Antagonistic compensation as a function of reduced weight bearing.
The principle of antagonistic compensation was presented by RIESENFELD in 1966 to explain the relative shortening and broadening of hypofunctional bones. Few studies have concerned themselves with this phenomenon, even though the causative agent(s) have not been delineated. In this study, RIESENFELD induced the hypofunction by complete unilateral bilateral forelimb amputation. The resulting hypofunctional condition may be attributed to the lack of muscle function or to the lack of weight bearing or both in combination. In the present study weight bearing was eliminated in such a manner as to preserve muscle functioning. This was accomplished by two techniques: (1) unilateral forearm amputation and (2) unilateral humeral resection. Statistically significant differences in interindividual scapular length and breadth as well as humeral and ulnar lengths are reported. In all cases, the bones of the operated side were shorter than those of the unoperated side and the scapular breadth of the unoperated side was relatively greater. This confirms the hypothesis that weight bearing is, at least, partially responsible for the morphological changes induced by hypofunction and described by the principle of antagonistic compensation. However, as the reduction in length was of a lesser magnitude than that reported by RIESENFELD, the input of muscle function cannot be ignored. Rather, as both muscle functioning and weight bearing induce compressive force on long bones (including the scapula), both may serve to initiate the observed morphological changes through the vehicle of reduced compression.
D000671:Amputation, Surgical; D000818:Animals; D001835:Body Weight; D001842:Bone and Bones / Q000502:physiology*; D005552:Forelimb; D006811:Humerus / Q000033:anatomy & histology / Q000502:physiology; D009119:Muscle Contraction; D011187:Posture; D051381:Rats; D012540:Scapula / Q000033:anatomy & histology / Q000502:physiology; D014457:Ulna / Q000033:anatomy & histology / Q000502:physiology