L14 Bone lesions affecting the jaws Flashcards

1
Q

What are the 3 broad groups that bone lesions can be categorised into?

A
  • Lesions of the jaw bones as part of a systemic bone diseases (most, if not all, bones affected e.g. osteogensis imperfecta)
  • Localised bone disease occuring in the jaws (may affect almost any bone, including the jaws, e.g. osteomyelitis)
  • Lesions occuring only in the jaw bones (e.g. dental cyst, ameloblastoma)
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2
Q

How can a surgical sieve be used to diagnose/differentiate between bone lesions?

A
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3
Q

Give examples of reactive processes, degenerative conditions and metabolic/endocrine deficiencies that can cause bone lesions.

A
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4
Q

Describe torus palatinus.

A
  • Slow growing, sessile exostosis in the midline of the vault of the palate
  • Symptomless, usually flat but may be lobular if large
  • Overlying mucosa may become ulcerated by trauma
  • Don’t typically require treatment
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5
Q

What is the inheritance pattern of torus palatinus?

A

Simple autosomal dominance
F:M (2:1)

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6
Q

When may torus palatinus be removed?

A

If they interfere with insertion of a denture

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6
Q

What type of bone is present in torus palatinus and mandibularis?

A
  • Cortical bone on the surface
  • Normal lamellar (cancellous) bone in the centre
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7
Q

Describe torus mandibularis.

A
  • Exostosis on the lingual aspect of the mandible in the premolar region
  • Broad base with smooth or lobular surface
  • Bilateral in 80% ofcases, can present more prominently on one side compared to the other
  • Affects 7% of Caucasion population
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8
Q

What is the inheritance pattern of torus mandibularis?

A

Autosomal dominant with 100% penetrance in females, 70% in males.

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9
Q

What is osteogenesis imperfecta?

A
  • Hereditary disease: usually autosomal dominant, recessive forms and spontaneous cases occur
  • Characterised by defects in type I collagen synthesis (25% chace of dental presentation)
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10
Q

What are the clinical features of osteogenesis imperfecta?

A
  • Generalised osteoporosis with slender bones, vulnerable to fracture
  • Long bones have narrow, poorly formed cortices composed of immature woven bone
  • Skull is thin, may be wormian bones in the skull (supernumerary)
  • Jaws are rarely affected
  • Sclera appear blue
  • Deafness due to distortion of ossicles
  • Joint hypermobility with lax ligaments
  • Translucent skin
  • Heart valve defects
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11
Q

What are the oral manifestations of osteogensis imperfecta?

A
  • 25% of cases are associated with dentinogenesis imperfecta, especially in primary dentition
  • Increased tendency to class III occlusion and impacted molar teeth
  • Dentinogenesis imperfecta: short roots, obliterated pulp chambers
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12
Q

List inflammatory conditions that can affect the jaws.

A
  • Fracture
  • Healing extraction socket
  • Dry socket
  • Chronic periodontal disease
  • Osteomyelitis
  • Actinomycosis
  • Syphilis
  • Osteoradionecrosis
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13
Q

Describe the stages of tooth socket healing following extraction.

A

1) Socket fills with blood, blood clots
2) Blood clot is organsied to form granulation tissue (macrophages remove clot at periphery, fibroblasts migrate into clot, endothelial ells produce new thin walled BVs)
3) Osteoclast resorption of crestal bone and spicules of bone detached during extraction
4) Gingival epithelial proliferation and migration across the defect, by 6 weeks the epithelium is normal thickness
5) Osteoblasts at the base of the socket replace granulation tissue with woven bone, by 6 weeks the socket is filled with woven bone
6) Remodelling of woven bone and removal of lamina dura of tooth socket

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14
Q

What is the prevalence of acute alveolar osteitis?

A
  • 1-3% of all extractions
    Most common in:
  • Molar teeth
  • Mandible
  • Local anaesthetic cases rather than GA
  • Complex extractions
  • Most commonly associated with lower 3rd molar extraction
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15
Q

What is acute alveolar osteitis?

