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CALCIUM METABOLISM.pptx
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- 2. CALCIUM METABOLISM R .Priya Darshini 1st year MDS DEPT OF PROSTHODONTICS
- 3. # CONTENTS • Introduction • Calcium •Dietary requirements • Sources • Functions • Homeostasis of calcium • Calcitriol • Parathyroid hormone • Calcitonin • Calcium absorption • Disorders due to Changes in Ca levels • Investigations of bone and Ca disorders • Prosthodontic considerations • Conclusion
- 4. # Introduction • Mineral (inorganic)elements constitute only small proportion of body weight. • Minerals - Principal elements (60-80%) - Trace elements • 7 principal elements are Calcium, Phosphorus, Magnesium, Sodium, Potassium, Chloride & Sulfur
- 5. # Calcium • Most abundantmineral in the body. • Constitutes about 2% of body weight. • Total content of Ca in adult is 1-1.5kg. • 99% - bones & teeth. • 1% - body fluids.
- 6. # Plasma calcium • Mostof the blood Ca is in plasma. • Normal conc – 9-11 mg/dl. • 5mg/dl – ionised form – most active. • 1mg/dl – in association with citrate & P. • 4-5mg/dl – bound to protien. • Ionised & citrate bound – diffusible • Protien bound – non-diffusible.
- 7. # Dietary requirements • Adultmen & women – 800mg/day • Pregnant, lactating &post menopausal women – 1.5 g/day. • Children (1-18yrs) – 0.8-1.2 g/day • Infants (<1yr) – 300-500 mg/day
- 8. # Sources • From milkand milk products. • And also beans, leafy vegetables, fish, cabbage, egg yolk.
- 9. # Biochemical functions • Developmentof bones and teeth • Muscle contraction • Blood coagulation • Nerve transmission • Membrane integrity and permeability • Activation of enzymes(lipase, ATPase, succinate dehydrogenase).
- 10. # • Calcium asintracellular messenger. Second messanger in liver glycogenolysis & third messanger for some hormones like ADH which acts through cAMP & then Ca. • Release of hormones (insulin, PTH, calcitonin)from endocrine glands. • Acts on myocardium and prolongs systole.
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- 12. # Homeostasis Of Calcium •Calcium is almost exclusively present in blood plasma or serum. • The hormones Calcitriol, Parathyroid hormone, Calcitonin are major factors that regulate plasma calcium (homeostasis of Ca) within normal range.
- 13. # Calcitriol • Active formof vit-D or 1 ,25- dihydroxycholecalciferol • Skin-photoactivation of 7-dehydrocholesterol to cholecalciferol (D3) Liver-25- hydroxycholecalciferol – Kidneys – by 1 – hydroxylase to 1,25- dihydroxycholecalciferol (conversion is mediated by PTH)
- 14. # FUNCTIONS to increaseplasma calcium increases absorption of Ca in intestines stimulates formation of calcium-binding protein in epithelial cells. promotes bone calcification and deposition by stimulating ca uptake by osteoblasts. inhibits secretion of PTH.
- 15. # Role of Calcitriol •Stimulates GI absorption of both calcium and phosphate • Stimulates renal reabsorption of both calcium and phosphate • Stimulates bone resorption Net effect of calcitriol - ↑ serum calcium ↑ serum phosphate
- 16. # Parathyroid Hormone • Parathyroidglands • Single chain polypeptide -84 AA • Synthesised as preproPTH – degraded to proPTH – active PTH • Formation and secretion of PTH is promoted by low ca conc. • Stimulus for secretion of PTH – low plasma calcium
- 17. # • PTH actson 3 independent tissues • Bone – demineralisation by osteoclasts. this is by PTH stimulated activity of enzymes pyrophosphate & collagenase which cause bone resorption. This leads to blood Ca levels. • Kidney- PTH Ca reabsorption by kidney tubules. PTH promotes production of calcitriol by stimulating 25-hydroxycholecalciferol by 1 hydroxylase. • Intestine – PTH increases intestinal absorption of Ca by promoting synthesis of calcitriol.
- 18. # FUNCTIONS to increaseplasma calcium activation of osteoclasts – stimulates absorption of Ca, P from bones decreases excretion of Ca by kidneys increases excretion of P by kidneys stimulates conversion of vitamin D to calcitriol (vitamin D hormon) in kidneys
- 19. # Role of PTH •Stimulates renal reabsorption of calcium • Inhibits renal reabsorption of phosphate • Stimulates bone resorption • Inhibits bone formation and mineralization • Stimulates synthesis of calcitriol Net effect of PTH - ↑ serum calcium ↓ serum phosphate
- 20. # Calcitonin • Parafollicular cellsof thyroid gland (C- cells). • peptide containing 32 amino acids. • stimulus for secretion – high plasma calcium. • Promotes calcification by increasing activity of osteoblasts.
