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Inflammatory Lesions of the jaw

Radiology Seminar
Ahmed Zarif Alaa Khaled
Mohamed Fathy Amr Ghareeb
“Identify your problems but
give your power to solutions”
Introduction
Inflammatory lesions are the most common pathologic condition of the jaws.

The jaws are unique from other bones of the body where direct
pathway for infectious and inflammatory agents to invade bone
by means of caries and periodontal disease are present

-The body responds to chemical, physical, or microbiologic


injury with inflammation, the inflammatory process is a response of
the body that aims to destroy the injurious stimulus and repair the
damaged tissue.
Periapical Osteomyelitis Osteoradionecrosis
Inflammatory lesions.
Pericoronitis Acute or chronice raditaion or bisphosphonates

Types of inflammatory lesions


Normally bone metabolism represent balance between; Osteoclastic bone resorption -> Osteoblastic bone formation.
Necrotic pulp -> periapical inflammatory lesion -> Spreading of infection along bone marrow -› Osteomyelitis
.
I- Periapical inflammatory lesions
Apical periodontitis/ Periapical abscess/granuloma/ Sclerosing osteitis

Definition:
• A periapical inflammatory lesion is a local response of the
bone around the apex of the tooth that occurs secondary
to pulpal necrosis or extensive periodontal disease.

Clinical features:

• Asymptomatic.
• Toothache.
• Sever pain with or without facial swelling.
• Fever.
•Lymphadenopathy
• Fistula (parulis).
I- Periapical inflammatory lesions

Radiographic feature:
• Early lesions show no radiographic signs but may be clinical signs only.
• Chronic lesions may show lytic (radiolucent) or sclerotic (radiopaque)
changes or both.

1- Location:

- Apical portion of periodontal ligament space.

2- Periphery:

- Ill defined with gradual transition from surrounding normal


trabeculation to abnormal pattern
I- Periapical inflammatory lesions

3- Internal structure: Early lesion-> no radiographic change


-> Widened PDL at apex -> a mixture of sclerosis and rarefaction

4- Effects on surrounding structures:

-Loss of Lamina dura - Sclerosis at apex - External apical root resorption


-Wider pulpal canal - New bone - halo shadow.
I- Periapical inflammatory lesions

Differential diagnosis:
• (vital lower mand. incisors-radiolucent, radiopaque, mixed.)
• Normal PDL space width, well defined periphery, no blending with surrounding bone
•Periapical granuloma: Small radiolucent lesion with well definedperiphery simulating a cortex.
• Cyst -› displacement of adiacent structures + expansion of outer cortical boundaries of jaw
>1 cm radicular cyst.

After RCT and periapical surgery - apical radiolucency -> apical scar.

Treatment:
1- RCT
2- Extraction
II- Pericoronitis /operculitis.

Definition:

Inflammation of the tissues surrounding the crown of a


partially erupted tooth.

Clinical and Radiographic features:

• Pain and swelling.


• Trismus may occur especially in lower third molar area
• Soft tissue inflammation-> no change.
II- Pericoronitis /operculitis.

1- Location: Most common site - mand 3rd molar region.

• In close proximity to bone or inside follicular space.


• Radiolucency or sclerotic with thick trabeculae.

• 2- Periphery: ill defined with gradual merging with sclerotic region.

3- Internal structure:
• Sclerotic with thick trabeculae Or radiolucency adjacent to crown.

4- Effect on surrounding structures:


• Sclerosis and rarefaction of surrounding bone.
• New bone formation at inferior cortex, posterior border of the ramus, and coronoid notch..
Acute Chronic
Osteomyelitis Osteomyelitis

III- Osteomylitis
Definition:
•Inflammatory process of bone that spread to all parts of bone causing destruction of endosteal surface of cortical bone.
• Development of sequestra which may resolve spontaneously or with antibiotic intervension.
A- Acute osteomyelitis
- Infection spreads to bone marrow. Elevating periosteum and
stimulating new bone formation.

Clinical features:
• Male predilection • More common in the mandible.
• Rapid onset, swelling of • Fever, lymph-adenopathy. •
•Involved Teeth are sensitive to percussion

Radiographic examination:

• Panoramic, intraoral periapical, and occlusal films.


• CT scanning is good for detecting periosteal new bone formation
• MRI displays abnormal bone marrow edema
A- Acute osteomyelitis

Radiographic features:

1- Location: posterior body of the mandible.


2- Periphery: ill defined with gradual transition to normal trabeculae.
3- Internal structure: Decrease in bone density - Loss of trabecular sharpness - Scattered
areas of radiolucency -› sequestra.

4-Effect on surrounding structures:


• Bone formation is parallel to bone surface and the periosteum.
• A radiolucent band separates this periosteal new bone from the bone surface.
• This is continue to form several radiopaque lines separated by radiolucent bands (Onion-skin
appearance)
A- Acute osteomyelitis

Differential Diagnosis:

• Fibrous displasia.-› bone enlargement inside the cortex, no onion- skin appearance.
• Malignant neoplasia (osteosarcoma, squamous cell carcinoma) -› periosteal bone
destruction, no sequestra

Management:

• Removal of inflammatory source-> tooth, RCT.


