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In the present study we evaluated the possible contribution of different factors to the occurrence of hip fractures in Israel. We assessed medical history, physical activity, body mass index, smoking status, bone turnover markers and calcium regulating hormones levels of 142 consecutive elderly hip fracture patients (HFP), and compared them to 96 community dwelling elderly people without a history of hip fracture. Age and female gender were the strongest predictors of hip fracture, p

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 µg/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.

Shallow or deep bowl-shaped depressions often develop after drilling an intraosseous conduit in the necrotic, avascular femoral head of rats. The etiopathogenesis of tissue loss at the articulation surface after a drilling procedure was elaborated in the authors’ previous reports. To scrutinize a large collection of femoral heads of rats in order to search for similar changes in cases in which no drilling procedure was carried out. This retrospective study comprised the specimens of 386 rats with vessels-deprived osteonecrosis of the femoral heads, none of the animals having undergone a drilling procedure. Shallow or deep bowl-shaped depressions were encountered at an incidence as low as 2.8% of the femoral heads of the above mentioned 386 rats. It is not feasible to distinguish histologically the “spontaneously” arising from and drilling-related depressions. No assured explanation can be offered for the evolving depressions of the surface of femoral heads of rats, which have not undergone a drilling procedure. It is hypothesized that the synovial fluid forces its way via slits in the articulation surface and bores cavities in the substance of femoral heads, which display a postosteonecrotic osteoarthritis-like disorder. The rising pressure in the arthritic joints results, firstly, in an enlargement of these cavities and, secondly, loss of fibro-cartilaginous tissue such that the cavities come to communicate with the articular space.

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.

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.

Following severance of the blood supply to the left femoral head of 6-month-old rats by incising the periosteum of the neck and cutting the ligamentum teres, a 21-gauge needle, inserted into the foveola, was pushed forward in the direction of the neck up to the opposite cortical bone. Femora were obtained for histological examination on postoperative days 32 and 42, from 22 and 12 rats, respectively. The right femoral heads were normal. In addition to the usual reparative and regressive changes characteristic of the second month after induction of osteonecrosis, the left femoral heads showed, compared to the femoral heads of otherwise untreated rats, lavish ingrowth of blood vessels and proliferation of mesenchymal cells. Moreover, 16 of the 34 femoral heads disclosed additional distinctive lesions, namely, partial fibrous replacement, surface depression, intraosseous tunneling, and subtotal destruction of the epiphysis. The results of this experiment, an attempt at modeling core decompresssion in man, parallel the frequently reported unsatisfactory outcome of the procedure in patients with osteonecrosis of the femoral head. They as well indicate that any therapeutic effects of producing an epiphyseal-metaphyseal conduit for the ingrowth of vessels and cells may only be achieved at the cost of a reduction in the mechanical load-bearing capacity of the femoral head.

A vascular necrosis (AVN) of the head of the femur is a potentially crippling disease which mainly affects young adults. Although treatment by exposure to hyperbaric oxygen (HBO) is reported as being beneficial, there has been no study of its use in treated compared with untreated patients. We selected 12 patients who suffered from Steinberg stage-I AVN of the head of the femur (four bilateral) whose lesions were 4 mm or more thick and/or 12.5 mm or more long on MRI. Daily HBO therapy was given for 100 days to each patient. All smaller stage-I lesions and more advanced stages of AVN were excluded. These size criteria were chosen in order to compare outcomes with an identical size of lesion in an untreated group described earlier. Overall, 81% of patients who received HBO therapy showed a return to normal on MRI as compared with 17% in the untreated group. We therefore conclude that hyperbaric oxygen is effective in the treatment of stage-I AVN of the head of the femur.

