Bone lesions of the jaw Flashcards
Bone structure (3)
• Gross structure • Blood supply • Microscopic structure – lamellar bone - mature – woven bone - immature (see this in embryology and healing or in a lesion)
Bone histology (5)
Cortical/ compact bone on outside
Cancellous bone on inside
-haemopoetic marrow and fat
In centre of traversian systems/ osteon are Haversian canals (contain BVs)
Osteocytes contained in holes you see on histology
Osteoblasts lining surface of woven bone
Bone turnover (4)
- Laid down by osteoblasts (some osteoblasts osteocytes)
- Removed by osteoclasts
- Turnover occurs in response to forces on bone
- Results in resting and reversal lines
Bone remodelling overseen by (4)
• Mechanical stimuli
• Systemic hormones
– parathyroid hormone (PTH) to stimulate resorption of bone to increase serum cacium
– vitamin D3 increases calcium absorption from diet and net absorption of calcium into bone
– oestrogen good at maintaining bone mass (loss of this in menopause can result in osteoporosis i.e. loss of bone mass)
– others: e.g. calcitonin for osteoclast function
• Cytokines (stimulus for osteoclasts and osteoblasts)
• Complex interactions promote growth of cells and
bone matrix
Special tests - bone biochemistry (5)
• Serum calcium - cheapest and simplest, analysis of bone metabolism • Osteoblast activity (bone formation) – serum alkaline phosphatase – osteocalcin • Osteoclast activity (bone resorption) – collagen degradation urine & blood • Parathyroid hormone: regulates serum calcium (specialised) • Vitamin D assays (specialised)
Oral developmental abnormalities of bone: torus (5)
• torus: developmental exostosis (i.e. growing out from surface of bone) • problem with fitting dentures • torus palatinus – midline of palate • torus mandibularis – bilateral on lingual aspect of mandible Histology: compact bone
Oral developmental abnormalities of bone: osteogenesis imperfecta (4)
– type 1 collagen defect – inheritance varied - 4 main types Clinical – weak bones, multiple fractures – sometimes associated with dentinogenesis imperfecta
Oral developmental abnormalities of bone: achondroplasia (3)
– autosomal dominant
– dwarfism
– poor endochondral ossification
Oral developmental abnormalities of bone: osteopetrosis (4)
– lack of osteoclast activity
– failure of resorption
– marrow obliteration
Made of compact bone only, becomes very fragile and has a tendency to fracture
Infections of bone and their prevalence (4)
Dry socket: very common
Sclerosing osteitis: relatively common
Osteomyelitis: rare
Osteonecrosis: rare, but increasingly more common
Dry socket (alveolar osteitis) -what does it affect -how is it caused -how might this have happened (6)
Usually affects molars, particularly impacted 3rd molars • Caused by loss of or failure of the clot to develop in a socket. This may be due to: • Excessive rinsing • Fibrinolysis of clot • Poor blood supply due to radiotherapy, Paget's disease • Excessive use of vasoconstrictors
Dry socket (alveolar osteitis) what is happening in the socket? (4)
Localised inflammatory reaction in bone adjacent
to socket
• Bone adjacent to socket becomes necrotic and is
removed by osteoclasts.
