How to improve the incorporation of massive allografts?

The incorporation of a bone graft is the result of creeping and substitutional activities that remove the original grafted bone and replace it by newly formed bone from the host cells. However, this intricate process is very limited in time and space. A bone allograft is poorly remodeled and is almost non viable even after several years of implantation. This lack of vitality accounts for the high rate of complications such as non union and fracture. One way to minimize the allograft complications is to improve its incorporation. The process of incorporation in animals and human beings is reviewed as well as the various avenues for a biologic improvement either through modulation on the host: the immune response, the inhibition of bone resorption, the use of bone morphogenetic proteins, the autogenous cell augmentation or through processing the bone allograft: bisphosphonate adsorption or bone perforations. In 2002, biologic enhancement of the incorporation is still in its infancy but will be in a near future a reality through influence on both the host and the allograft.     

Corin: a key protein of an adaptive renal mechanism to respond to salt variation?

The protease corin generates atrial natriuretic peptide and affects blood pressure and salt-water homeostasis. Under dietary salt challenge, corin knockout mice show blood pressure exacerbation and significant weight gain due to water and salt retention. This phenotype involves the epithelial sodium channel but is independent of the renin-angiotensin-aldosterone system. This suggests that corin has an important role in a new adaptive mechanism of the response to variations of salt in the diet.     

Do trauma centers have the capacity to respond to disasters?

BACKGROUND: Concern has been raised about the capacity of trauma centers to absorb large numbers of additional patients from mass casualty events. Our objective was to examine the capacity of current centers to handle an increased load from a mass casualty disaster. METHODS: This was a cross-sectional study of Level I and II trauma centers. They were contacted by mail and asked to respond to questions about their surge capacity as of July 4, 2005. RESULTS: Data were obtained from 133 centers. On July 4, 2005 there were a median of 77 beds available in Level I and 84 in Level II trauma centers. Fifteen percent of the Level I and 12.2% of the Level II centers had a census at 95% capacity or greater. In the first 6 hours, each Level I center would be able to operate on 38 patients, while each Level II center would be able to operate on 22 patients. Based on available data, there are 10 trauma centers available to an average American within 60 minutes. Given the available bed capacity, a total of 812 beds would be available within a 60-minute transport distance in a mass casualty event. CONCLUSIONS: There is capacity to care for the number of serious non-fatally injured patients resulting from the types of mass casualties recently experienced. If there is a further continued shift of uninsured patients to and fiscally driven closure of trauma centers, the surge capacity could be severely compromised.     

How to deal with glenoid type B2 or C? How to prevent mistakes in implantation of glenoid component?

Background

Although TSA has been shown to significantly yield better outcomes than hemiarthroplasty, glenoid prosthesis loosening remains the most common complication. Inadequate primary fixation enables the glenoid component to move. In primary glenohumeral osteoarthritis (GHOA), glenoid involvement and proper morphology vary considerably. Postero-inferior glenoid hypoplasia could be associated with some degree of osteoarthritis. According to Walch, 24 % of glenoids in GHOA are type B2 or C (excessive posterior retroversion), which increases the challenge for the glenoid component fixation.

Materials and methods

A total of 30 cases of TSR with glenoid type B2 (20 cases) and type C (10 cases) were reviewed. Mean follow-up was 11.2 months. A metal-backed (MB) glenoid component was implanted, with a posterior bone graft reconstruction. Pre- and post-operative clinical evaluation was done using the Constant–Murley score and the SST from Matsen.

Results

There is no glenoid loosening, no joint narrowing and no radiolucent line. There was no bone graft osteolysis. With 4 patients revised (4 conversions from TSR to RSR for 3 instabilities and 1 secondary rotator cuff tear), on the overall 30 patients cohort, Constant score pain increased from 1.6 to 13.4, forward flexion from 92° to 146° and Constant score from 27 (36 %) to 70 (95 %). The statistical difference between pre- and post-operative values is greatly significant.

Conclusion

Although MB prostheses have been noted to have a higher rate of loosening than full-cemented PE, this is not our experience, even in case of glenoid type B2 or C, where the technical challenge is demanding and most of the time a posterior bone graft is necessary.     

How many pathways to pheochromocytoma?

Pheochromocytomas, like several other tumors, may be either sporadic or the manifestation of a familial cancer syndrome. Recently, major advances have occurred in both the understanding of diverse molecular mechanisms leading to pheochromocytoma and the diagnostic modalities available for detection of the disease. Familial pheochromocytoma may be a manifestation of multiple endocrine neoplasia type 2 (MEN-2), von Hippel-Lindau (VHL), or neurofibromatosis-1 (NF 1) disease. Tumor-suppressor genes responsible for the familial occurrence of extra-adrenal pheochromocytoma, called paraganglioma, have been identified. This wealth of genetic information, coupled with the availability of sensitive and specific biochemical tests as well as imaging studies, allows for genetic screening and early diagnosis of pheochromocytoma. In addition, genetic screening of relatives at risk is now feasible. In this article, we review recent clinical and molecular advances in our understanding of pheochromocytoma.