In view of the lifelong persistence of the physis, the femoral head of rats may serve to model Perthes disease and slipped capital femoral epiphysis. To produce osteonecrosis, the blood supply of one femoral head of 133, 6-month-old animals was severed by circumferentially incising the periosteum of the neck and cutting the ligamentum teres. The rats were killed 7 days to 90 days postoperatively. Associated with resorption of the necrotic bone and marrow, remodeling of the epiphysis was characterized by an ingrowth of vascularized fibrous tissue, formation of new bone and some cartilage, architectural deformation and flattening of the head. In 22 of 83 rats killed 30 days or more postoperatively, gaps in the continuity of the physeal cartilage were occupied by osseous bridges, connecting newly formed epiphyseal bony trabeculae with either the preexisting or newly formed metaphyseal osseous trabeculae. This healing mode may follow ischemic death of physeal chondrocytes or be owing to another mechanism, e.g., release of mediatory substances of inflammation. These findings raise the possibility that fixation of the healing epiphysis of a child's previously necrotic femoral head to the metaphysis occurs by transphyseal osseous growth in cases in which the physis is involved in the necrotic process.

This report describes an animal model of chondrolysis, i.e., acute necrosis of the articular cartilage. The blood circulation of rats' femoral heads was disrupted by incising the periosteum at the base of the femoral neck and cutting the ligamentum teres. The joint cartilage was necrotic in 18 of the 30 and 21 of the 39 osteonecrotic femoral heads of rats killed on the 30th and 42nd postoperative day, respectively. Chondrolysis was limited to the superficial cartilage layer in mild cases. It involved the entire cartilage in the more severely affected instances. Chondroclasts abutted on the necrotic cartilage where fibrous tissue replaced the subchondral bone plate. At the most advanced stage, the cartilage was segmentally absent, polished bone constituting the articular aspect. Chondrolysis, rarely detected in otherwise healthy children, commonly occurs in patients with a slipped capital femoral epiphysis, a disorder commonly associated with osteonecrosis of the femoral head. The herein presented model may serve the study of necrosis of the cartilaginous and osseous compartments of the femoral head in a small laboratory animal.

The blood supply of rats' femoral heads was severed by cutting the ligamentum teres and stripping the periostium. Histologically, necrosis of the marrow was apparent on the 2nd postoperative day, necrosis of the bone on the 5th postoperative day and fibrous ingrowth on the 7th postoperative day. During the following 5 weeks, progressive resorption of the intertrabecular necrotic debris and necrotic bony trabeculae and subchondral bone plate and, concurrently, appositional and intramembranous new bone formation resulted in remodeling of the femoral heads. In 2 of 7 femoral heads, replacement of the necrotic bone by viable bone was complete at the 42-day postoperative interval. Also, the articular cartilage of the deformed and flattened femoral heads was undergoing degenerative changes. Reduplicating the pathogenically inferred clinical settings of blood supply deprivation, it is proposed that this model, in a small laboratory animal, satisfies the requirements sought for preclinical studies of treatment modalities of avascular osteonecrosis in man.

We describe the unusual occurrence of giant-cell reparative granulomas in the rat. Cutting the ligamentum teres and incising the periosteum around the base of the femoral neck induced femoral capital necrosis. Giant-cell reparative granuloma-like lesions developed in ~0.8% of 366 rats during the early reparative stages of osteonecrosis. Resorption of the necrotic bone, hematopoietic tissue, and adipocytes was exceptionally widespread in these three rats. Overexpression of macrophage-fusing cytokines may account for the increased number of multinucleated giant cells, which on a plump stromal cell background imitate a giant-cell reparative granuloma of the bone.

