1. Metabolic bone disease

2. Metabolic bone disease are of 3 main types: 1.Osteoporosis : the quantity of bone mass is abnormally low 2.Osteomalacia : osteoid tissue is present but poorly mineralized 3.Osteitis fibrosa :PTH over production leads to bone resorption and replacement by fibrous tissue

3. Clinical assessment The clinical features are those of : Skeletal failure : pain, fracture, deformity Hypercalcaemia : anorexia, nausea, vomiting, abdominal pain, depression, renal stone Clinical features of underlying disorder * history : duration of symptoms, relation to previous disorders, drug history, previous operation,,,etc * Examination : patient general appearance

4. Clinical assessment X-ray :decreased bone radio density is a late sign ( up to 30 % decrease is needed to be detected radiologically) The earliest sign is the loss of horizontal trabeculae of the vertebral bodes, vertical trabeculae are more conspicuous, the vertebral cortices are sharply etched There may be signs of fractures old or new in the spine, ribs, pubic rami, cortico-canclous junction of the long bones

5. Clinical assessment In the vertebra, there may be compression fracture, minor wedging at multiple levels bi concave distortion of end plates There may be x-ray finding of the underlying disorder

6. Clinical assessment *Measurement of bone mass Radiographic absorptiometry Single energy x-ray absorptiometry Dual energy x-ray absorptiometry Quantitative CT

7. Clinical assessment Biochemical tests Serum calcium and phosphate Serum alkaline phosphatase PHT activity Vit D activity Urinary calcium and phosphate Urinary hydroxyl proline * bone biopsy

8. Osteoporosis A state of which the bone is fully mineralized, but it’s structure is abnormally porous and it’s length is less than normal for the person at the same age and sex i.e. there is significant decrease in the bone mass per unit volume of bone tissue and this is accompanied by increase fragility Osteoporosis can be regional where it is confined to bone or group of bones or generalized

9. Osteoporosis Osteoporosis is usually divided into : 1.Primary Osteoporosis : no cause is found, usually due to aging and decrease gonadal activity 2.Secondary Osteoporosis : due to a variety of metabolic, endocrine, neoplastic disorders

10. Primary Osteoporosis There is 2 types : 1.Early post menopausal syndrome : due to rapid increase in the osteoclastic resorption ( type I or high turn over Osteoporosis ) 2.Senile Osteoporosis : due to decrease in osteoblastic activity and the appearance of the dietary insufficiency and chronic ill health ( type II or low turn over Osteoporosis )

11. Post menopausal Osteoporosis women at menopause and next 10 years loose bone at rate of 3 % per year, compared to 0.3 % during the preceding decade, due to increased bone resorption Risk factors : white, positive family history, amenorrhea, early hysterectomy, alcoholism, cigarette smoking, lack of exercise

12. Post menopausal Osteoporosis Clinical features :bone pain, backache, increase thoracic kyphosis X-ray :wedging or compression of one or more vertebral bodies Diagnosis : mentioned previously Prevention and treatment :women approaching menopause should maintain adequate dietary levels of calcium and phosphate and vitamin D,and keep a high level of physical activity, no smoking, no alcohol consumption

17. Post menopausal Osteoporosis Drugs used : 1.Estrogen medication (hormone replacement therapy ) 2.Biphosphonates 3.Calcitonin 4.Fluride

18. Senile osteoporosis Fifty years after menopause or in the seventh or eighth decade in men there is loss of bone mass by 0.5 % per year, this is universal to be considered as physiological manifestations of aging Risk factors : similar to post menopausal osteoporosis, but in addition there is prolonged menopausal bone loss, chronic illness, dietary insufficiency, lack of exposure to sun light

19. Senile osteoporosis Clinical features : exaggeration of sign and symptoms of post menopausal osteoporosis, there is fracture ribs, pubic rami, the classical fracture is neck of femur with minimal trauma X-ray : decrease trabecular marking of neck of femur and spine Serum biochemistry are normal unless there ids a sign of osteomalacia

20. Senile osteoporosis Treatment : correction of the underlying disorder Drugs have very limited role because of the very slow bone turn over at this age Sometimes we can use HRT, biphosphonate

