Bone Pathology Flashcards

1
Q

What factors can initiate bone remodelling?

A

Mechanical stimuli

Systemic hormones
- Parathyroid hormone
- Vitamin D3
- Oestrogen

Cytokines

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2
Q

Why is osteoporosis more common in post-menopausal women?

A

Osteoclasts have receptors for oestrogen- usually oestrogen is high before menopause and this reduces the activation of osteoclasts.

During menopause, oestrogen production is low.
- osteoclasts become active and start to break down bone.

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3
Q

Describe the action of parathyroid hormone.

A

When blood calcium levels drop- PTH is released from the parathyroid gland.

PTH acts to activate osteoclasts to resorb bone, which will increase serum calcium levels back to normal.

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4
Q

What is a torus?

A

Developmental abnormality of bone.

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5
Q

What problems may arise with a torus?

A

Ill-fitting dentures

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6
Q

What are the different types of Torus present in the oral cavity?

A

Torus Palatinus- usually unilateral, in the midline of the palate.

Torus Mandibularis- usually bilateral but not symmetrical. In the area of the premolars.

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7
Q

How would a torus present on a CBCT?

A

Uniformly radiopaque.

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8
Q

What is Osteogenesis Imperfecta?

A

Type 1 collagen defect

Weak bones, multiple fractures.
Sometimes associated with dentinogenesis Imperfecta.

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9
Q

What is Achondroplasia?

A

Poor endochondral ossification

Dwarfism

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10
Q

What is Osteoporosis?

A

Lack of osteoclast activity- failure of resorption.

End up with very dense bone.

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11
Q

What is fibrous dysplasia?

A

Genetic defect whereby the patient presents with asymptomatic bone swelling and the bone is replaced with fibrous tissue and calcified.

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12
Q

When is fibrous dysplasia active?

A

Usually stops at 20 years old or once the patient stops growing.

Serum biochemistry is normal.

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13
Q

What are the clinical phenotype of fibrous dysplasia?

A

Monostotic- one bone
- most common.
- Usually in the maxilla.
- Present with facial symmetry.

Polyostotic- many bones

May present as part of a syndrome- Albright’s syndrome.

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14
Q

What might a patient present with if they have fibrous dysplasia?

A

Patient will still be in the growth period.

Facial asymmetry- one side of the mandible larger than the other, one side of the maxilla larger than the other.

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15
Q

What is the radiographic appearance of fibrous dysplasia?

A

Variable appearances- ground glass, orange peel, fingerprint whorl.

Bone maintains approximate shape but becomes more radiopaque.

On an OPT- bone looks enlarged and more radiopaque- compare with other side.

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16
Q

What further investigations might you request for fibrous dysplasia?

A

CBCT
Biopsy- incisional.

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17
Q

Describe the histology of fibrous dysplasia?

A

Fibrous replacement of bone- cellular fibrous tissue.
Bone present but will remodel and increase in density.

18
Q

What is Sclerosing Osteitis?

A

Localised increase in bone density in response to low grade inflammation.

Usually around the apex of a necrotic pulp.

Uniform radiopaque shape.

May cause external root resorption if chronic.

19
Q

What is idiopathic osteoclerosis?

A

Localised increase in bone density of unknown cause.

Most common in premolar/molar region
Always asymptomatic
No bony expansion and no effect on adjacent teeth/structures.

20
Q

What further tests would you want to do after discovering this?

A

Sensibility test- if the tooth is non-vital, likely to be sclerosis osteitis.

Ask about symptoms in the history.

21
Q

What is osteomyelitis?

A

Rare endogenous infection of bone.

Caused by Actinomyces.
- bacteria invades the cancerous bone and causes soft tissue inflammation and oedema in the closed bone marrow spaces.
- Oedema here leads to increase in hydrostatic pressure, increases blood pressure.
- Results In tissue necrosis- bacteria continue to proliferate because normal blood borne defences do not reach the tissues.

