9 - Bone pathology Flashcards
1
Q
What are the key components of bone?
A
- osteon (Haversian system)
- interstitial, concentric and circumferential lamellae
- periosteum
2
Q
What are Haversian canal?
A
Bony canal that contains blood vessels
3
Q
What are volksman’s canal?
A
Bony canal that runs perpendicular to Haversian canal that contains blood vessel
4
Q
What cells are contained within lacunae?
A
Osteocytes
5
Q
How does bone histology change as it matures?
A
Becomes less cellular
6
Q
What stimulates bone remodelling?
A
- mechanical stimuli
- systemic hormones
- cytokines
7
Q
What systemic hormones stimulate bony remodelling?
A
- PTH
- vitamin D3
- oestrogen
8
Q
How does oestrogen influence bone?
A
- acts like a brake on osteoclasts
- when oestrogen levels drop, osteoclasts become more active
9
Q
What special tests can be done for bone biochemistry?
A
- can’t take biopsy
- serum alkaline phosphatase
- osteocalcin
- PTH
- vitamin D assays
10
Q
What is a torus?
A
- developmental exostosis
- palatinus/mandibularis
- thickening of cortical bone
11
Q
What is osteogenesis imperfecta?
A
- type 1 collagen defect
- inheritance varied
- weak bones, multiple fractures
- associated with dentinogenesis imperfecta
12
Q
What is achondroplasia?
A
- autosomal dominant condition
- poor endochondral ossification
- causes dwarfism
13
Q
What is osteopetrosis?
A
- lack of osteoclast activity
- bone fails to resorb and marrow is obliterated
- bone becomes very dense like stone
14
Q
What is fibrous dysplasia?
A
- uncommon gene defect
- slow growing, asymptomatic bony swelling where bone is replaced by fibrous tissue
- stops progressing after growth period
15
Q
What are the different types of fibrous dysplasia?
A
- monostotic
- polyostotic
- syndromic (Albright’s syndrome)
16
Q
What is monostotic fibrous dysplasia?
A
- single bone (continues to grow)
- most common phenotype
- maxilla>mandible
- causes facial asymmetry
17
Q
What is polyostotic fibrous dysplasia?
A
Many bones affected by fibrous dysplasia
18
Q
What is Albright’s syndrome?
A
Characterised by multiple bones with fibrous dysplasia, early puberty and increased melanin pigment
19
Q
Describe the radiographic appearance of fibrous dysplasia.
A
- “ground glass”, “cotton wool”, “orange peel”
- lacks trabecular pattern
- margins blend into surrounding bone
- bone maintains approximate shape
- becomes more radiopaque as lesion matures
20
Q
Describe the histology of fibrous dysplasia.
A
- “fibro-osseous” lesion
- fibrous replacement of bone
- cellular fibrous tissue around metaplastic or woven bone which increases in density
- no capsule
21
Q
What is rarefying osteitis?
A
- localised loss of bone in response to inflammation
- process rather than disease
- occurs secondary to another form of pathology
- if at apex of tooth, consider apical periodontitis, periapical granuloma or periapical abscess
22
Q
What is sclerosing osteitis?
A
- localised increase in bone density in response to low grade inflammation
- most common around apex of tooth with necrotic pulp
- periapical radiopacity that is poorly defined
- can cause external root resorption
23
Q
What is idiopathic osteosclerosis?
A
- localised increase in bone density of unknown cause
- most common in premolar/molar region of mandible
- asymptomatic
- no bony expansion or effect of adjacent structures
24
Q
What is alveolar osteitis?
A
- dry socket
- complication of extraction
- causes severe pain, loss of clot and bone sequestra
25
What is osteomyelitis?
- endogenous infection
- acute or chronic (suppuration is rare)
- presents similarly to sequestra, actinomycosis, chronic diffuse sclerosing osteomyelitis or periostitis
26
What is Garre's sclerosing osteomyelitis?
- only seen in children
- any infection can cause
- suppuration present
- painful hard swelling
27
What are the different aetiologies of bone necrosis?
- osteomyelitis
- avascular necrosis (age related ischaemia or anti-resorptive medication)
- irradiation (ORN)
28
What are the different types of metabolic bone disease?