Achievement of adequate vitamin D3 level is crucial for the treatment of hip fracture patients. Currently used vitamin D3 supplementation in Israel ranges between 200 and 800IU/day. The study objectives were to evaluate the effects of 800IU/day vitamin D3 and 1.200mg of calcium carbonate supplementation to achieve adequate vitamin D3 level of 30ng/ml in elderly hip fracture patients. One hundred and twenty-two elderly patients after surgical hip fracture correction aged 73.0+/-9.5, who were enrolled in a post-surgical treatment program (PSTP). The patients received 800IU of vitamin D3 and 1.200mg of calcium carbonate daily. Serum 25(OH)D and plasma PTH levels were assessed during initial hospital stay and at quarterly follow-up visits for 2 years. At baseline, 120 patients (98.4%) had 25(OH)D serum level30ng/ml. Forty-two patients (34.4%) had 25(OH)D serum level10ng/ml and these were considered as vitamin D(3) deficient. After 3 months, 29 patients (23.8%) were fully adherent to the supplement, 32 were (26.2%) partially adherent. The dropout rate at 1 year was 55.7%. The major reason for the discontinuation of participation was non-compliance. We conclude that the majority of elderly hip fracture patients had inadequate 25(OH)D serum levels. Compliance with calcium and vitamin D3 supplements was extremely low. An adequate vitamin D status was not achieved with daily vitamin D3 supplementation of 800IU. Supplementation strategies using a periodic single high dose of vitamin D3 might be more appropriate and should be considered in these patients.

Background: The population is progressively aging and an increasing number of elderly patients face surgical treatment. Objective: The current study was designed to examine the perioperative morbidity and mortality of elderly patients undergoing orthopedic or urologic surgery and look for predictors for adverse outcome. Methods: This is a prospective study of elderly patients, 80 years of age and older, who underwent elective or emergent orthopedic or urologic surgery in our institution during a 5-month period. Data were collected on age, gender, chronic diseases, number of regular medications, whether or not the patient was bedridden before surgery, American Society of Anesthesiologists (ASA) class, type of surgery and anesthesia, duration of hospitalization, and 30-day postoperative morbidity and mortality. We studied correlations between pre- and intraoperative parameters and postoperative complications. Results: During the study period, 39 patients underwent urologic surgery and 147 patients underwent orthopedic surgery. Age ranged from 80 to 98 years (85 ± 4.2 years, mean ± SD). One patient had an intraoperative complication, 5 patients had postoperative complications within 1 day of surgery, and 23 had complications within 1 month of surgery. Five (2.7%) patients, all of whom were operated urgently, died after surgery. Postoperative complications correlated significantly to poor ASA class (p = 0.01), urgency of the procedure (p = 0.03), and extent (p = 0.02) and duration (p = 0.01) of surgery. No significant correlation was found between outcome and any other pre- or intraoperative factors. Conclusions: Elderly surgical patients with poor ASA class or following urgent, extensive or long surgery are at a higher risk for postoperative morbidity and mortality, mandating special perioperative care.

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. Female Sprague–Dawley rats with interrupted blood circulation of the femoral head were treated with alendronate and compared to controls. There was no distortion of the femoral heads in the alendronate-treated animals. 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.

After producing bilateral osteonecrosis of the femoral head, rats were medicated alendronate according to one of 6 schedules. In group 1 injection was administered one week prior to the operation of devascularization and thereafter was continued for another 42 days. In group 2, medication started on the day of the operation. The control group 3 was similarly handled except that they were given injections of physiological saline. Group 4 animals were subjected to drilling of the right femoral head and treated with alendronate a week before the operation and 42 days thereafter, while in group 5 medication begun on the day of the operation. Control group 6 was similarly handled, but received physiological saline. The furthest advanced changes occurred in groups 3 and 6 (in which an advanced stage of an osteoarthritis–like disorder were observed) followed by groups 4 and 5 (in which alterations were mild to moderate), and finally by groups 1 and 2 (in which there were but mild changes). In addition, all changes were less pronounced in the animals which had been treated with alendronate for one week prior to the operation than in those given the first dose from the operative day. These findings demonstrate that bisphosphonate medication preserves the shape of rats’ femoral heads in the early post–necrotic phase to a greater degree than in the Authors’ earlier, diverse attempts to arrest the disastrous progression of the post–necrotic remodeling towards hip osteoarthritis. The presented findings warrant the preclinical trial of bisphosphonate therapy in patients admitted for the management of osteonecrosis of the femoral head.