- 21. # FUNCTIONS to decreaseplasma calcium and phosphates inhibits osteolysis – decreases absorption of Ca, P from bones stimulates incorporation of Ca, P to bones decreases absorption of Ca, P in kidneys decreases the effect of PTH on bones – PTH antagonist
- 22. # Calcium Absorption Absorption ofCa occurs in duodenum by energy dependent active process. Factors promoting Ca absorption 1. Vit-D induces synthesis of Ca binding protein in intestinal epithelial cells & promotes Ca absorption. 2. PTH – by synthesis of calcitriol.
- 23. # 3. Acidity (lowpH) 4. Lactose promotes Ca uptake by intestinal cells. 5. AA Lysine & Arginine. Factors inhibiting ca absorption 1. Phytates & oxalates by forming insoluble salts. 2. High content of dietary P results in formation of insoluble Ca P &prevents Ca uptake.
- 24. # • Alkaline (highpH) • High content of dietary fiber interferes with Ca absorption. • Free fatty acids react with Ca to form insoluble Ca soaps.
- 25. # CHANGES IN CA2+ PLASMALEVEL Hypocalcemia • Muscle tetany : Carpopedal spasm-trousseaus sign Chvostek’s sign • Dilatation of heart • Increased cell membrane permeability • Impaired blood clotting • Replacement therapy includes vit-D & calcium supplements.
- 26. # Dental considerations • Dentaltreatment complicated by- tetany, seizures, psychiatric problems & learning disability. • There may be facial parasthesia &facial twitching caused by tetany (chvostek’s sign). • Local anesthesia satiafactory • Consious sedation after replacement therapy
- 27. # Hypercalcemia • Serum calciumlevel elevated • Associated with hyperparathyroidism in which there is serum phosphate and also alkaline phosphatase activity. • Diagnosis can be done by determination of ionised serum calcium level (elevated to 6-9mg/dl) .
- 28. # Conditions associated: • Depressionof nervous system, reflex activity. • Increased heart contractility. • Lack of appetite & constipation. • Abdominal pain, peptic ulcers • Formation of calcium phosphate crystals(urinary calculi). • Bone diseases like osteitis fibrosa cystica.
- 29. # Dental considerations • Dentaltreatment complicated by renal diesease, peptic ulcer & bone frgility. • LA main means of pain control. • Conscious sedation with nitrous oxide & O2. • General anesthesia complicated b’cos of cardiovascular complications and sensitivity to muscle relaxants.
- 30. # Osteoporosis • Disease –low bone mass and micro- architectural deterioration of bone tissue, leading to enhanced bone fragility and an increase in fracture risk. • Most common in advanced age and also women are more prone b’cos of loss of estrogen production which accelarates bone loss.
- 31. # Causes • Etiology unknown •May be due to the ability to produce calcitriol from vitamin-D is decreased with age. • Immobilised or sedentary individuals tend to decrease bone mass. • Post menopausal, deficiency of oestrogen has implicated in development of osteoporosis.
- 32. # Clinical features • Mildtaumatic or non-traumatic injuries cause fractures • Chief complications- fracture of neck of femur, distal radius or humerus, or vertebral bodies causing gradual collapse of spine. • Low back pain.
- 33. # Risk factors -Increasing age -Earlymenopause -Female sex -Immobility -Smoking -Excess alcohol -Nutrition(low ca diet, high protein intake for long time) Diseases Endocrine -Cushing syndrome -Hyperparathyroidism -Hypogonodism -Acromegaly -typeI diabetes mellitus Joint -Rheumatiod arthritis Other -Chronic liver failure -Chronic renal failure -Mastocytosis -Anorexia nervosa -Inflammatory bowel disease -Coeliac disease Drug therapy -Corticosteroids -Heparin -Ciclosporin -Cytotoxics
- 34. # Investigations • If fractureis suspected - plain radiographs. - bone scintigraphy(pelvis or vertebrae fracture) • Bone density – DXA(dual energy x-ray absorptiometry)
- 35. # Dental considerations • Thereseems to be correlation between osteoporosis and excessive alveolar bone loss in elderly edentulous patients. • Jaw osteoporosis is particularly a problem in women. • Systematic treatment may improve jaw bone density. • There may be risk during general anesthesia, if there is vertebral collapse and chest deformities
- 36. # Treatment • Diet with1000mg of Ca daily and 400-800 IU of vit-D. • 30min of wt bearing exercises 3 times a week. • Smoking cessation • Hormone replacement therapy. • Combination therapy of calcium with vitamin-D.
- 37. # Rickets & Osteomalacia •Inadequate mineralisation of bone matrix. • Usually caused by a defect in vit-D availability or metabolism. • In children calcification delayed & vascularisation impaired. • In adults osteiod width & delayed mineralisation assessed by double- tetracycline labelling.
- 38. # Etiology Rickets • In urbanareas that were deprived of sunlight. • Failure of vit-D synthesis in skin.(lack of exposure to sun light). Osteomalacia • Postmenopausal women with history of low dietary calcium intake and little exposure to ultra violet rays.
