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In response to low calcium, what are the combined effects of vitamin D and PTH?
- Stimulate bone calcium mobilisation (osteoclasts)
- Increase renal reabsorption of calcium in the distal tubule (mainly PTH)
- Stimulate intestinal calcium and PHOSPHATE absorption (vitamin D)
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In response to high calcium?
Osteoclast action is inhibited.
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Ricketts/osteomalacia (adults) causes failure of calcification due to?
- Deficiency of or resistance to actions of Vit D.
- Mineralisation of osteoid is not normal. (Dependant on Ca and PO4, which vit D maintains)
- In growing children Ricketts can therefore cause deformaties.
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What are the causes of deficiency or resistance to vit D?
- Lack of UV
- Malabsorption (Coeliac)
- Renal disease
- Drugs e.g. phenytoin, degrades vit D into inactive form.
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Dental abnormalities of rickets?
- Enamel hypoplasia
- Increased width of predentine
- Increased interglobular dentine
- Deficient growth of condylar carlilage- lack of growth of vertical ramus
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Hyperparathyroidism leads to:
- Increased osteoclastic activity
- Increased absorption
- Increase reabsorption
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Hyperparathyroidism can be primary or secondary, give an example of each:
- Primary - hyperplasia of the gland
- Secondary - Reactive hyperplasia due to persistent hypocalcaemia e.g chronic renal disease
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Clinical fts of hyperparathyroidism:
- Generalised Osteoporosis
- Bone lesions - Giant cell lesions (Brown Tumours) (epulis)
- Metastatic Calcification- renal stones
- Dental Rad - loss of lamina dura, ground glass
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Investigation findings for hyperparathyroidism:
- Increased Calcium
- Increased alkaline phosphatase
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What is osteoporosis?
- Reduced bone density and mass, leading to increased risk of fracture.
- Imbalance between bone formation and resorption.
- Increased bone resorption due to osteoclasts activity compared to new bone formation.
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Risk factors for osteoporosis:
immobilisation, post menopausal, steroids, age, smoking, alcohol.
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Clinical fts of osteoporosis:
- Fractures in 3 common sites - Neck of femur, Ribs and sternum, lumbar vertebrae
- Compression fractures in vertebra can slowly lead to deformity and distortion of skeleton, loss of height
- Compression - lead to nerve problems, increased pain.
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Dental fts (osteoporosis):
- Atrophic mandible/maxilla (edentulous)
- Pathological fracture of jaw
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Tx (osteoporosis):
- Assess predisposing factors
- Prevention
- Excercise
- Ca intake
- Bisphosphonates
- OestrogenRT
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What hormone is in excess in acromegaly?
Growth hormone. Due to hyperplasia or neoplasm of anterior pituitary.
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Clinical fts of acromegaly:
- In adults, bone growth is reactivated. Large hands/feet/ears/nose
- Prognathism, gaps in teeth
- Macroglossia
- Diabetes
- Hypertension
- Thick skin
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What is pagets disease?
Chronic disorganised remodelling of bone unrelated to functional requirements. Bone is enlarged, abnormal, brittle. Older patients affected.
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Clinical fts (Pagets disease):
- Progressive enlargement and deformity of affected bones (skull, femur, spine, pelvis, sternum, jaws)
- Maxilla x2 than mandible. Spacing of teeth.
- Narrowing of foramina can cause CN deficits.
- Hypercementosis and ankylosis of teeth
- Risk of malignancy (sarcomatous transformation) 0.1 percent.
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Radiographic features (Pagets):
- Ground glass appearance of trabeculae.
- Hypercementosis
- Skull vault will show scalloped circumscribed zones of osteoporosis
- Later, deposition of sclerotic bone - cotton wool appearance.
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Investigations (Pagets):
Raised serum alkaline phosphatase level
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Histopathology (Pagets):
- Osteolytic phase
- Mixed phase
- Osteosclerotic phase
- Mosaic appearance
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Diff dx of radiographic appearance (Pagets):
- Diffuse sclerotic OM
- Osteosarcoma
- FOD
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Treatment (Pagets):
- Analgesia
- Calcitonin
- Biphosphonates
- Mithramycin
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Dental problems (Pagets):
- Endo, root canal may be decreased in size, or obstructed.
- Extractions (hypercementosis, ankylosis)
- Haemostasis (increased vasc. of pagetic bone)
- Osteomyelitis may develop post XLA or surgery
- Pros appliances remade.
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What is a central giant cell granuloma?
A giant cell lesion in bone. Its aetiology unknown, possible haemodynamic disturbance in bone marrow.
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Who gets CGCG?
- Younger people <30years
- Mandible>maxilla
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Clinical features of CGCG:
- Swelling of bone (rapid), can perforate soft tissue
- Can get a peripheral version, primarily in soft tissue (epulis)
- Asymptomatic
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Radiographic features of CGCG:
- Demarcated Radiolucent Area
- Thinning / Expansion of cortical plates
- Multi/Unilocular
- Teeth Displaced / Root Resorption
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Histology of CGCG:
- Multinucleated Giant Cells (Osteoclast-like)
- Vascular Stroma
- Haemorrhage / Haemosiderin
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Treatment CGCG:
Curettage
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