Individuals affected with mild to moderate rheumatoid arthritis are disabled as compared with the general population. There is a severe negative impact on mobility and functional capacity when the disease process begins to affect their feet.
Background-Subacromial corticosteroid injections are commonly used in the nonoperative management of rotator cuff disease. The effects of corticosteroid injection on injured rotator cuff tendons have not been studied. Our aims were to characterize the acute response of rotator cuff tendons to injury through the analysis of the type-III to type-I collagen expression ratio, a tendon injury marker, and to examine the effects of corticosteroid on this response.
Background-Chronic alcohol consumption reduces bone mass and strength, increasing fracture risk for alcohol abusers. Mechanisms underlying this vulnerability involve modulation of bone remodeling. Direct effects of alcohol on bone formation have been documented; those on bone resorption are less well studied. Skeletal effects of exposure to high blood alcohol concentrations (BAC's) attained during binge drinking have not been studied. We examined the effects of repeated binge-like alcohol treatment on bone resorption, bone mineral density and vertebral compressive strength in adult male rats treated with the aminobisphosphonate, risedronate.
Bone loss following OVX can be significantly increased by concurrent binge alcohol treatment. The effects of alcohol and OVX are compensated by concurrent intermittent treatment with PTH. These results suggest that postmenopausal women who abuse alcohol may place their skeleton at additional risk for osteoporotic fracture.
Decreased bone mass and bone strength can result from excess alcohol consumption in humans and alcohol treatment in the rat. Although the specific mechanism is unknown, the damaging effects of alcohol abuse modulate the bone remodeling cycle and increase bone turnover. Chronic alcohol consumption models have shown an inhibition of bone formation. We previously reported that binge alcohol treatment increases bone resorption and that alcohol-induced damage can be prevented by treatments with intermittent parathyroid hormone and bisphosphonates. In this study we hypothesized that an effective dose of vitamin D (cholecalciferol) or a single dose of ibandronate would prevent bone loss caused by binge alcohol treatment in male rats. Forty-eight adult (450 gram) male Sprague-Dawley rats were randomly assigned to 6 treatment groups (n=8): a) saline, i.p.3 days/ week (C); b) binge alcohol, 3g/kg i.p., 3 days/week (A); c) vitamin D, 5,000 IU/kg daily s.c., (D); d) binge alcohol and vitamin D (AD); e) e) ibandronate, (120 ug, given as a single i.p. injection (I); f) alcohol and ibandronate (AI). After 4 weeks of treatment proximal tibia and L3 and L4 vertebrae were analyzed for bone mineral density (BMD) by quantitative computerized tomography and compressive strength-to-failure using an Instron materials testing machine. Type-I collagen crosslinked c-telopeptide, calcium, and 25-OH vitamin D levels were measured in serum collected at the time of sacrifice. Binge alcohol significantly decreased cancellous BMD by 58% in tibia and 23% in lumbar spine (p < 0.05). Binge alcohol treatment decreased L3 and L4 compressive strength-tofailure by 21% (p <.05). Treatment with vitamin D at 5,000 IU/kg/day prevented alcohol-induced bone loss, significantly increasing both tibial and vertebral cancellous BMD values (161% increase in tibia and 40% increase in vertebra, respectively, p < 0.05) compared to alcohol alone groups. Pretreatment with the single dose of 120 ug ibandronate prevented alcohol-induced bone loss, increasing cancellous BMD by 186% in tibiae and by 46% in vertebrae compared to the alcohol alone group (p < 0.05). In summary, binge alcohol-induced tibial and vertebral bone loss can be prevented using an effective dose of vitamin D or a single dose of ibandronate even during high blood alcohol concentrations that have been shown to impair osteoblast functions and increase bone resorption.
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