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F - SCR > BDS4 bone pathology > Flashcards

BDS4 bone pathology Flashcards

1
Q

what is systemic hormones of bone remodelling?

A
  • Parathyroid hormone (PTH)
  • Vitamin D3
  • Oestrogen
  • others
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2
Q

what is special tests of bone biochemistry?

A
  • Blood calcium
  • Osteoblast activity (bone formation)
    *Serum alkaline phosphatase
    *Osteocalcin
  • Osteoclast activity (bone resorption)
    *Collagen degradation urine & blood
  • Parathyroid hormone
  • Vitamin D assays (>50 nmol/L adequate)
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3
Q

what is types of torus?

A

Torus
* Developmental
* Exostosis

Problem with fitting dentures

Types
* Torus palatinus
*Midline of palate
* Torus/tori mandibularis
*Bilateral on lingual aspect of mandible (usually premolar region)

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4
Q

what is this?

A

Torus mandibularis

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5
Q

what are types of developmental abnormality conditions

A

Osteogenesis imperfecta
Achondroplasia
Osteopetrosis
Fibrous dysplasia

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6
Q

what are characteristics and clinical features of osteogenesis imperfecta?

A
  • Type 1 collagen defect
  • Inheritance varied – 4 main types
  • Clinical features
    *Weak bones, multiple fractures
    *Sometimes associated with dentinogenesis imperfecta
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7
Q

what is characteristics of achondroplasia?

A
  • Autosomal dominant
  • Poor endochondral ossification
  • Dwarfism
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8
Q

what is characteristics of osteopetrosis

A
  • Lack of osteoclast activity
  • Failure of resorption
  • Marrow obliteration
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9
Q

what are characteristics of fibrous dysplasia?

A

Uncommon
* Gene defect
Slow growing, asymptomatic bony swelling
* Bone replaced by fibrous tissue
Active under 20 years
Stops growing after active growth period (usually…)
Serum biochemistry norma

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10
Q

what are clinical phenotypes of fibrous dysplasia?

A
  • Determined by timing of gene mutation
  • Monostotic: single bone
    *More common
    *Maxilla > mandible
    *Facial asymmetry
  • Polyostotic: many bones
  • May be syndromic – Albright’s syndrome
    *Melanin pigment
    *Early puberty
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11
Q

what does fibrous dysplasia look like radiographically?

A
  • Variable appearances
  • Margins often blend into adjacent bone
  • Bone maintains approximate shape (initially)
  • Becomes more radiopaque as lesion matures
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12
Q

what is histology of active fibrous dysplasia?

A

Fibrous replacement of bone
* Cellular fibrous tissue
* Bone – metaplastic or woven, but
will remodel & increase in density

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13
Q

what is rarefying osteitis?

A

Localised loss of bone in response to inflammation
* Always occurring secondary to another form of pathology
* If at apex of tooth consider apical periodontitis, periapical granuloma or periapical abscess

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14
Q

what is sclerosis osteitis?

A
  • Localised increase in bone density in response to low-grade inflammation
  • Most common around apex of tooth with a necrotic pulp
    *Periapical radiopacity, often poorly-defined
    *May eventually lead to external root resorption if chronic
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15
Q

what is idiopathic osteosclerosis?

A

Localised increase in bone density of unknown cause
* a.k.a. dense bone island
* Most common in premolar-molar region of mandible
* Always asymptomatic
* No bony expansion & no effect on adjacent teeth/structures

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16
Q

how to tell difference between idiopathic osteosclerosis and sclerosing osteitis

A

Carry out sensibility testing on the tooth involved

17
Q

what is aetiology of bone necrosis?

A
  • Osteomyelitis
    *Acute or chronic
  • Avascular necrosis
    *Age-related ischaemia
    *Anti-resorptive medication
  • Irradiation
    *Osteoradionecrosis
    **Prone to infections
18
Q

what are osteoclast inhibitors used for?

A
  • osteoporosis
  • Paget’s
  • bone metastases
19
Q

what are types of metabolic bone disease?

A
  • Osteoporosis
  • Rickets & Osteomalacia
  • Hyperparathyroidism
20
Q

what is osteoporosis and clinical and radiographic features?