A
  • Dry socket
  • Localised inflammation of bone following failure of blood clot to form, or premature loss/disintegration of clot
  • Bone is exposed to saliva, food debris and bacteria
  • Bone becomes necrotic with inflammation in adjacent bone
  • Healing is slow; necrotic bone is gradually seperated by osteoclasts and bony sequestra form
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16
Q

Name the various types of osteomyelitis.

A
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17
Q

What does the term osteomyelitis mean?

A

Inflammation of the bone

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18
Q

Describe acute suppurative osteomyelitis.

A
  • Usually due to spread of local infection (e.g. from periapical infection)
  • Occassionally due to haematogenous spread
  • Relatively rare condition
  • Predisposing factors: reduced host resistnace, virulent bacteria
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19
Q

Why is acute suppurative osteomyelitis more common in the mandible than the maxilla?

A
  • Mandible has thicker bone trabeculae and cortical plates
  • Therefore the blood supply is more easily compromised
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20
Q

Describe the radiology of acute and chronic osteomyelitis.

A

Acute:
- Ragged, moth eaten radiolucency
- Subperiosteal bone formation
- May be sequestra

Chronic:
- Ragged, moth eaten radiolucency
- Sequestra present
- Sclerosis of surrounding bone
- Involucrum formation (layer of new bone growth)

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21
Q

Explain the pathogenesis of acute suppurative osteomyelitis.

A
  • Infection of marrow leads to acute inflammatory reaction
  • Tissue necrosis and suppuration follow
  • Thrombosis may produce widespread necrosis of osteogenic tissues
  • Inflammation, nerosis and suppuration extends through marrow spaces
  • Pus reaches periosteum (which is elevated), reducing blood supply
  • Pus may discharge through sinuses to mouth and skin
  • Granulation tissue seen in marrow spaces beyond areas of necrosis, osteoclasts seperate off necrotic bone and form sequestrum
  • New bone (involucrum) may form beneath the elevated periosteum
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22
Q

Describe the histological features of osteomyelitis.

A
  • Loss of osteocytes
  • Non-vital bone
  • Fibrous replacement of bone marrow with mixed inflammation (PMNs and granulation tissue)
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23
Q

Describe radiation osteomyelitis and osteoradionecrosis.

A
  • Radiotherapy involving the jaw causes ischaemia (lack of blood supply = lack of oxygen)
  • Ischaemia is caused by proliferation of intima of BVs (endarteritis obliterans) which can occlude vessels
  • Central mandibular artery may be occluded
  • Ischaemic and possibly necrotic bone
  • Bone now susceptible to infection from teeth, periodontium, XLA, mucosa
  • Extensive painful necrosis of bone with sloughing of overlying mucosa exposing more bone to infection
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24
Q

Describe MRONJ.

A
  • Medication related osteo-necrosis of the jaw
  • Associated with bisphosphonates, antiangiogenic agents, RANKL inhibitors and m-TOR inhibitors (inhibit osteocalst formation and migration and reduce bone turnover)
  • Increased risk with IV delivery
  • Causes exposed bone, localised pain and failure of extraction socket to heal
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25
Q

How is MRONJ managed?

A
  • Daily irrigation and antimicrobial rinses
  • OHI
  • Abx if there is secondary infection
  • Remove looses pieces of bone with tweezers or gently grind bone away to allow for soft tissue coverage
26
Q

How is MRONJ staged?

A

Stage 1 is asymptomatic.

27
Q

What are the types of fibro-osseus lesions?

A
28
Q

Describe fibrous dysplasia.

A
  • Developmental or reactive lesions
  • 25% affect the head and neck
  • Can present in single or multiple bones
  • Affects those aged 15-30
  • Painless smooth swellings
  • Maxilla most frequent site in head and neck
  • Poorly demarcated radiopacity
  • 3 types: monostotic, polystotic, McCune-Albright’s
29
Q

Describe monostotic fibrous dysplasia.