- osteoporosis
- rickets/osetomalacia
- hyperparathyroidism
29
What is osteoporosis?
- bone atrophy (resorption>formation)
- endosteal net bone loss
- quantitive deficiency (bone that is formed is normal)
- symptomless, weak bones, sinus enlargement
30
What are the radiographic features of osteoporosis?
Loss of normal bone markings
31
What is the aetiology of osteoporosis?
- sex hormone status
- age
- calcium status and physical activity
- secondary osteoporosis caused by hyperparathyroidism, cushings, thyrotoxicosis, diabetes, long term steroids
32
What is rickets/osteomalacia?
- rickets in children, osteomalacia in adults
- osteoid forms but fails to calcify
- qualitative deficiency
33
What is the aetiology of rickets/osteomalacia?
Vitamin D deficiency
34
How does rickets present?
- children with bow legs
- poor endochondral bone
- law calcium and raised alkaline phosphatase
35
What is hyperparathyroidism?
- increased levels of parathyroid hormone
- calcium is mobilised from bones causing generalised osteoporosis, brown tumours and metastatic calcification in kidneys
36
What are the different types of hyperparathyroidism?
- primary (neoplasia/hyperplasia)
- secondary (hypocalcaemia due to vit D deficieny)
- tertiary (hyperplasia due to prolonged secondary)
37
What is the incidence of primary hyperparathyroidism?
- 1 in 100
- postmenopausal women
- 3:1 F:M
- 90% caused by parathyroid adenoma
38
What is osteitis fibrosa cystica?
- aka brown's tumour
- giant cell lesions which with mulitnucelated giant cells and blood vessels which give brown colour
39
What are the different types of giant cell lesion in the jaw?
- peripheral giant cell epulis
- central giant cell granuloma
40
What is a central giant cell granuloma?
- grows along jaw
- mandible>maxilla
- 10-25 years
- central lesion may "burst" out which is first clinal sign
41
What is cherubism?
- rare condition in children
- autosomal dominant inheritance (FH important)
- multicystic/locular lesions in multiple quadrants
- grow before 7 years then regress after puberty
- vascular giant cell lesions
42
What is the management of cherubism?
- no active management
- may require orthodontic treatment to realign once condition is resolved
43
What is Paget's disease?
- presents with bone swelling, pain and nerve compression
- unknown aetiology
- monostotic or polystotic
- >40 years M>F
44
Describe the radiographic appearance of Paget's disease.
- bone pattern changes as disease progresses
- osteoporotic in early stages, becoming osteosclerotic in mature disease
- causes loss of lamina dura, hypercementosis and migration
45
Describe the histology of Paget's disease.
- active increased bone turnover
- osteoblastic and osteoclastic activity next to each other which indicates disordered turnover
46
What are the complications of Paget's disease?
- infection
- pathological fracture
- tumours (osteosarcoma)
47
What is an osteoma?
- solitary bone tumour
- if multiple, consider Gardner syndrome which has high polyp cancer risk
48
What is an osteoblastoma?
- rare bone tumour
- very active growth
49
What is an ossifying fibroma?
- slow growing bone tumour
- affects wide age range
- mandible
- radiologically well defined as has capsule
50
Describe the histology of an ossifying fibroma.
- cellular fibrous tissue
- immature bone
- acellular calcifications
51
What are the different types of cementum lesions?
- cementoblastoma
- cemento-osseous dysplasia
52
What is a cementoblastoma?
- neoplasm attached to root
- commonly found in lower 4 anteriors
- histology same as osteoblastoma
- PDL space is continuous on radiograph
53
What is a cemento-osseous dysplasia?
- not neoplastic
- periapical COD (lower 4 anteriors)
- focal COD (one)
- florid COD (all quadrants)
- starts as radiolucency then calcifies
54
What complication is associated with cemento-osseous dysplasia?
Risk of osteomyelitis if extraction is carried out in area of COD
55
What is an osteosarcoma?
- rare tumour
- 30s, if older Paget's related
- mandible>maxilla
- local destruction
- recurrence is high and metastasis common
