Bone lesions of the jaw

Question 1

Bone structure (3)

Answer 1

• Gross structure
• Blood supply
• Microscopic structure
– lamellar bone - mature
– woven bone - immature (see this in embryology and healing or in a lesion)

Question 2

Bone histology (5)

Answer 2

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

Question 3

Bone turnover (4)

Answer 3

• Laid down by osteoblasts (some osteoblasts osteocytes)
• Removed by osteoclasts
• Turnover occurs in response to forces on bone
• Results in resting and reversal lines

Question 4

Bone remodelling overseen by (4)

Answer 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

Question 5

Special tests - bone biochemistry (5)

Answer 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)

Question 6

Oral developmental abnormalities of bone: torus (5)

Answer 6

• 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

Question 7

Oral developmental abnormalities of bone: osteogenesis imperfecta (4)

Answer 7

– type 1 collagen defect
– inheritance varied - 4 main types
Clinical
– weak bones, multiple fractures
– sometimes associated with dentinogenesis
imperfecta

Question 8

Oral developmental abnormalities of bone: achondroplasia (3)

Answer 8

– autosomal dominant
– dwarfism
– poor endochondral ossification

Question 9

Oral developmental abnormalities of bone: osteopetrosis (4)

Answer 9

– lack of osteoclast activity
– failure of resorption
– marrow obliteration
Made of compact bone only, becomes very fragile and has a tendency to fracture

Question 10

Infections of bone and their prevalence (4)

Answer 10

Dry socket: very common
Sclerosing osteitis: relatively common
Osteomyelitis: rare
Osteonecrosis: rare, but increasingly more common

Question 11

Dry socket (alveolar osteitis)
-what does it affect
-how is it caused
-how might this have happened 
(6)

Answer 11

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

Question 12

Dry socket (alveolar osteitis) what is happening in the socket? (4)

Answer 12

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

Question 13

Differential diagnosis for sclerosing osteitis (3)

Answer 13

Hypercementosis, cementoblastoma, osteoma

Question 14

What is sclerosing osteitis and who/ where does it affect? (4)

Answer 14

• Focal bone reaction to low-grade inflammation e.g. chronic pulpitis
• Any age
• Commonly affects mandibular molars
• Asymptomatic, incidental finding

Question 15

Sclerosing osteitis - radiography (2)

Answer 15

• Uniform opacity at apex tooth,

* Often with peripheral lucency

Question 16

Treatment for sclerosing osteitis (1)

Answer 16

Cause of inflammation

Question 17

Osteomyelitis 
-what is it?
-who does it affect?
-subtypes
(5)

Answer 17

• 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)

Question 18

Causes of osteomyelitis (6)

Answer 18

Problems with:
• Blood supply:
– Age related
– Paget's disease
– Radiotherapy
• Host response
• Immunosuppression
• Poor nutrition
• Other causes:
– bisphosphonates

Question 19

Acute osteomyelitis aetiology (3)

Answer 19

Most commonly infectious (Staphylococci,
Streptococci)
• Extension of periapical abscess
• Physical injury/fracture

Question 20

Acute osteomyelitis acute inflammatory response (4)

Answer 20

Pain, pyrexia, lymphadenopathy, malaise

Question 21

Acute osteomyelitis histology (3)

Answer 21

• Acute inflammatory infiltrate
• ↑ Bone resorption
• ↓ Bone formation

Question 22

Chronic osteomyelitis aetiology (2)

Answer 22

• Low-grade inflammatory reaction

* May be progression from acute osteomyelitis

Question 23

Chronic osteomyelitis - Chronic inflammatory response associated with low-grade infection (4)

Answer 23

Pain, swelling, bone loss, sequestrae

Question 24

Chronic osteomyelitis histology (4)

Answer 24

• Chronic inflammatory infiltrate - lymphocytes and plasma cells
• Both osteoclastic and osteoblastic activity
• Reversal lines
• Osteonecrosis

Question 25

What is proliferative periostitis? (1)

Answer 25

chronic osteomyelitis with periosteal inflammation

Question 26

Chronic osteomyelitis radiograph (3)

Answer 26

Radiolucency, focal opacity, ‘moth eaten’ Indistinct margins Sequestrae

Question 27

Osteomyelitis - patient management (3)

Answer 27

* Resolve source of infection * Remove infected bone * Hyperbaric oxygen

Question 28

Osteonecrosis of the jaws - causes (8)

Answer 28

``` • 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 ```

Question 29

Osteonecrosis of the jaws - patient management - prevention (4) - low risk (2) - high risk (2)

Answer 29

``` • 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 ```

Question 30

Types of bone neoplasms (4)

Answer 30

Benign: osteoma, osteoblastoma Malignant: osteosarcoma, chondrosarcoma

Question 31

Osteoma - clinical (4)

