ Pain, Swelling, Lymphodenopathy andTrismus
▪ Radiographic Features;
▪ Location; When bone changes are present; they are centered on the follicular space or the
portion of the crown still embedded in bone or in close proximity to bone.
▪ Periphery; The periphery is ill defined, with a gradual transition of the normal trabecular
pattern into a sclerotic region.

18. Pericoronitis
▪ Internal Structure.
▪ The internal structure of bone adjacent is most often is sclerotic with thick trabeculae.
▪ An area of bone loss or radiolucency immediately adjacent to the crown that enlarges
the follicular space may be seen
▪ Effects on Surrounding Structures.
▪ May cause the typical changes of sclerosis and rarefaction of surrounding bone.
▪ Differential Diagnosis; enostosis and fibrous dysplasia, the sclerotic form of
osteosarcoma and, in older patients, squamous cell carcinoma.
▪ Management; Extraction but not in the acute phase

20. Osteomyelitis
▪ An inflammation of bone.
▪ The inflammatory process may spread through the bone to involve the marrow, cortex,
cancellous portion, and periosteum.
▪ In the jaws pyogenic organisms that reach the bone marrow from abscessed teeth or
postsurgical infection usually cause osteomyelitis.
▪ In some instances hematogenous spread is presumed to be the origin
▪ No infectious organs identified; Prior AntibioticTherapy or Inadequate methods of
bacterial isolation
▪ The hallmark of osteomyelitis is the development of Sequestra.
▪ A sequestrum is a segment of bone that has become necrotic because of ischemic injury
caused by the inflammatory process.

21. Osteomyelitis
▪ Acute Phase
▪ Chronic Phase
▪ Garré’ s Osteomyelitis; an exuberant periosteal response to inflammation.
▪ Diffuse sclerosing osteomyelitis; chronic form of osteomyelitis with a pronounced
sclerotic response.
▪ Osteomyelitis may resolve spontaneously or with appropriate antibiotic intervention.
▪ Infection may persist and continue to spread and become chronic in about 20% of
patients

22. Acute Osteomyelitis
▪ Acute Suppurative osteomyelitis
▪ Pyogenic osteomyelitis
▪ Subacute Suppurative osteomyelitis
▪ Garr é ’ s osteomyelitis
▪ Proliferative periostitis,
▪ Periostitis ossificans

23. Acute Osteomyelitis
▪ The medullary spaces of the bone contain an inflammatory infiltrate consisting
predominantly of neutrophils and mononuclear cells.
▪ In the jaws the most common source of infection is a periapical lesion from a non-vital tooth.
▪ Trauma or hematogenous spread.
▪ More common in younger people because the periosteum is loosely attached and has greater
osteogenic potential
▪ Mandible > Maxilla
▪ Rapid onset, pain, swelling of the adjacent soft tissues, fever, lymphadenopathy, and
leukocytosis.Affected teethTTP and Mobile
▪ Plain X-Rays;CBCT; MRI

24. Acute Osteomyelitis
▪ Location; Posterior body of the mandible.
▪ Periphery; Most often presents an ill-defined periphery with a gradual transition to normal
trabeculae.
▪ Internal Structure. The first radiographic evidence is a slight decrease in the density of the
involved bone, with a loss of sharpness of the existing trabeculae.
▪ Resulting in an area of radiolucency in one focal area or in scattered regions throughout
the involved bone
▪ Later, the appearance of sclerotic regions becomes apparent.
▪ Sequestra may be present but usually are more apparent and numerous in chronic forms

27. Differential Diagnosis
▪ Fibrous dysplasia; the new bone is manufactured on the inside of the mandible; thus
the outer cortex which may be thinned, is on the outside and contains the lesion.
▪ Malignant neoplasia (e.g., osteosarcoma, squamous cell carcinoma)
▪ Management; Removal of the source; Antimicrobial treatment along with establishing
drainage.

28. Chronic Osteomyelitis
▪ Chronic diffuse sclerosing osteomyelitis
▪ Chronic non-Suppurative osteomyelitis
▪ Chronic osteomyelitis with proliferative Periostitis
▪ Garré’s chronic non-Suppurative sclerosing osteitis
▪ Sequela of inadequately treated acute osteomyelitis, or it may arise de novo
▪ The symptoms are generally are less severe and have a longer history than those of
the acute form.
▪ They include intermittent, recurrent episodes of swelling, pain, fever, and
lymphadenopathy, paresthesia and drainage with sinus formation

29. Chronic Osteomyelitis
▪ Chronic Recurrent Multifocal Osteomyelitis (CRMO) ; Condition that often occurs
symmetrically in the long bones in children.
▪ It is characterized by pain of the affected bone with or without swelling and non-
purulent osteomyelitis with negative microbiologic cultures
▪ NSAIDs
▪ Bisphosphonates therapy

32. Chronic Osteomyelitis
▪ SAPHO syndrome
▪ Synovitis [Inflammatory arthritis ]
▪ Acne [Pustulosa]
▪ Pustulosis [Psoriasis, Palmoplantar pustulosis]
▪ Hyperostosis [Acquired ]
▪ Osteomyelitis
▪ These lesions are refractory to antibiotic therapy,
▪ Responding to anti-inflammatory agents such as steroids and NSAIDs.