22
Q

What signs and symptoms would suggest someone has osteomyelitis?

A

Usually systemically unwell.

Usually in the mandible because of the dense overlying cortical bone- limits penetration of periostea blood vessels.

Usually in immunocompromised individuals.

Usually a precipitating factor- fractured mandible, odontogenic infections.

23
Q

How does osteomyelitis present radiographically?

A

Typically a radiolucent lesions- destruction of bone, moth-eaten appearance.

If chronic- the radiolucent lesions can start to become radiopaque.

24
Q

What might cause bone to become necrotic?

A

Osteomyelitis

Avascular necrosis-
- Age-related ischaemia
- Anti-resorptive medication- MRONJ

Irradiation- ORN

25
Q

What is osteoporosis?

A

Bone atrophy- bone resorption exceeds formation.
- the bone that is formed is normal but there is just less of it.

26
Q

What is the aetiology of osteoporosis?

A

Sex hormone status- post-menopausal women

Age

Calcium status and physical activity

Secondary osteoporosis
- Hyperparathyroidism
- Cushing’s syndrome
- Thyrotoxicosis
- Diabetes Mellitus

27
Q

What is Rickets and Osteomalacia?

A

Both arise because of vitamin D deficiency but Rickets occurs in children and Osteomalacia occurs in adults.

Osteoid forms but fails to calcify

28
Q

Why might vitamin D deficiency occur?

A

Lack of vit D in the diet
Lack of sunlight
Malabsorption
Renal causes

29
Q

What is Primary hyperparathyroidism?

A

Caused by hyperplasia or neoplasia- usually a tumour in the parathyroid gland.

Causes release of PTH, increased calcium in serum caused by the resorption of bone by osteoclasts.

30
Q

How might hyperparathyroidism present in the mouth?

A

Brown’s tumour (Osteitis fibrosa cystica)- caused by increased calcium in the blood.

Enlarged mandible, expansion bucco-lingually.
Multilocular appoearance.
Radiolucent
Pushes teeth out the way but doesn’t resorb the roots.

31
Q

Describe the histology of a Brown’s tumour (Osteitis FIbrosa Cystica)?

A

Giant cell lesions

Focal osteolytic lesions

32
Q

What is Cherubism?

A

Autosomal dominant condition that results in multicystic/multilocular lesion in multiple quadrants.

Usually in children before the age of 7.

33
Q

What is the management of cherubism?

A

Monitor- should resolve by itself.

34
Q

What is Paget’s disease?

A

Characterised by increase in osteoclast activity, disordered bone formation and increased bone vascularity.

Can be monostotic or polyostotic.

35
Q

How would Paget’s disease present clinically?

A

Bone swelling
Pain
Nerve compression
Patients may say their denture is becoming tighter

36
Q

What dental changes might you see in Paget’s disease?

A

Loss of lamina Dura
Hypercementotiss- make extractions more difficult.
Migration of teeth due to bone enlargement- difficult for prostheses to be fabricated.

37
Q

Describe the histology of Paget’s disease?

A

Bone resorption (osteoclasts) and bone deposition (osteoblasts) occurring simultaneously.

38
Q

What are the potential complications of Paget’s disease?

A

Infection
Tumour- osteosarcoma.

39
Q

What is an ossifying fibroma?

A

Benign tumour that occurs when bone is encompassed in fibrous tissue.

Has a capsule- differs from fibrous dysplasia.

40
Q

What is a Cementoblastoma?

A

Neoplasma of cementum that is attached to the root.
- Radiopaque area of bone.

Commonly found in lower and anterior teeth.

41
Q

What is Cemento-osseous dysplasia?

A

Fibro-osseous disease of the jaws.

Periapical COD- at the apex of a vital tooth
Focal OCD- appears in one area of the jaw bone
Florid COD- present in all 4 quadrants.

Starts as a radiolucency and then later calcifies.