Card Set Information
Metabolic disorders of bone - Miranda Pring
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)
In response to high calcium?
Osteoclast action is inhibited.
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.
What are the causes of deficiency or resistance to vit D?
Lack of UV
Drugs e.g. phenytoin, degrades vit D into inactive form.
Dental abnormalities of rickets?
Increased width of predentine
Increased interglobular dentine
Deficient growth of condylar carlilage- lack of growth of vertical ramus
Hyperparathyroidism leads to:
Increased osteoclastic activity
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
Clinical fts of hyperparathyroidism:
Bone lesions - Giant cell lesions (Brown Tumours) (epulis)
Metastatic Calcification- renal stones
Dental Rad - loss of lamina dura, ground glass
Investigation findings for hyperparathyroidism:
Increased alkaline phosphatase
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.
Risk factors for osteoporosis:
immobilisation, post menopausal, steroids, age, smoking, alcohol.
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.
Dental fts (osteoporosis):
Atrophic mandible/maxilla (edentulous)
Pathological fracture of jaw
Assess predisposing factors
What hormone is in excess in acromegaly?
Growth hormone. Due to hyperplasia or neoplasm of anterior pituitary.
Clinical fts of acromegaly:
In adults, bone growth is reactivated. Large hands/feet/ears/nose
Prognathism, gaps in teeth
What is pagets disease?
Chronic disorganised remodelling of bone unrelated to functional requirements. Bone is enlarged, abnormal, brittle. Older patients affected.
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.
Radiographic features (Pagets):
Ground glass appearance of trabeculae.
Skull vault will show scalloped circumscribed zones of osteoporosis
Later, deposition of sclerotic bone - cotton wool appearance.
Raised serum alkaline phosphatase level
Diff dx of radiographic appearance (Pagets):
Diffuse sclerotic OM
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.
What is a central giant cell granuloma?
A giant cell lesion in bone. Its aetiology unknown, possible haemodynamic disturbance in bone marrow.
Who gets CGCG?
Younger people <30years
Clinical features of CGCG:
Swelling of bone (rapid), can perforate soft tissue
Can get a peripheral version, primarily in soft tissue (epulis)
Radiographic features of CGCG:
Demarcated Radiolucent Area
Thinning / Expansion of cortical plates
Teeth Displaced / Root Resorption
Histology of CGCG:
Multinucleated Giant Cells (Osteoclast-like)
Haemorrhage / Haemosiderin