A
  • Single skeletal lesion
  • Ribs and femur are most common sites
  • 25% of lesions in head and neck
  • Affects men and women equally, typically aged 15-30
30
Q

Describe polystotic fibrous dyplasia and McCune-Albright syndrome.

A
  • Multiple lesions
  • 50% of cases present with head and neck lesions
  • Affects those aged under 15
  • May be part of McCune-Albright syndrome: Cafe au lait spots, endocrinopathies
31
Q

Describe the oral manifestations of fibrous dysplasia.

A
  • Maxilla more commonly affected
  • Gradually increasing painless swelling
  • Produces facial asymmetry
  • May cause tooth displacement
  • Usually smooth surfaced
  • More pronounced bucally than palatally
  • Maxillary lesions may involve sinus, zygomatic process, floor of orbit
32
Q

Describe the radiographic features of fibrous dysplasia.

A
  • Localised lesion within normal bone
  • Appearance varies depending on age of lesion
  • Begin more radiolucent due to more fibrous tissue, gradually become more calcified with ground glass or orange peel effect
  • Poorly demarcated, margins blend with normal bone
  • Loss of lamina dura! (Key feature)
  • Enlargement of bone
  • Teeth displaced
  • Antrum may be involved
33
Q

Describe the histological features of fibrous dysplasia.

A
  • Replacement of normal bone by fibrous tissue containing islands and trabeculae of metaplastic bone
  • Fibrous tissue may be cellular
  • Overtime fibrous contents decrease and amounts of bone increase
  • Newly formed trabeculae are delicate and irregularly shaped, lace like
  • Consist of coarse fibred woven bone
34
Q

What is the management of fibrous dysplasia?

A

No requirement for treatment.
Surgery may be indicated for aesthetic reasons only.

35
Q

What gene is mutated in McCune-Albright syndrome?

A

GNAS1 gene

36
Q

Describe ossifying fibromas/cemento-ossifying fibromas.

A
  • A type of fibro-osseus lesion
  • Benign osteogenic neoplasm
  • Age 20-40
  • Females twice as likely to be affected
  • Usually found in the mandible, in the premolar or molar region
  • Trabeculae, island or ‘cementicles’ of bone present
37
Q

Describe the radiographic presentation of ossifying fibromas.

A
  • Well defined radiolucency
  • Islands of bone present
  • Mixed pattern of radiolucent and radiopaque areas
  • Root resorption occurs
  • Can cause expansion of bone
38
Q

Describe the management of ossifying fibromas.

A

Require complete surgical excision.

39
Q

Describe the histological presentation of ossifying fibromas/cemento-ossifying fibromas.

A

Cellular fibrous tissue containing trabeculae of bone.
Pattern of bone and cellularity is highly variable.
Cementoid like bodies present.

40
Q

Summarise the differences between fibrous dysplasia and ossifying fibroma.

A
41
Q

Describe central giant cell granulomas.

A
  • Aka giant cell lesions
  • Reactive or hyperplastic lesions
  • Benign but may be locally destructive
  • First clinical presentation is typically a gingival swelling
  • Growth is sometimes rapid (radiological features are not typical if growth is rapid)
  • Age 10-30
  • 60% of cases are women
42
Q

Where are giant cell lesions most commonly found?

A
  • Mandible more common than the maxilla
  • Anterior region of jaws most common (in the site of the primary dentition)
43
Q

Describe the radiology of central giant cell granulomas.

A
  • Well defined radiolucent area
  • May be multilocular (small lesions may be unilocular)
  • Thinning and often expansion of the cortex
  • Involved teeth may be displaced
  • Root resorption is common
44
Q

Describe the histological features of central giant cell granulomas.

A
  • Cellular stroma mostly composed of fibroblasts and macrophages
  • Variable numbers of multinucleated giant cells
45
Q

How are central giant cell granulomas managed?

