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BACKGROUND: Surgical osteonecrosis of the rat femoral head was induced by detaching the ligamentum teres and stripping the femoral neck periosteum. Bone and marrow necrosis were found from the fifth postoperative day and replaced by creeping substitution. Osteonecrosis of the femoral head results in the flattening to various degrees of roundness and osteoarthritic changes of the hip joint. Alendronate, an osteoclast inhibitor, slows down bone resorption and remodeling. The purpose of this study was to evaluate objectively the influence of alendronate treatment on the rat femoral head shape after six weeks of daily treatment, when compared with controls. MATERIALS AND METHODS: The blood circulation of right femoral head of 20 female Sprague-Dawley rats was interrupted. Twelve were treated by alendronate injections of 200 microg/kg/day and eight controls were treated with saline, both for a total of 42 days. Both femoral head specimens were obtained for computed-assisted morphometry. For each rat, the right operated head was compared with the left, and the alendronate treated group was compared with the control group. RESULTS: No differences were found in shape factor and femoral head height/length ratios in the alendronate treated femoral heads. Among the nontreated control group, shape-factor differences were found between the operated and the nonoperated femoral heads. CONCLUSION: Alendronate treatment prevented the distortion and destruction of the femoral head. Osteoclast inhibition might prolong the bone creeping substitution process and could enable secondary bone maturity and mineralization that increases bone strength. Alendronate preserved the femoral head architecture, which might reduce morbidity and disability due to femoral head collapse.

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INTRODUCTION: In animals with a disrupted blood supply and drainage of the femoral head, the dead epiphyseal bone undergoes osteoclastic osteolysis and is replaced by newly synthesized, immature, and weak bone, which cannot withstand the daily loads and, therefore, the articular surface caves in. METHODS: Female Sprague-Dawley rats with interrupted blood circulation of the femoral head were treated with alendronate and compared to controls. RESULTS: There was no distortion of the femoral heads in the alendronate-treated animals. INTERPRETATION: Alendronate medication interferes with osteoclastic activities, slowing down bone turnover. These observations verify our hypothesis that osteoclastic activity is detrimental to the conservation of a hemispherical femoral head because of the rapidly occurring replacement of the dead by living tissues. Hence, halting the activities of the osteoclasts by alendronate stops the hasty new bone formation which is responsible for early femoral capital disfigurement.

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Current pain treatment guidelines advise against providing analgesics for postoperative pain using intramuscular injections, as this generally provides poor pain relief. However, this route remains the most prevalent treatment method. Intravenous or epidural patient-controlled-analgesia methods reduce pain effectively but are expensive, labor intensive, and available to only a limited number of patients. We propose administering the analgesics using oral analgesics and have developed a simple protocol for treating postoperative pain by use of oral morphine. After a variety of orthopedic surgeries, patients were given "around-the-clock," oral, immediate-release morphine. Efficacy of the treatment (pain scores and adverse effects) was assessed 24 +/- 2 hours after surgery. Data were collected prospectively from 95 patients, who received an average of 61 +/- 30 (SD) mg morphine. Average pain scores were 2.4/10 (+/- 1.4) at rest and 4.0/10 (+/- 1.4) during movement in bed. Nausea and vomiting, the most common adverse effects, were reported by 22 (23 percent) patients. Naloxone was not administered to any of the patients. Oral morphine given in the early postoperative time to patients after a variety of orthopedic surgeries was effective and safe.

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Osteonecrosis of the femoral head was produced in rats by cutting the ligamentum teres and incising the cervical periosteum. As of the second postoperative week, fibrous tissue pervaded the necrotic epiphyses, macrophages and osteoclasts removed the debris, osteoblasts deposited lamellar-fibred and woven-fibred intramembranous bone, and remodeling began. In 16% of the rats killed during the 2nd postoperative week, the epiphyses contained big fragments of necrotic bone enclosed by densely packed, capillary-sized vessels. Ingrowth of this hypervascularized, pyogenic granuloma-like tissue is presumably due to the presence of excessive growth factors, reflecting an exaggerated pathophysiological reaction within the framework of organization of the necrotic epiphyses.

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The blood supply of one femoral head of 6-month-old rats was severed by incising the periosteum of the neck and cutting the ligamentum teres. The rats were killed on the 30th postoperative day and the femoral bones were obtained for semiquantification of the reparative processes in the necrotic heads. Fourteen rats were treated with enoxaparin and 14 untreated animals served as controls. Statistically, the amounts of necrotic bone in the epiphysis were less, the extent of remodeling of the femoral heads was milder, and the articular cartilage degeneration was slighter in the enoxaparin-treated than untreated rats. There was no significant difference in the quantities of newly formed bone in femoral heads of treated and untreated rats. These findings are in agreement with the known effects of unfractionated and low-molecular-weight heparins which enhance osteoclastic bone resorption and angiogenesis and decrease osteoblastic bone formation. The former activities, operative in minimizing the structural distortion of the femoral head, oppose the crucial event in the pathogenesis of post-osteonecrotic osteoarthritis.

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