A
  • Bone atrophy: resorption exceeds formation
    *Endosteal net bone loss
    *Quantitative deficiency (bone formed is normal)
  • Clinical features
    *Symptomless
    *Weak bone
    *Antrum enlarged
  • Radiographic features
    *Loss of normal bone markings
21
Q

what is aetiology of osteoporosis?

A
  • Sex hormone status
  • Age
  • Calcium status & physical activity
  • Secondary osteoporosis
    *Hyperparathyroidism
    *Cushing’s syndrome
    *Thyrotoxicosis
    *Diabetes mellitus
    others
22
Q

what is characteristics of rickets and ostemalacia?

A
  • Vitamin D deficiency
    *Lack of sunlight – daylight hours
    *Diet
    *Malabsorption
    *Renal causes
  • Osteoid forms but fails to calcify
  • Rickets
    *Poor endochondral bone
    *Low calcium
    *Raised alkaline phosphatase
23
Q

what is hyperparathyroidism and types?

A
  • Calcium mobilised from bones
    *Generalised osteoporosis
    *Osteitis fibrosa cystica (“brown tumours”)
    *Metastatic calcification – kidney
  • Types
    *Primary: neoplasia / hyperplasia
    *Secondary: hypocalcaemia (e.g. due to vitamin D deficiency)
    *Tertiary: hyperplasia as a result of prolonged secondary
24
Q

what is increased primary hyperparathyroidism?

A
  • mainly posmenopausal women
  • 90% parathyroid adenoma (→ increased parathyroid hormone)
    *Hypercalcaemia
    *Increased bone turnover
25
Q

what is giant cell lesions of the jaws?

A
  • Peripheral giant cell epulis
  • Central giant cell granuloma
    *Age 10-25
    *Mandible>maxilla
    *May be multilocular
  • Differential diagnosis
    *Osteitis fibrosa cystica
    *Aneurysmal bone cyst
    *Giant cell tumours (very rare)
  • Central lesions may “burst out”
26
Q

what is cherubism? histology

A
  • Rare condition
  • Autosomal dominant inheritance
  • Multicystic/multilocular lesions in multiple quadrants
  • Grow before about 7 years & regress after puberty
  • Histology: vascular giant cell lesions
27
Q

what is paget’s disease of bone?

A

Age > 40, M>F
3% of routine autopsies
Aetiology unknown
* Racial predilection
* Viral?
Monostotic or polyostotic
Serum biochemistry
* Raised alk phos
Clinical
* bone swelling, pain, nerve compression

28
Q

what is bone patterns and dental changes of paget’s disease of bone?

A

Variable bone pattern
* Changes as disease progresses
* Osteoporotic / mixed / osteosclerotic
Dental changes
* Loss of lamina dura
* Hypercementosis
* Migration (due to bone enlargement)

29
Q

what is histology and complications of paget’s bone disease?

A

Histology
* Active: increased bone turnover
* Osteoclastic & osteoblastic activity
* Will burn out
Complications
* Infection
* Tumour

30
Q

what are types of bone tymours?

A
  • Osteoma
    *Solitary
    *Mostly cortical bone
    *Slow growing
    *If multiple osteomas:
    **Consider Gardner syndrome
  • Osteoblastoma
    *Rare
    *May be a Giant Osteoid Osteoma
    *Often very active growth
31
Q

what is clinical and histological features of ossifying fibroma?

A
  • Clinical
    *Slow growing
    *Wide age range
    *Mainly mandible
    *Radiologically well-defined
  • Histology
    *Cellular fibrous tissue
    *Immature bone
    *Acellular calcifications
32
Q

what are types of cementum lesions?

A

Cementoblastoma
*Neoplasm attached to root
*Histology same as osteoblastoma
Cemento-osseous dysplasias
*Nomenclature problem, probably not neoplastic
*Types:
**Periapical COD
**Focal COD
**Florid COD
*Starts as radiolucency → later calcification

33
Q

what is osteosarcoma charcateritics?

A

Age 30’s
*If elderly, likely Paget’s-related

Characteristics
* Mandible > maxilla
* Varied clinical & x-ray presentation
* Local destruction
* Recurrence & metastasis

34
Q
A

cementoblastoma

F - SCR (32 decks)

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