A
  • Surgical curettage
  • Recurrence is rare
46
Q

What conditions do you need to exclude when diagnosing central giant cell granuloma?

A
  • CGCG is histologically identical to Browns tumours caused by hyperparathyroidism
    Also need to differentiate from:
  • Cherubism
  • Aneurysmal bone cyst
  • Fibrous dysplasia
  • Giant cell tumour of bone
47
Q

What are the 3 forms of hyperparathyroidism?

A
  • Primary: often due to adenoma of parathyorid gland
  • Secondary: often due to unerlying chronic renal disease
  • Tertiary: following prolonged secondary hyperparathyroidism
48
Q

Describe primary hyperparathyroidism.

A
49
Q

What are the skeletal effects of hyperparathyroidism?

A

Skull:
- Osteopenia ‘pepper pot skull’

Jaws:
- Osteopenia ‘ground glass appearance;
- Loss of lamina dura and other corticated structures
- No bony expansion
- Associated with Brown tumours

50
Q

Describe Brown tumours.

A
51
Q

Name bone tumours that can affect the jaws.

A
  • Benign primary bone tumours
  • Malignant primary bone tumours
  • Malignant bone marrow tumours
  • Malignant secondary bone tumours (metastases commonly from breast, prostate, kidney)
  • Odontogenic tumours
52
Q

What tissues of the jaw can bone tumours arise from?

A
  • Bone
  • Cartilage
  • Bone marrow
  • Vascular tissue
  • Fibrous tissue
  • Odontogenic tissue
53
Q

Give examples of bone tumours of the jaws.

A
  • Osteoma
  • Haemangioma of bone
  • Langerhans cell histiocytosis
  • Osteosarcoma
  • Malignant secondary bone tumours
54
Q

What is an osteoma?

A
  • Benign, slow growing tumour
  • Mandbile more commonly affected
  • Comprised of well-differentiated mature bone
  • Well defined margin
55
Q

What syndrome is associated with multiple osteomas?

A

Gardener’s syndrome
- Autosomal dominant
- Also causes polyposis coli and fibrous tumours and epidermoid cysts of the skin

56
Q

What is a haemangioma of bone?

A
  • Rare benign tumour
  • More common in soft tissue than bone
  • More common in mandible
  • May produce swelling, but can also present as an incidental radiographic finding
  • Osteolytic, often multilocular honey comb appearance
  • Aspiration reveals fresh blood
  • Extraction of teeth may produce severe haemorrhage!!
57
Q

What is Langerhans cell histiocytosis?

A
58
Q

What is osteosarcoma?

A
  • Malignant tumour
  • Rarely presents in the jaws
  • If present in the jaw, usually around 30 years of age
  • More common in mandible than maxilla
  • Rapidly enlarging swelling, may be pain, numbness of lip, trismus, displacement of teeth
  • Occasionally seen in elderly; may complicate Paget’s disease or radiotherapy
59
Q

Describe the radiographic appearance of osteosarcoma.

A
  • Variable appearance dependent on amount of normal bone destroyed
  • Elevation of periosteum
  • Deposition of radiating trabeculae produces sunburst appearance
60
Q

Describe the histological presentation of osteosarcoma.

A
  • Considerable variation in histological appearance
  • Tumour cells produce thin bone or osteoid
  • Cells of varying sizes present
61
Q

What is the long term prognosis for patients with osteosarcoma?

A
  • Prone to local recurrence
  • 5 year survival rate of 40%
  • Metastasise infrequently
62
Q

Describe malignant secondary bone tumours.

A
  • The jaws are a rare site for secondary tumours, account for approx. 1% of malignant tumours of the oral cavity
  • Mandible more common than the maxilla
  • Most common primary sites are breast, bronchus and kidney
  • Majority are osteolytic (bone destroyed) some (breast and prostate) may be osteoblastic
  • Symptoms are highly variable but may include: pain, paraesthesia or anaesthesia of lip due to involvement of ID nerve, swelling, loosness of teeth
  • Many are asymptomatic