Answer 31

``` • 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) ```

Question 32

Osteoma - histopathology: composed of (2)

Answer 32

• Compact bone • Compact and cancellous bone

Question 33

Osteosarcoma (6)

Answer 33

* 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

Question 34

Osteosarcoma of the jaws (3)

Answer 34

• Age 20-40 years • Males slightly more common • Mandible > maxilla

Question 35

Why is early dx essential in osteosarcoma of the jaws (3)

Answer 35

* Rapidly growing swelling * Pain * Nerve involvement

Question 36

Osteosarcoma of the jaws - radiographic features (2)

Answer 36

• Radiolucency with bone formation (sunray) • Loss of lamina dura is an important sign

Question 37

Osteosarcoma - patient management (3)

Answer 37

* Neo-adjuvant chemotherapy * Wide local excision +/- radiotherapy * 5 year survival – about 50%

Question 38

Fibro-osseus lesions (1)

Answer 38

Lesions where the normal bone is replaced by fibrous | tissue in which abnormal bone is laid down

Question 39

Fibro-osseus lesions - radiographically (3)

Answer 39

• 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

Question 40

Types of fibro-osseus lesions (4)

Answer 40

``` • Neoplastic: (Cemento) ossifying fibroma • Developmental: Fibrous dysplasia • Reactive: (Cemento) osseous dysplasia Osteodystrophy • Idiopathic: Paget's disease ```

Question 41

Ossifying fibroma (6)

Answer 41

• 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

Question 42

Ossifying pt management (3)

Answer 42

``` • Conservative enucleation • Resection • Low recurrence rate ```

Question 43

Fibrous dysplasia (7)

Answer 43

``` • 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 ```

Question 44

Fibrous dysplasia - radiographically (2)

Answer 44

• Stippled “orange peel” appearance • Merges with the surrounding bone

Question 45

Clinical variants of fibrous dysplasia: monostotic (single bone involved) (5)

Answer 45

* Single skeletal lesions * Ribs and femur most common site * 25% of lesions in head and neck * Age 15-30 (average 25) * Males = females

Question 46

Clinical variants of fibrous dysplasia: polyostotic (multiple bones involved) (5)

Answer 46

* Multiple lesions * Head & neck involved in 50% * Age: <15 * 75% in females * May be part of McCune-Albright’s syndrome

Question 47

Fibrous dysplasia: patient management (5)

Answer 47

• 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

Question 48

Fibrous dysplasia vs ossifying fibroma (4)

Answer 48

Poorly defined vs well defined No margin vs clear margin M=F vs F>M Often maxilla vs often mandible

Question 49

Cemento-osseus dysplasias (5)

Answer 49

• 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

Question 50

Classification of osseus dysplasias (3)

Answer 50

Focal: single lesions Perapical: multiple mixed radiodensity lesions at apex of teeth Florid: multiple lesions throughout jaws

Question 51

Familial gingatiform cementoma (3)

Answer 51

• 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

Question 52

Paget's disease (4)

Answer 52

* 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

Question 53

Paget's disease epidemiology (4)

Answer 53

``` • More common in Western Europe, USA, Canada, Australia, New Zealand • Rare in Asia, Africa • Cause unknown. • Possible genetic/hereditary association or infective cause ```

Question 54

Paget's disease clinical features (3)

Answer 54

``` • 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 ```

Question 55

Paget's disease: dental implications (4)

Answer 55

``` • 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 ```

Question 56

Giant cell lesions of the jaws: what are they and types (4)

Answer 56

``` Characterised by replacement of bone by fibrous tissue containing numerous multi-nucleate giant cells (osteoclasts) • Cherubism • Central giant cell granuloma • Hyperparathyroidism ```

Question 57

Cherubism (5)

Answer 57

• Developmental condition • Autosomal dominant inheritance • Bilateral expansion of posterior mandible • May regress after puberty Histology: vascular multinucleated giant cell lesions

Question 58

Giant cell lesions of the jaws (6)

Answer 58

* Reactive or hyperplastic lesions * Benign but may be locally destructive * Age: 10-30 * 60% in females * Usually mandible * Characterised by osteoclasts

Question 59

Central giant cell granuloma (3)

Answer 59

* Well demarcated radiolucency * Composed of giant cells - osteoclasts * May be destructive

Question 60

Giant cell lesions of the jaws: patient management (4)

Answer 60

* Blood biochemistry (serum calcium initially) * Curettage * Resection * 20% recurrence rate

Question 61

Hyperparathyroidism types and tests (5)

Answer 61

``` Hyperparathyroidism: – Primary: parathyroid adenoma (90%) – Secondary: renal failure, malabsorption – Hereditary: autosomal dominant • Blood biochemistry: – Raised serum Calcium, Phosphate – Parathyroid hormone ```

Question 62

Hyperparathyroidism mnemonic (1)

Answer 62

Stones, bones, groans and moans

Question 63

Hyperparathyroidism giant cell lesion (3)

Answer 63

• Radiolucent lesion • “Brown tumour” – Identical to central giant cell granuloma • Management: – Treatment of hyperparathyroidism (surgery)