Introduction: Extracorporal Shock Wave Therapy (ESWT) has become a useful adjunct for the treatment of various musculo-skeletal inflammatory conditions.

The aim of the study is prospective assessment of the efficacy of ESWT for the treatment of recalcitrant greater trochanteric bursitis (GTB).

Material and Methods: Prospective evaluation and follow-up of fourteen patients with persistent GTB two of them with bilateral problem. All the patients failed to response to conventional treatment with oral NSAID’s, physiotherapy, US and more than one steroid injection to the grater trochanter region. All patients underwent compete physical examination. A Comprehensive VAS Score (grading from 0–10) which were obtained prior to therapy and at follow-up. ESWT was applied in six consequitive courses each of 1500 impulses of 0.32mj/mm^2 to the lateral side of the grater trochanter region.

Results: Mean age of 60.6 ± 11.6 (mean ± SD) years (range 81 to 38 years). Mean duration of symptoms 14.2 ± 8.1 months, up to 37 months. Mean VAS dropped from 7.9 ± 0.9 to 1.6 ± 0.8 (p< 0.0001). There were no side effects except minimal local discomfort during the session time.

Conclusion: ESWT is an effective treatment for recalcitrant GTB, with minimal side effect.

During the second Lebanon war, between 12/07/06 to 14/08/06, 241 war injuries were admitted to Rambam Medical Center emergency room: 202 soldiers and 39 citizens. (Post traumatic stress disorders victims were not included). Majority of the injured soldiers (98%) were mobilized by the Israeli Air Force helicopters. More then 40 helicopters had landed in the hospital heliport during the war. Distribution of injuries according to the injury type:

110 patients (44% of all injured) had Orthopedic injuries (including hand injuries)

Distributions of soldier’s injuries among soldiers were similar to the above :

81 soldiers (41%) Orthopedic injuries (including hand injuries)

About 75 % of the injured soldiers suffered from orthopedic injuries. Vast majority of the injuries were shrapnel injuries, which were divided to 3 levels:

Mild soft tissue damage due to few or superficial shrapnel injury – 107 (49%) soldiers.

Organs injury distribution:

24 Patients total of 54 fractures, 24 of those had been long bone fractures

Amputation – 5 soldiers were underwent completion of traumatic lower limb amputation. One soldiers had bilateral below knee amputation, 1 above knee amputation and 3 unilateral below knee amputation.

Two hundred and three orthopedic surgery interventions were done by Orthopedics’ B’ department in Rambam Medical Hospital, during the Second Lebanon War.

Introduction: In avascular necrosis [AVN] of the femoral head the dead bone undergoes osteoclastic osteolysis and is replaced by newly synthesized, immature, weak bone, which cannot withstand the daily loads. The articular surface might caves in because of these changes, and osteoarthritic joint changes can develop. Alendronate interferes with the osteoclastic activities, it can slow-down the bone turnover of the necrotic bone and can differ these changes.

The aim of this study is to delay the speedy renewal of living epiphyses by alendronate medication in order to describe the effects of it on the fate of the necrotic femoral heads in rats.

Methods: Sixty female sprague-dawley rats, 6-month old weighing about 400–500 grams, underwent surgical AVN of the right femoral heads. Forty-four rats, the treated group, were treated with alendronate 200 μgm/kg/day. Sixteen rats, the control group, were treated with saline. Both groups were daily injected subcutaneously for six weeks and sacrificed. Both femoral heads were harvested and were evaluated microscopically and stained by H& E.

Results: The necrotic femoral heads of the control group, which were not treated by alendronate, were severely distorted with osteoarthrosis features as; collapse of the epiphysis, pannus formation, filling of spaces by chronically and mildly inflamed densely textured fibrous tissue which was polluted by numerous tiny particles of necrotic bone. Additionally, large chunks of necrotic articular cartilage were haphazardly scattered in the fibrous tissue. All hematopoietic and fat cells of the intertrabecular spaces of the epiphysis were replaced by fibrous tissue. More often than not, the cartilage of the physis was focally or entirely absent such that osseous trabeculae of the epiphysis and metaphysis linked with each other, forming so-called epiphyseal-metaphyseal bridges. The above described alterations were encountered in all animals, yet their severity varied.

The decisive difference between the necrotic femoral heads of otherwise untreated in opposition to the alendronate-medicated rats was the preservation of a hemispherical configuration of the femoral heads. There was no distortion of the femoral heads in the alendronate-treated animals and the femoral heads preserved their roundness.

All femoral heads of the non-operated left hips were microscopically normal.

Discussion: It has become clear that the degree of architectural distortion of the femoral epiphyses depends on the extent of bone turnover leading to resorption of all debris and its replacement by living osseous and soft tissues. The more rapidly and more extensively the reconstruction of living epiphyses progresses, the smaller is the prospect of reshaping a hemispherical or near-hemispherical femoral head. The recently rebuilt epiphyses cannot carry daily transarticular loads without caving in. The revascularization-related reconstitution of weak bony trabeculae is blamed for the collapse of the femoral heads. If this indeed is the case, the remodeling of the necrotic femoral heads should be delayed, rather than sped-up. Alendronate interferes with the osteoclastic activities and hence, slowing-down the bone turnover.

The osteoclastic activity is detrimental for the conservation of a hemispherical femoral head because of the rapidly occurring replacement of the necrotic bone by living tissues. Halting the activities of the osteoclasts by a biphosphonate would stop the hasty osteoneogenesis, which is responsible for the early femoral capital disfigurement and might delay the regeneration of osteo-arthiritic changes of the joint later on.