• Healing is very slow
– Irrigation
– Antiseptic dressing
• Very rarely develops into osteomyelitis
Differential diagnosis for sclerosing osteitis (3)
Hypercementosis, cementoblastoma, osteoma
What is sclerosing osteitis and who/ where does it affect? (4)
- Focal bone reaction to low-grade inflammation e.g. chronic pulpitis
- Any age
- Commonly affects mandibular molars
- Asymptomatic, incidental finding
Sclerosing osteitis - radiography (2)
- Uniform opacity at apex tooth,
* Often with peripheral lucency
Treatment for sclerosing osteitis (1)
Cause of inflammation
Osteomyelitis -what is it? -who does it affect? -subtypes (5)
• Inflammation within marrow cavities of bone
• Can affect any age
• Acute or chronic
Subtypes:
• Sclerosing osteomyelitis - nightmare for pt and to treat
• Proliferative periostitis (Garré’s osteomyelitis)
Causes of osteomyelitis (6)
Problems with: • Blood supply: – Age related – Paget's disease – Radiotherapy • Host response • Immunosuppression • Poor nutrition • Other causes: – bisphosphonates
Acute osteomyelitis aetiology (3)
Most commonly infectious (Staphylococci,
Streptococci)
• Extension of periapical abscess
• Physical injury/fracture
Acute osteomyelitis acute inflammatory response (4)
Pain, pyrexia, lymphadenopathy, malaise
Acute osteomyelitis histology (3)
- Acute inflammatory infiltrate
- ↑ Bone resorption
- ↓ Bone formation
Chronic osteomyelitis aetiology (2)
- Low-grade inflammatory reaction
* May be progression from acute osteomyelitis
Chronic osteomyelitis - Chronic inflammatory response associated with low-grade infection (4)
Pain, swelling, bone loss, sequestrae
Chronic osteomyelitis histology (4)
- Chronic inflammatory infiltrate - lymphocytes and plasma cells
- Both osteoclastic and osteoblastic activity
- Reversal lines
- Osteonecrosis
What is proliferative periostitis? (1)
chronic osteomyelitis with periosteal inflammation
Chronic osteomyelitis radiograph (3)
Radiolucency, focal opacity, ‘moth eaten’
Indistinct margins
Sequestrae
Osteomyelitis - patient management (3)
- Resolve source of infection
- Remove infected bone
- Hyperbaric oxygen
Osteonecrosis of the jaws - causes (8)
• Osteoradionecrosis – Complication of irradiation – Head and neck malignancies – Compromised vasculature - endarteritis obliterans • Bisphosphonate/Medication related osteonecrosis of the jaws – MRONJ, BRONJ, DRONJ • Associated with certain medications – Bisphosphonates – Denosumab • Diabetes • Smoking • Poor OH • Prolonged drug use • Dental extractions
Osteonecrosis of the jaws - patient management
- prevention (4)
- low risk (2)
- high risk (2)
• Prevention – Dental assessment – Oral hygiene – Smoking cessation – Limiting alcohol • Low risk – Osteoporosis – Atraumatic extractions • High risk – Malignancy/ Paget's/ immunosuppressed/ history of MRONJ – Refer to OS/OMFS
Types of bone neoplasms (4)
Benign: osteoma, osteoblastoma
Malignant: osteosarcoma, chondrosarcoma
Osteoma - clinical (4)
• Localised bony nodule on maxilla or mandible • Shows continued growth • Distinguish from tori • May be associated with syndromes (multiple osteomas --> Gardener's syndrome - colon cancer)
Osteoma - histopathology: composed of (2)
• Compact bone
• Compact and cancellous
bone
Osteosarcoma (6)
- Malignant tumour which produces bone
- Very rare - 120 cases per year all sites
- Most in long bones
- 2% to 10% in the jaws
- About 10 jaw lesions per year in UK
- Young adults
Osteosarcoma of the jaws (3)
• Age 20-40 years
• Males slightly more
common
• Mandible > maxilla
Why is early dx essential in osteosarcoma of the jaws (3)
- Rapidly growing swelling
- Pain
- Nerve involvement
Osteosarcoma of the jaws - radiographic features (2)
• Radiolucency with
bone formation (sunray)
• Loss of lamina dura is an
important sign
Osteosarcoma - patient management (3)
- Neo-adjuvant chemotherapy
- Wide local excision +/- radiotherapy
- 5 year survival – about 50%
Fibro-osseus lesions (1)
Lesions where the normal bone is replaced by fibrous
tissue in which abnormal bone is laid down
Fibro-osseus lesions - radiographically (3)
• Initially radiolucent because of bone loss
• Later more mixed radiodensity lesion as the abnormal bone is laid down.
