What are rickets and osteomalacia?







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RICKETS AND   OSTEOMALACIA


Def.: reduction in bone mineralization
Rickets and  osteomalacia  are  conditions  characterized by pathological defects in bone matrix mineralization. Rickets refers specifically to osteomalacia, where the defect occurs in growing bone.
The  aetiological  factors  are  diverse,  but the  end  result  is  an  increased  quantity  of unmineralized bone matrix  (osteoid).



Etiology  of  osteomalacia
The  conditions  may  arise  in  three  distinct situations:
™ •  Deficiency or abnormal metabolism  of vitamin D
™ •  Phosphate  depletion
™ •  Chronic metabolic  acidosis.


 Lack of vitamin D is often  due to a combination of poor exposure to sunlight and dietary  deficiency. The elderly  are particularly at risk.
Phosphate  depletion  is  a  less  common  cause  of  rickets than  deficiency  or  altered  metabolism  of  vitamin  D
 Chronic metabolic acidosis, usually resulting  from renal tubular disorders, may lead  to  rickets or  osteomalacia. The  bone  lesions  usually heal  satisfactorily following treatment  to correct  the acidosis.
Clinical  features:
™ In  children,  failure  of  bone  mineralization  gives  rise  to classic  bone  deformities,  which  include  widening  of  the metaphyses,  prominence  of  costochondral  junctions  and  varus or valgus abnormalities of  the  knee  joints.  The  bones  are  painful  and growth is reduced.
™  In adults, bone pain and tenderness  are the  most  prominent  features.  A  characteristic  proximal myopathy may develop, and is more common  in cases  due to vitamin D  deficiency.

Investigation:
™ Biochemical
™ In osteomalacia  due to deficiency or abnormal  metabolism of  vitamin  D,  investigations  typically demonstrate  a  low normal   plasma   calcium, a low plasma phosphate.
Vitamin  D  deficiency  may  be confirmed  by  measurement  of 25-hydroxyvitamin D  in plasma.

XRAY FINDINGS:

RICKETS
                                
  •                    Thickening and widening of physes,                               
  •                    Cupping of metaphysis, 
  •                     Wide metaphysis,          
  •                    Bowing of diaphysis,




XRAY FINDINGS:

OSTEOMALACIA
                                  stress  Fracture with healing lacking calcium, on compression side of long bones. 
                                    Codfish vertebrae













Management:

™ Dietary  vitamin  D  deficiency  is  treated  by  oral  replacement  of  vitamins  D2  or  D3  in  physiological  quantities(500-1000  units/day). This  can  conveniently  be  given  as combined  calcium  with  vitamin  D  tablets. 

™ Osteomalacia   associated   with anticonvulsant therapy requires higher doses of vitamin D  (3000-6000 units/day)unless a change in An anticonvulsant is clinically feasible.

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