- 39. # CAUSES Renal disease -Chronic renaldiesease -Renal osteodystrophy -Bone disease due to dialysis -Tubular disorders Miscellaneous -Multiple myeloma -X-linked hypophosphataemia -Mesenchymal tumours Vitamin D deficiency -Inadequate sunlight exposure -Low dietary intake -Malabsorption coeliac disease intestinal resection chronic cholestasis
- 40. # Clinical features Osteomalacia- • Remodellingof bone in absence of adequate calcium – results in softening and distortion of skeleton and an increased tendency to fracture • Vague symptoms of bone or muscle pain and tenderness. • Fractures rare and asymptomatic. • Proximal myopathy- waddling gait. • Occasionally, tetany or other hypocalcemic features.
- 41. # Clinical features Rickets • Atbirth- craniotabes (thin deformed skull) • First few years of life- widened epiphysis at wrists and beading at costochondral junctions, producing ‘rickety rosary’ or harrison’s sulcus (groove in mid rib). • In older children lower limb deformities.
- 42. # Investigations • Serum alkalinephosphatase – increased osteoblastic activity • Plasma calcium – low or normal raised PTH. • Serum 25-hydroxyvitamin-D3 low. • X-rays • Iliac crest biopsy.
- 43. # Dental considerations • Dentaldefects seen in unusally severe cases, eruption may be retarded. • Jaws shows abnormal radiolucency. • Vit-D deficient rickets, skull suture are wide and frontal bossing present which are known mostly by dental complaints. • Teeth – large pulp chambers & abnormal dentin calcification –liable to pulpitis and dental abscesses.
- 44. # Treatment • Increase indietary vit-D intake and sunlight exposure. • Also multiple formulations of vit-D and its metabolites are available. • Nutritional deficiency-replacement doses needed - 400-800 IU daily. • Gasterectomy malabsorption, liver disease or hypoparathyroidism – upto 40,000-100,000 IU
- 45. # Investigations of boneand calcium disorders • Total plasma calcium (9-11mg/dl) • PTH & 25-hydroxyvit-D – useful where hypervitaminosis D or interaction with antiepileptic drugs is suspected in hypocalceamia or in hypercalceamia. • Urinary calcium (normal-2.5-7.5mmol/24hrs) – increased when renal tubular resorption of Ca is decreased or in hypercalceamia.
- 46. # • Markers ofbone formation – Alkaline phosphatase – Serum osteocalcin – Type I collagen propeptides • Markers of bone resorption -Pyridinoline cross links of collagen -N-terminal and C-terminal crosslinked telopeptides • Diagnostic imaging -Plain radiographs -Radionuclide scans -Magnetic resonance imaging
- 47. # • Bone densitymeasurements -Conventional radiographs -Dual energy x-ray absorptiometry -Quantitative Ctscan -Quantitative ultrasound • Bone biopsy
- 48. # Conclusion • Calcium playsa key role in many physiologic processes, including contraction of muscles, blood clotting, transmission of nerve impulse etc. • 0.1 % of total body calcium is in extracellular fluid, 1% in the cells and rest is stored in bones. • Many hormones regulate Calcium homeostasis and any abnormalities in this process could lead to hyper or hypo calcemic states leading to altered functions
- 49. # Conclusion • Residual ridgeresorption is a primary concern in edentulous elderly patients and the effects of hormones and other physical factors should be remembered when considering prosthodontic treatment.
- 50. # References • Hirai T,Ishijima T, Hashkawa Y, Yajima T: Osteoporosis and reduction of residual ridge in edentulous patients. J Prosthet Dent. 1993 Jan;69(1):49-56. • Zmysłowska, Ledzion, Jędrzejewski: Factors affecting mandibular residual ridge resorption in edentulous patients: a preliminary report. Folia Morphol. Vol. 66, No. 3, pp. 346–352 • Deshpande s, sarin p: Evaluation of the relationship between Systemic osteoporosis, dietary ca intake and the reduction of Residual ridges in an edentulous patient:an in vivo pilot study. Journal of Clinical and Diagnostic Research. 2009 Aug;7(3):1706-1708. • Wowern N, Lollerup G: Symptomatic osteoporosis: a risk factor for residual ridge reduction of the jaws. J Prosthet Dent. 1992 May;67(5):656-60.
- 51. # References • Shipley, BlackCM, Comptson J and O’ Gradaigh: Rheumatology and bone disease. In: Praveen Kumar, Micheal Clark (eds) Clinical Medicine, 5th edition, Saunders, 2002. • Scully C, Cawson RA: Medical Problems in dentistry, 5th edition, Elsevier, 2005. • Neville, Damm, Allen, Bouquot: Oral and maxillofacial pathology, 2nd Edition, Elsevier, 2004. • Shafer, Hine, Levy: A text book of Oral Pathology, 4th edition, A prism India edition, 1993. • Sembulingam K, Sembulingam P: Essentials of medical physiology, 3rd edition, Jaypee, 2004. • Chaudhary: Consise medical physiology. • Satyanarayana U: Biochemistry, 2nd edition, Books and allied pvt ltd, 2002.