S TRESS ENHANCEMENT and stress deprivation have been shown to exert paramount influences on connective tissue homeostasis. The mechanisms by which the physical environment influences cells remains obscure, but there can be little doubt about the importance of these interactions on connective tissue well-being. Factors that alter the loading conditions on synovial joints can be expected to have far-reaching effects on all tissues which compose the articular structures. In the case of joint disorders, such as osteoarthritis, which create functional disability, restriction of motion, and altered loading of the joints, the secondary effects of connective tissue deterioration will be superimposed because of the altered loading conditions. Depending on the anatomic region, loading may exceed either the high or low boundary conditions for connective tissue health. A compound downward spiral in the ability of the synovial joint tissues to sustain the necessary functional needs is the inevitable outcome. With this deterioration inevitably comes further anatomic distortion and mechanical incongruity, with increased wear debris, ligament laxity, capsular stiffness, and pain. The purpose of this report is to review the effects of altered loading on para-articular connective tissue and to propose mechanisms by which the osteoarthritic joint may be further compromised by these processes. Both stress deprivation and stress enhancement influence morphologic and biomechanical characteristics of connective tissue. Data from experimental animals and from descriptive clinical studies on humans accumulated over the past two decades is sufficient to place stress deprivation effects on a secure foundation in qualitative terms.‘.’ Quantitative data on the process remain sketchy, but enough information has been accumulated to suggest a few generalizations that may be used to introduce the subject and provide guidelines for future research priorities. Unfortunately, data on exercise effects on connective tissue other than muscle and bone remain meager. The available evidence infers that hypertrophy of tendon and possibly of ligament occurs in exercising animals.3 Recent studies on exercise effects in humans and animals clearly show that sustained exercise produces bone hypertrophy, a finding of importance with respect to the osteoporosis of an aging population. The problem of recovery from stress deprivation has been shown to have a much greater time requirement than that which induced the effect, a matter of frustration to physicians who are required to use casts in the treatment of injuries or deformities, and a matter of even greater frustration to patients forced to undergo prolonged rehabilitation programs to regain prior functional strength, mobility, and agility of the affected extremity.4 A brief resume of pertinent supporting data for these conclusions follows.