Shoulder arthroscopy is usually performed under general anesthesia or interscalene block. General anesthesia may be contraindicated and interscalene block sometimes fails. We had 8 patients who were at high-risk and, therefore, shoulder arthroscopy and decompression were performed under local anesthesia in the beach-chair position. We used 50 mL of 1% lidocaine; 30 mL were infiltrated into the skin and underlying tissues and into the glenohumeral joint, and the rest was infiltrated into the subacromial joint. Before the infiltration, all patients were given 5 mg midazolam and 0.1 mg fentanyl intravenously. All 8 patients were satisfied with the analgesia provided by the anesthesia. We conclude that arthroscopy and subacromial decompression can be readily performed under local anesthesia in combination with efficient sedation.

An impeded blood flow through the femoral head is incriminated in the etiopathogenesis of osteonecrosis of the femoral head. The disorder is either primary (idiopathic avascular osteonecrosis) or secondary to one condition or another, say, corticosteroid medication, fracture of the neck, coagulation defects, physical or thermal damage, storage disorders, alcoholism, and infectious, autoimmune as also marrow infiltrating diseases. In the wake of the necrosis, several mediators are released in increased amounts, prime among which is the vascular endothelial growth factor. The intermediates recruit endothelial progenitor cells, macrophages, osteoclasts, fibroblasts, and osteoblasts, which, pervading throughout the necrotic areas, initiate the reparative processes. The dead, soft and hard tissular debris is substituted by fibrous - later on by hematopoietic-fatty tissue - and bone. The newly formed, appositional and intramembranous bone is deficient in its mechanical properties. The ordinary load-carrying functions suffice to deform these weakened femoral heads so that osteoarthritic changes develop. Considering contemporary assumptions of the causes of osteonecrosis, oxygenation, revascularization, and core decompression are the realistic therapeutic interventions. Necrosis of rats' femoral heads is studied as a model of osteonecrosis in both adults and children. In view of rodents' lifelong persisting physeal cartilage, vascular deprivation-induced osteonecrosis in rats mimics children's Perthes disease. The experimental model, which is well suited to test treatment modalities, has been used to investigate the effects of exposure to hyperbaric oxygen with and without non-weight bearing, medication of enoxaparin, and creation of an intraosseous conduit on the remodeling of the avascular necrotic femoral head. Intriguingly, the shape of treated rats' femoral heads is disfigured to a greater degree than that of untreated animals. This is most likely due to the reduced yield strength and elastic modulus as well as the raised strain-to-failure of the recently formed bone making up the post-necrotic femoral heads. It follows that expedited osteogenesis is, counter intuition, detrimental to maintaining the hemispherical shape of the femoral head, and thus to an articulation with congruent load-bearing surfaces. If this is indeed the case, the remodeling of the necrotic femoral head should be delayed, rather than sped up, as the present day paradigm would have it. Bearing in mind that the dead osseous structures keep their mechanical attributes for quite a while, a slowed down new bone formation would favor the gradual replacement of the necrotic by living bone. Therefore, management of the adult patients with osteonecrosis and children with Perthes disease should focus on a slowly progressive substitution so that the decline of the bone's mechanical properties is kept to a minimum. One viable therapeutic mode is a medication of inhibitors of the vascular endothelial growth factor.

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.

Osteonecrosis of rat femoral heads was induced by stripping the periosteum of the neck and cutting the ligamentum teres. The epiphyseal marrow and bone were necrotic on the 5th postoperative day. Specimens obtained 18 and 36 days postoperatively showed fibrous and hematopoietic-fatty tissue in the intertrabecular spaces, osteoclastic bone resorption, osteogenesis, and degeneration of the joint cartilage. Morphometrically, the means of the height-to-length ratios of the control, 6-day, 18-day, and 36-day femoral heads were 0.26, 0.28, 0.48, and 0.29, respectively. The shape factor of the femoral heads of the control rats was higher than 0.81 in 80% of the cases, while those of rats killed on the 6th, 18th, and 36th postoperative day were higher than 0.81 in 65, 60, and 50% of cases, respectively. Statistically, the means of the height-to-length ratios and the values of the shape factors of the femoral heads of the rats killed 18 days postoperatively differed significantly from those of the other three groups of rats. The quantitatively gauged data of the remodeled epiphyses negate the authors' subjective impression concerning early flattening of the femoral heads after surgically produced osteonecrosis.

