Metabolic Bone Diseases

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abnormalities of metabolism and harmonal immbalance causes many bone  More

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Metabolic Bone Diseases : Metabolic Bone Diseases Vinod Naneria Consultant orthopaedic surgeon Choithram Hospital & Research Centre Indore , India


Skeleton: Skeleton 1 – 2 kg calcium, 1 kg phosphates


Skeleton: Skeleton


Metabolic bone disease: Metabolic bone disease


Importance: Importance Past : Deficiency disease Present : Disabling disease Future : Space age disease


Key-words: Key-words


Key-players: Key-players


Slide8: Kidney G.I.Tract Bone Target Organs


BMU‘S Bone Metabolic Unit: BMU‘S Bone Metabolic Unit Battle field


BMU- steps: BMU- steps Activation: Osteoclasts Resorption: Bone matrix Reversal: pre-osteoblasts Formation: osteoid formation Mineralization: Quiescence Blue – the lining resting cell layer, Red – newly deposited osteoid, Green- mineralized bone, Dark green – old mature bone.


Remodelling: Remodelling


BMU: One BMU lasts about 11 seconds and represents about 6 months of real time. A micro-crack starts the process, the osteocytes sense damage and send signals into the marrow space. Preosteoclasts turn into multi-nucleated osteoclasts and start resorption, meanwhile preosteoblasts turn into osteoblasts and start forming osteoid (orange) which then mineralizes (green) BMU


Slide13: The same thing is shown in the linear un animated slide.


Calcium: Calcium


Calcium metabolism: Calcium metabolism


Osteomalacia: Osteomalacia Reduced mineralization of bone matrix due to calcium deficiency. Calcium deficiency Osteomalacia results when the osteoid does not have mineral.


Menopausal Osteoporosis: Menopausal Osteoporosis Reduced bone mineral mass Normal mineral to matrix ratio. Estrogen deficiency The resorption cavities go a little deeper and resorption lasts a little longer, and the bone formation increases but doesn't quite match the higher resorption rate.


Paget’s Disease: Paget’s Disease Increase rates of bone turn-over with development of disorganized woven bone.


Slide21: Fast bone turn over


Tetracyline labeling: This animation shows a slice through a piece of bone about a millimeter long. It lasts 13 seconds and shows 30 months of real time. -10 BMU's in this view, each at a different stage. The bone formation rate in this movie is a bit above average, but within the normal range. -The shades of green represent the mineralization density: newly formed bone is not very dense (pale green) and older bone is denser (dark green). Tetracyline labeling


Steroid induced bone disease: Steroid induced bone disease


Slide24: Steroid Induced osteoporosis Corticosteroids increase the bone resorption rate and depth, similar to menopause. The steroids block action of osteoblasts, so the bone formation does not increase.


Osteopetrosis: Osteopetrosis Failure of osteoclastic and chondroclastic resorption. Failure of remodelling Genetic disorder


Fluorosis: Fluorosis Abnormal matrix mineralization. Crystals of fluoroapatite replace calcium phosphate crystals of hydroxyapatite. Endemic in India Iatrogenic fluorosis


PTH: PTH Change of shape of osteoblast  secretion of neutral collagenase by osteoblast cells. Collagenase digests the protective layer of matrix  exposing the bone surface for osteoclastic resorption. PTH receptors only on Osteoblasts


PTH -> hypocalcemia: PTH -> hypocalcemia Calcium homeostasis


Slide29: Hyper calcemia Hypo phoshphatemia Hyper calciuria High alk.phosphatase level PTH immune assay Ultrasosnography of neck. Disease of Stone & Bone


Vitamin D: Vitamin D The active hormone is 1,25(OH)2D3 responsible for the absorption of calcium from gut. Probably it acts indirectly by increasing serum calcium level thus reducing the effect of PTH on bone. Synthesized in Skin


Deficiency of Vit. D: Deficiency of Vit. D Disease of Affluent class


Vitamin D Resistant Rickets: Vitamin D Resistant Rickets Defective final conversion of Vit. D in to active form.


Slide33: Effect at growth end plate


Slide34: Cupping of the epiphyses. Bones incapable of withstanding mechanical stresses and lead to bowing deformities. Eventual length of the long bones is diminished. ( short stature) Cont…..


Slide35: Genu valgus Wrist cupping Tri radiate pelvis Looser’s zones Wrist widening Wide metaphysis


Renal bone disease: Renal bone disease


Renal Osteodystrophy: Renal Osteodystrophy


Calcitonin: Calcitonin Anti - PTH


Calcitonin: Calcitonin


Estrogen: Estrogen Reloxiphen selectively on bone & not on breast


Estrogen: Estrogen positive calcium balance.


RELOXIPHEN: RELOXIPHEN This movie shows the effect of Raloxifene in women with osteoporosis.


Bisphosphonates : Bisphosphonates Anti osteoclast  Anti resorptive


Slide44: After the estrogen deficiency in the first 6 months show high turnover; then the little blue diamonds representing a bisphosphonate start to attach to the bone; resorption stops suddenly and formation stops after a few months. The bone continues to become more mineralized (darker), and only a few BMU's are still active.


Bone Markers: Bone Markers


Bone Markers: Bone Markers


Space age bone disease: Space age bone disease


Space age bone disease: Space age bone disease Weightlessness in “Zero G”. Minimal mechanical stress on bone.  numbers of osteoblasts. Osteoclast number – normal. NASA projects hPTH(1-31) as potent osteoblastic agent under extensive study. Effect of exercises in “Zero G”.


Slide50: Bon Voyage


Slide51: DISCLAIMER • Information contained and transmitted by this presentation is based on personal experience and collection of cases at Choithram Hospital & Research centre, Indore, India, during last 25 years. • It is intended for use only by the students of orthopaedic surgery. Many GIF files are taken from Internet. • Views and opinion expressed in this presentation are personal opinion. • Depending upon the x-rays and clinical presentations viewers can make their own opinion. • For any confusion please contact the sole author for clarification. Every body is allowed to copy or download and use the material best suited to him. I am not responsible for any controversies arise out of this presentation. • For any correction or suggestion please contact naneria@yahoo.com


Slide52: THANK YOU