33. Chronic Osteomyelitis
▪ Radiographic Features
▪ Location; Posterior mandible.
▪ Periphery; better defined than in the acute phase, but it is still difficult to determine
the exact extent
▪ Usually a gradual transition is seen between the normal surrounding trabecular
pattern and the dense granular pattern characteristic of this disease.
▪ Active; more radiolucent and have poorly defined borders.

34. Differential Diagnosis
▪ Very sclerotic, radiopaque chronic lesions of osteomyelitis may be difficult to
differentiate from fibrous dysplasia, Paget’s disease, and osteosarcoma.
▪ More difficult if considerable remodeling and loss of a distinct original cortex have
occurred.
▪ In these cases, inspection of the bone surface at the most peripheral part of the lesion
may reveal subtle evidence of periosteal new bone formation.
▪ The presence of Sequestra indicates osteomyelitis.
▪ Paget ’ s disease affects the entire mandible.

37. SoftTissue Imaging
▪ MRI and CT may be used to differentiate soft tissue neoplasia from inflammatory lesions.
▪ MRI can be used in theT2 orTI with gadolinium and fat suppression modes to detect the
presence of soft tissue edema.
▪ CT usually is used with intravenous contrast.
▪ The CT image characteristics that suggest the presence of a soft tissue inflammation include
abnormal fascial planes, thickening of the overlying skin and adjacent muscles, streaking of
the fat planes and abnormal collections of gas in the soft tissue.
▪ Over time the contrast between soft tissue planes may disappear, and the presence of an
abscess may become evident as a well-defined region of low density surrounded by a wide
border of contrast-enhanced (more radiopaque) tissue.
▪ Lymphadenopathy resulting from infections such as tuberculosis of the head and neck may
be visualized on magnetic resonance and CT images

41. Osteoradionecrosis
▪ Inflammatory condition of bone (osteomyelitis) that occurs after the bone has been
exposed to therapeutic doses of radiation usually given for a malignancy of the head
and neck region.
▪ It is characterized by the presence of exposed bone for a period of at least 3 months
occurring at any time after the delivery of the radiation therapy.
▪ Doses above 50 Gy usually are required to cause this irreversible damage.
▪ Hypo-cellular and Hypo-vascular.
▪ In many cases dental extraction and denture trauma after radiation therapy
▪ Secondary infection is common

42. Osteoradionecrosis
▪ The mandible is much more commonly affected than the maxilla is.
▪ Posterior mandible is affected more often; direct field of the radiation treatment.
▪ Loss of mucosal covering and exposure of bone is the hallmark of osteoradionecrosis.
▪ Pathologic fracture also may occur.
▪ Pain may or may not be present.
▪ Intense pain may occur, with intermittent swelling and drainage extra-orally.
▪ Radiologic Examination; CT being the imaging modality of choice.

43. Osteoradionecrosis
▪ Radiographic Features
▪ Radiographic changes seen in bone that has received a considerable amount of
therapeutic radiation.
▪ An early characteristic change is a well-defined area of bone resorption within the
outer cortical plate of the mandible
▪ Later changes are quite variable and may be predominantly lytic or sclerotic or a
mixture

44. Osteoradionecrosis
▪ Differential Diagnosis
▪ Recurrence of the malignant neoplasm
▪ Management

47. BRONJ
▪ Bisphosphonate-RelatedOsteonecrosis of the Jaws
▪ Multiple myeloma, hypercalcemia of malignancy, metastatic bone tumors, and
osteoporosis.
▪ Amino-bisphosphonates IV and after an invasive dental surgical procedure
▪ Clinical Features
▪ Exposed bone after an invasive dental surgical procedure.
▪ Ulceration of palatal tori resulting in bone exposure is most likely the result of trauma.
▪ Most common areas affected are the posterior mandible (60%) and the maxilla (40%) and
both (9%).
▪ Recent studies suggest that approximately 3% of patients receiving these drugs will have
exposed bone.The areas may be asymptomatic or present with pain and swelling.

48. BRONJ
▪ Radiographic Features
▪ More oftenThere are no specific radiographic findings with the clinically exposed
bone.
▪ In other cases the radiographic changes are not dissimilar to osteoradionecrosis or
chronic osteomyelitis with the presence of Sequestra
▪ Other reported findings include an increase in bone sclerosis, widening of the
periodontal membrane space, and thickening of the lamina dura

51. References
▪ Chapter 20: Inflammatory Lesions of the Jaws

52. THANKYOU!