Acute compartment syndrome (ACS) is a devastating complication of rhabdomyolysis caused by muscle tamponade secondary to increased intracompartmental pressure (Pi). ACS requires emergency surgical decompression when Pi greater than 30 mmHg (normal less than 4.0 mmHg) and clinical signs exist. The present study was undertaken to examine whether mannitol which has been used extensively for prevention of acute renal failure in rhabdomyiolysis may also improve muscular hemodynamics in ACS. ACS was produced in dogs by injecting dog plasma into the anterolateral compartment of the hind limb. The Pi was directly monitored. Control dogs received saline, whereas experimental dogs received intravenously 20% mannitol (0.15 ml/min/kg) over a period of 1 h. The initial Pi was set arbitrarily at 100 mm Hg. Following the establishment of ACS, the spontaneous mean decrease in Pi in the control group was 40% of initial value over 60 min (n = 5) versus a decrease of 65%/60 min in the experimental (mannitol) group (n = 7, p less than 0.01). The net mean decompressive effect of mannitol treatments was approximately 28 mm Hg (mean control Pi minus mean experimental Pi at time 60 min). Extrapolated to man with ACS, such a decrease in Pi induced by mannitol theoretically could relieve compartmental tamponade noninvasively.

The healing of vascular deprivation-induced necrosis of the femoral head of rats exposed to hyperbaric oxygen was compared with that in untreated rats. The amount of necrotic bone, extent of osteoneogenesis, degree of remodeling, and changes of the articular cartilage were histologically graded on a semiquantitative scale of 0 to 3+. On the 2nd, 7th, and 21st postoperative days, there were no differences between the two groups. Newly formed appositional and intramembranous bone was more abundant and remodeling was more advanced in the femoral heads of the hyperbaric oxygen-treated than untreated rats sacrificed on the 42nd postoperative day; also there was less necrotic debris in the femoral heads of the treated rats. There were no differences in the severity of the degenerative changes of the articular cartilage of the treated and untreated rats. Exposure of rats to hyperbaric oxygen does not preserve tissue viability after all arteries supplying the femoral head are severed. Yet, resulting in an increased oxygen tension of the tissues, it seems to provide the optimal settings for reparative processes. The results suggest that hyperoxygenation-mediated relief of ischemia enhances the fibroblastic, angioblastic, osteoblastic, and osteoclastic activities such that healing of the rats' necrotic femoral heads is expedited.

Summary The reparative processes following vascular deprivation induced necrosis of the femoral head were studied histologically in rats sacrificed 2, 7, 14, 21, 42 and 92 days postoperatively. The blood supply was severed by incision of the periosteum at the neck of the femoral head and transection of the ligamentum teres. Granulation tissue and a well-vascularized fibrous tissue originating from the joint capsule invaded the necrotic marrow spaces. With progressive resorption of the necrotic tissues and osteoneogenesis, both appositional and intramembranous, within the fibrotic intertrabecular spaces, the remodeling process led to a shift of the normal spongy architecture of the femoral head to a compacta- like one. In a few cases, osseous bridges bisected a necrotic physeal cartilage at the latest time intervals. The remodeling was associated with flattening of the femoral heads as well as with degenerative, regenerative and reparative alterations of the articular cartilage. In one of the two femoral heads obtained three months postoperatively, cystic spaces developed in the fibrous subchondral zone. Our findings are consistent with the view that ineffective attempts at restoring the prenecrotic state of the femoral head by replacing the necrotic with viable tissue triggers the collapse of the femoral head. Thickening and condensation of the subchondral bone, leading to increased stiffness of the subchondral zone, result in the osteoarthritis-like disorder. Mimicking the well-known phases of human osteonecrosis, the model readily allows for preclinical studies of therapeutic regimens.