• Surgical incision and drainage.
• Antimicrobial treatment.
• Definition:
it is a state of balance in which bone metabolism is tipped toward
bone formation producing sclerotic radiographic appearance.

Clinical picture:

• Intermittent pain • Swelling • Fever • Lymphadenopathy.


• Drainage with sinus formation
• May spread to TMJ cause septic arthritis & ear infection.
B-Chronic Osteomyelitis:
Garre's osteomylitis.
B-Chronic Osteomyelitis:

Radiographic features:

1- Location: posterior mandible.


2- Periphery: Better defined than the acute phase. In acute exacerbation periphery is radiolucent.
3- Internal structure:
Lesion is more radiopaque and may be equivalent to cortical bone.
Small regions of radiolucency may be scattered. CT is superior for revealing sequestra
4- Effects on surrounding structures:
New periosteal bone in series of radioqaue lines (onion skin) parallel to the cortical bone surface.
Apical widening of PDL space of non-vital tooth.
Well -defined break in outer cortex (draining fistula).
B-Chronic Osteomyelitis:

Differential diagnosis:
Diagnostic imaging of soft tissue infections:
• Fibrous dysplasia -› no new periosteal bone formation, no sequestra.
• Paget's disease-› affect the entire mandible. • MRI can detect soft tissue edema.
• Osteosarcoma -› sunray - like appearance. • CT inflammatory lesion-› abnormal facial
planes, thickening overlying skin & muscle.
• Management: • Abscess -› well defined low density area
surrounded by wide border of radiopacity
• Surgical -* sequestrectomy, decortication or resection.
Hyperbaric oxygen therapy and long term
antibiotic therapy.
IV- Osteoradionecrosis
Definition:
• Inflammatory condition of bone (osteomylitis) that occur after the
bone has been exposed to therapeutic doses of radiation for
treatment of malignancy of head & neck.
• Bone should exposed to radiation at least 3 months .
.

Clinical features:

• The mandible is more common especially posterior part.


.• Loss of mucosal covering & bone exposure is evident.
• Pain may be present.
• Sequestration of bone with swelling.
• Extraoral drainge.
B-Chronic Osteomyelitis:

Radiographic features:
Similar to chronic osteomylitis.
1- Location: posterior part of the mandible.
2- Periphery: ill - defined , irregular cortical resorption.
3- Internal structure: more bone formation (sclerotic) with or without areas of radiolucency .
4- Effects on surrounding structures:
-Stimulation of sclerosis -No new periosteal bone formation.

Management:
• Preventive therapy is more effective than curative one.
• Removal of periodontally involved tooth before radiation treatment with good oral hygiene are
main obiectives of preventive therapy
V- Bisphosphonate- Related Osteonecrosis
Bisphosphonates are synthetic analogs of pyrophosphates that act to inhibit osteoclasts and reduce bone metabolism.

• They are used for treatment of the following conditions:


1- bone lesions of multiple myeloma
2- hypercalciemia of malignancy
3- Metastatic bone tumors.
4-osteoporosis

Clinical features

• Patients have area of exposed bone after invasive dental surgical procedures (e.g. extraction, periodontal surgery).
• It is more common in posterior mandible (60%) & maxilla (40%) and both (9%).
• Incidence: 3% of patients receiving these drugs will have exposed bone
V- Bisphosphonate
- Related Osteonecrosis

Staging
• At Risk (0) : no apparent exposed /necrotic bone in patient who have
been treated with either IV or oral Bisphosphonates.
• Stage I: exposed bone, no pain or infection
• Stage II- exposed bone with infection and pain
•Stage III pathological fracture,
large volume of necrotic bone, no response to antibiotics
V- Bisphosphonate-
Radiographic features
Related Osteonecrosis
• There are no specific radiographic findings with clinically exposed bone.
• Presence of sequestra.
• Increase in bone sclerosis.
• Widening of PDL space
• Thickening of lamina dura.

Management

• Preventive treatment as patient should have dental examination


to exclude any source of infection before drug intake.
• Treatment is aimed at controlling the symptoms of pain and
infection with antibiotics and mouth washes.
References
Radiopaque Jaw Lesions: An Approach to the Differential Diagnosis
Joel K. Curé, Surjith Vattoth, Ritu Shah
Guide to the Diagnosis of Jaw Lesions According to Radiographic Manifestations
Ines Velez, DDS, MS, Luis Tamara, MD, Maritzabel Hogge, Tulia Gonzalez
Indian J Radiol Imaging. 2021 Jan; 31(1): 224–236.
Published online 2021 Jun 1. doi: 10.1055/s-0041-1729769
PMCID: PMC8299495
PMID: 34316130
Radiolucent Jaw Lesions: Imaging Approach
Avril L, Lombardi T, Ailianou A et al. Radiolucent lesions of the mandible: a pattern-based approach to diagnosis. Insights Imaging. 2014;5(01):85–101. [PMC free article] [PubMed] [Google Scholar] Sumi M, Ichikawa Y, Katayama I, Tashiro S, Nakamura T. Diffusion-weighted MR imaging of ameloblastomas a
nd
keratocystic odontogenic tumors: differentiation by apparent diffusion coefficients of cystic lesions. AJNR Am J Neuroradiol. 2008;29(10):1897–1901. [PMC free article] [PubMed] [Google Scholar]
Thank
You!

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