metabolic bone diseases

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abnormalities of metabolism and harmonal immbalance causes many bone diseases like osteomalasia,osteoporosis, renal bone disease, flurosis, rickets, & space age disease.

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By: tamam (26 month(s) ago)

thanks alot it's great work

 

By: dr_nano (66 month(s) ago)

it's good work and i hope to have more better

Presentation Transcript

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