21. Rickets and osteomalacia They are different expression to the same disease : defective mineralization of the bone, the bone tissue throughout the skeleton is incompletely calcified and softened In the children there are effects on physical growth and ossification, resulting iin deformity of endochondral ossification (rickets )

22. Rickets and osteomalacia Causes: calcium diffecincy, defects any ehre in the metabolic pathway for vitamin D, decrease intake, lack of exposure to sunlight, intestinal malabsorption, defective hydroxylation in the liver and kidney

23. Rickets and osteomalacia Clinical fetures :children : tetany, convulsions, failure to thrive, muscle flaccidity, deformity in the skull ( craniotabes ), thickening of the knees, ankle, wrist from physeal over growth, enlargement of costochondral junction ( rickety rosary ), lateral indentation of the chest ( Harrison sulcus ) tibial bowing When the child starts to walk, there is knock n\knees, bow legs, swollen joints, disturbed gait

24. Rickets and osteomalacia Adults Coarse is slow, patients complains of backache, bone pain, muscle weakness, vertebral collapse causes loss of weight Unexplained pain in the hip or one of the long bones precede the stress fractures X-ray : in active rickets there is thickening, widening of growth plate, cupping of metaphysis, bowing of the diaphysis ( which may remain after healing )

25. Rickets and osteomalacia In osteomalacia : the looser zone which is a thin transverse band of rarefaction in an other wise normally looking bone, in the shaft of long bones and the axillary border of the scapula, due to incomplete stress fracure which heal with callus lacking of calcium There is also biconcave vertebrae from disk pressure ) lateral indentation of the acetabulum, spontaneous fracture of ribs, pubic rami, femoral neck

26. Rickets and osteomalacia Biochemistry : changes common in all types of Rickets and osteomalacia are : Decrease serum calcium and phosphate, increase serum alkaline phosphatase, decrease urinary excretion of calcium The calcium phosphate product derived by multiplying calcium and phosphate pruduct expressed in mmol per liter normally about 3, it is decreased in Rickets and osteomalacia and value below 2.4 is diagnostic Treatment : according to the cause

27. Hyperparathyroidism Paget disease (osteitis deformans ) Characterized by enlargement and thickening of bone, the internal architecture of the bone is abnormal and the bone is brittle

28. Paget disease Pathlogy It affects one or more sites, it starts at one end of the bone and extends towards the diaphysis, the characteristic cellular changes is a marked increase in osteoblastic and osteoclastic activity at an alternating pattern at both endosteal and periosteal surface leading to increased thickness of bone it’s structure is weak and easily deformed

29. Paget disease Clinical features :men and women are affected equally, usually after 50 year of age and the commonest sites are the pelvis, tibia, while the femur, skull and spine are next common It’s asymptomatic, it’s discovered because of pain, deformity and complication Pain is dull ache, constant, worse in bed, if it is severe, it is due to fracture or sacromatous comlication

30. Paget disease Deformity seen mainly in the lower limbs where long bones tend to bend, the tibia anteriorly, the femur anteriolaterally, the limb look bend, feel thick, with worm skin hence called osteitis deformans, if the skull is affected it enlarges Cranial nerves entrapment : leads to impaired vision, fascial palsy, trigeminal neuralgia, deafness, vertebral thickening lead to spinal stenosis, nerve entrapment

31. Paget disease Radiology During the resorptive phase, there are localized areas of osteolysis, later the bone becomes thick and sclerotic with coarse trabeculae with or without fine cracks on the convex sides of the shaft of long bones

33. Paget disease Biochemistry Serum calcium and phosphate are normal, serum alkaline phosphatase is increase, increased hydroxyl purine excretion

34. Paget disease Complications Pathological fracture, OA, nerve compression, spinal stenosis, high output cardiac failure, hypercalcaemia sacromatous transformation

35. Paget disease Treatment Most patients have never symptoms and require no treatment Indications for specific treatment : 1.Persistent bone pain 2.Repeated fracture 3.Neurological complications 4.High output cardiac failure 5.Hypercalcaemia Drugs that suppress bone turn over are :cacitonin and biphosphonates