• the extent of this varies with the lesion and some lesions
are almost always radio-opaque or radiolucent
Types of fibro-osseus lesions (4)
• Neoplastic: (Cemento) ossifying fibroma • Developmental: Fibrous dysplasia • Reactive: (Cemento) osseous dysplasia Osteodystrophy • Idiopathic: Paget's disease
Ossifying fibroma (6)
• Benign neoplasm composed of fibrous tissue
which forms spicules, islands or cementicles of
bone
-pattern of bone and cellularity is variable
-lesion has well defined margin and is separated from the cortical bone
• Age: 20-50, average 35 years
– Children may be affected
• Females > males (>3:1)
• Mandible overall most common site (65%)
– Premolar or molar region
– May be in craniofacial bones
Ossifying pt management (3)
• Conservative enucleation • Resection • Low recurrence rate
Fibrous dysplasia (7)
• Developmental disorder of bone – Mutations in GNAS1, not inherited • 25% affect head and neck • Age: 15-30 • Males = females • Painless smooth enlargement/swellings • Maxilla most frequent site in H&N • Poorly demarcated radiopacity
Fibrous dysplasia - radiographically (2)
• Stippled “orange peel”
appearance
• Merges with the surrounding bone
Clinical variants of fibrous dysplasia: monostotic (single bone involved) (5)
- Single skeletal lesions
- Ribs and femur most common site
- 25% of lesions in head and neck
- Age 15-30 (average 25)
- Males = females
Clinical variants of fibrous dysplasia: polyostotic (multiple bones involved) (5)
- Multiple lesions
- Head & neck involved in 50%
- Age: <15
- 75% in females
- May be part of McCune-Albright’s syndrome
Fibrous dysplasia: patient management (5)
• Growth stabilises over time (skeletal maturity)
• Debulking and contouring of bone
-recurrence if during growth phase
-can reactivate in pregnancy
• Surgical removal
• Orthodontics and orthognathic surgery
• Very low risk of malignant transformation
Fibrous dysplasia vs ossifying fibroma (4)
Poorly defined vs well defined
No margin vs clear margin
M=F vs F>M
Often maxilla vs often mandible
Cemento-osseus dysplasias (5)
• A clinicopathological spectrum of reactive lesions
• Age: 30-50
• Often females
• Often multiple radiopacities in the tooth bearing
areas of the jaws
• Composed of irregular trabeculae of woven bone
and ‘cementum’ in fibrous stroma
Classification of osseus dysplasias (3)
Focal: single lesions
Perapical: multiple mixed radiodensity lesions at apex of teeth
Florid: multiple lesions throughout jaws
Familial gingatiform cementoma (3)
• Usually described as a variant of Florid OD
-appears to be a different entity to Florid OD
-autosomal dominant inheritance pattern
• M=F
• Found in white patients
Paget’s disease (4)
- Rare disorder affecting all bones
- Bone turnover is increased and no longer related to functional demands
- Early stages bone becomes very vascular: may result in heart failure
- Later stages bone becomes sclerotic and shows numerous resting and reversal lines
Paget’s disease epidemiology (4)
• More common in Western Europe, USA, Canada, Australia, New Zealand • Rare in Asia, Africa • Cause unknown. • Possible genetic/hereditary association or infective cause
Paget’s disease clinical features (3)
• Legs become bowed • Enlargement of the skull causing constriction of foramen: deafness, hats do not fit etc • Jaws become enlarged: tooth spacing and dentures do not fit
Paget’s disease: dental implications (4)
• Bone sclerotic: difficulty with extractions and prone to infections • Hypercementosis: difficulty with extractions • Bisphosphonates may complicate matters • Increased incidence of osteosarcomas and other bone malignancy
Giant cell lesions of the jaws: what are they and types (4)
Characterised by replacement of bone by fibrous tissue containing numerous multi-nucleate giant cells (osteoclasts) • Cherubism • Central giant cell granuloma • Hyperparathyroidism
Cherubism (5)
• Developmental condition
• Autosomal dominant inheritance
• Bilateral expansion of posterior mandible
• May regress after puberty
Histology: vascular multinucleated giant cell lesions
Giant cell lesions of the jaws (6)
- Reactive or hyperplastic lesions
- Benign but may be locally destructive
- Age: 10-30
- 60% in females
- Usually mandible
- Characterised by osteoclasts
Central giant cell granuloma (3)
- Well demarcated radiolucency
- Composed of giant cells - osteoclasts
- May be destructive
Giant cell lesions of the jaws: patient management (4)
- Blood biochemistry (serum calcium initially)
- Curettage
- Resection
- 20% recurrence rate
Hyperparathyroidism types and tests (5)
Hyperparathyroidism: – Primary: parathyroid adenoma (90%) – Secondary: renal failure, malabsorption – Hereditary: autosomal dominant • Blood biochemistry: – Raised serum Calcium, Phosphate – Parathyroid hormone
Hyperparathyroidism mnemonic (1)
Stones, bones, groans and moans
Hyperparathyroidism giant cell lesion (3)
• Radiolucent lesion
• “Brown tumour”
– Identical to central giant cell granuloma
• Management:
– Treatment of hyperparathyroidism (surgery)
