1. Aneurysmal bone cyst
2. Hyperparathyroidism
3. Central giant cell granuloma
4. Granuloma

A focal area of granulomatous inflammation – consisting of multinucleate macrophages

Histology:

• Epithelioid appearance of macrophages, surrounded by mononuclear leukocytes (mainly lymphocytes and plasma cells)
• As lesion matures – develops a rim of fibrous CT

Infectious granulomas – also called immune granulomas because:

• Macrophages ingest resistant bacteria (eg. Mycobacteria) → activate T cells → produce IFN gamma → causes transformation of macrophages into giant cells
• Giant cells – also observed in foreign body reactions eg. sutures and amalgam

Asymptomatic condition that is discovered on routine radiography

Etiology: It is possibly derived from the PDL

Epidemiology: Poorly understood predilection for black female patients, 5th and 6th decades

Clinical:

• Lower anterior region
• Associated teeth usually – vital pulps
• Common complication: Osteomyelitis after extractions – due to poor vascularity of bone

Clinical subtypes:

• Single (< 1.5 cm diameter)
• Multiple
• Florid (familial tendency)

Radiology:

• Early – Circumscribed radiolucencies involving apical area of anterior teeth.
• Late – Mixed radiolucency to ”cotton wool” appearance

Histology: Trabecular/sclerotic areas of lamellar bone OR cementum-like material interspersed in fibrous matrix

Management: Surgical curettage with care, the lesions does not separate clearly from bone

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A well demarcated and occasionally encapsulated neoplasm – containing varying amounts of calcified tissue resembling bone or cementum or both

Clinical: Asymptomatic swelling – causing facial asymmetry, mandible > maxilla

Radiology: A well defined unilocular lesion, may have a sclerotic border

Histology:

• Encapsulated lesion – composed of cellular fibrous matrix + calcified material, which may be either cementum or bone
• Osteoblasts are visible (but not osteoclasts)
  

Management: Enucleation, with good prognosis

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Juvenile ossifying fibroma

An aggressive variant of OF – seen in patients under 15

Common sites: Orbital, frontal bones & paranasal sinuses

Radiology: Varying degrees of radiolucency and opacity

Histology:

• Cell rich stroma + spindle shaped cells
• Scanty collagen + small strands of immature osteoid with some areas of woven bone

Management: Surgical enucleation, 30-58% recurrence

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A benign developmental condition – replacement of normal medullary bone with abnormal fibrous CT proliferation with the capacity to form new metaplastic bone

Clinical: 3 main presentations, all of which involve the skull and jaws

1. Monostotic disease – Painless swelling
2. Polyostotic non syndromic disease.
3. Polyostotic syndromic type:
   • Jaffe type:
     – Polyostotic FD
     – Cutaneous pigmentation (café au lait spots)
   • McCune Albright syndrome:
     – Polyostotic FD
     – Cutaneous pigmentation (cafe au lait spots)
     – Endocrine hyperfunction – precocious puberty, acromegaly, hyperthyroidism, hyperparathyroidism, hyperprolactinaemia

• Asymptomatic, self limiting, stabilizing at puberty and growing slowly thereafter

Etiology:

• Gs alpha mutation (chromosome 20) – which transcribes transmembrane signaling proteins.
• Resultant dysfunction in cAMP signaling affects multiple systems.
• In the musculoskeletal system:
  – Osteoblasts secrete abnormal bone
  – ↑ IL-6 – ↑ Osteoclastic bone remodeling
• The severity of the condition depends of the timing of the mutation and the size of the affected cell mass:
  • a) Mutations in embryonic life -Polyostotic and syndromic types (20 %).
  • b) Postnatal mutations – Monostotic types (80 %)

Common site: Maxilla > mandible, with jaws being the most common site but ribs, femur and tibia are also commonly affected

Radiology:

• Early lesions – Radiolucent, with a unilateral “ground glass” appearance being acquired in the process of calcification.
• Ill defined margins
• Bucco-lingual expansion pattern
• Loss of lamina dura around root
• No displacement of teeth and no resorption

Lab: Serum laboratory values are normal

Histology:

• Irregularly shaped trabeculae – of immature woven bone – in cellular, loosely arranged
  fibrous stroma.
• Metaplastic deposits of curvilinear bone arranged in ”chinese letter” pattern
• Few osteoblasts, no osteoclasts and no inflammatory cells – except 2⁰ infection

Management:

• Surgical recontouring/bone shaving
• Alleviate pain, pressure and deformity
• Bisphosphonates
• May recur (25%)

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• Reactive/dysplastic/neoplastic lesions → replacement of normal bone by fibrous tissue
• Contains mineralized product – deposited by metaplastic cells (derived from the fibrous tissue)
• Include:
  • Dystrophic normal bone
  • Dense sclerotic cementum-like calcifications
  • Or mixed hard tissues

Common fibro-osseous lesions

1. Fibrous dysplasia of bone
2. Cemento-osseous dysplasia
   • Periapical cemento-osseous dysplasia
   • Focal COD.
   • Florid COD – all 4 quadrants
3. Ossifying fibroma
4. Cherubism – Hereditary craniofacial malformations

Common radiology

• Early – well circumscribed radiolucencies.
• Late – mixed radiolucency to ”cotton wool” appearance

Difference between fibrous dysplasia and ossifying fibroma

Pathways of spread:

• Direct extension
• Lymphatic/ vascular dissemination
• Intraspinal seeding (through Batson plexus of veins)

Most frequent sites: Vertebrae, ribs, pelvis, skull

Common sources of jaw metastases: Breast, prostate, lungs, colorectal & kidneys

Clinical:

• Elderly patient
• Pain
• Swelling
• Loosening of teeth
• A mass
• Paraesthesia
• Hx primary tumour

Histology: Poorly differentiated malignant cells with little resemblance to the tissue of origin,
confirmation usually done with immunohistochemistry

Management: Low survival rates because metastases usually implies that patient is in Stage IV. Most patients do not survive more than 1 yr

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Etiology:

• There are common mutations between this tumour and the primitive neuroectodermal tumour of bone (PNET)
• All cause myc overexpression
  • t(11;22) – 85% of ES & PNET
  • t(24;12) – 5 – 10%
  • t(7;22) – < 1%

Radiology:

• Irregular lytic bone destruction with ill-defined margins.
• “Onion skin” periosteal reaction

Histology:

• Small round cells – well-delineated nuclear outlines + ill-defined cellular borders
• Areas of necrosis and hemorrhage

Diagnosis: 75% of tumors have glycogen in the cytoplasm, so they are PAS positive

Management:

• Combined surgery + Radiotherapy + Multidrug chemotherapy

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• Benign tumours composed of mature compact or cancellous bone
• Those arising on the surface of bone = Periosteal osteoma
• Those arising within bone = Endosteal osteoma

Clinical: Slow progressive enlargement of the affected area.

Histology:

• Compact type with normal appearing bone tissue – minimal bone marrow
• Cancellous type with trabeculae of bone and fibro – fatty marrow

Radiology: Circumscribed sclerotic mass

Management: Surgical enucleation

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• Benign vascular, osteoid and bone forming tumour
• Osteoblastic origin
• May be aggressive

Common sites:

• Rare in jaws – molar premolar region, mandible > maxilla.
• Femur
• Tibia
• Phalanges

Clinical:

• Aggressive
• Pain
• Intact cortical expansion

Histology:

• Well demarcated mass
• Oval/round osteoblast like cells + some osteoclasts,
• Partially calcified osteoid
• Vascular spaces

Radiology: Poorly defined radiolucency

Management: Surgical excision

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