A study in vivo of the effects of a static compressive load on the proximal tibial physis in rabbits.

BACKGROUND: The effect of compression on the physis is generally defined by the Hueter-Volkmann principle, in which decreased linear growth of the physis results from increased compression. This investigation examined whether mechanically induced compression of rabbit physes causes changes in gene expression, cells, and extracellular components that promote physeal resilience and strength (type-II collagen and aggrecan) and cartilage hypertrophy (type-X collagen and matrix metalloprotease-13). METHODS: Static compressive loads (10 N or 30 N) were applied for two or six weeks across one hind limb proximal tibial physis of thirteen-week-old female New Zealand White rabbits (n = 18). The contralateral hind limb in all rabbits underwent sham surgery with no load to serve as an internal control. Harvested physes were divided into portions for histological, immunohistochemical, and quantitative reverse transcription-polymerase chain reaction analysis. Gene expression was statistically analyzed by means of comparisons between loaded samples and unloaded shams with use of analysis of variance and a Tukey post hoc test. RESULTS: Compared with unloaded shams, physes loaded at 10 N or 30 N for two weeks and at 10 N for six weeks showed histological changes in cells and matrices. Physes loaded at 30 N for six weeks were decreased in thickness and had structurally disorganized chondrocyte columns, a decreased extracellular matrix, and less intense type-II and X collagen immunohistochemical staining. Quantitative reverse transcription-polymerase chain reaction analysis of loaded samples compared with unloaded shams yielded a significantly (p ≤ 0.05) decreased gene expression of aggrecan and type-II and X collagen and no significant (p > 0.05) changes in the matrix metalloprotease-13 gene expression with increasing load. CONCLUSIONS: Compressed rabbit physes generate biochemical changes in collagens, proteoglycan, and cellular and tissue matrix architecture. Changes potentially weaken overall physeal strength, consistent with the Hueter-Volkmann principle, and lend understanding of the causes of pathological conditions of the physis.

Accuracy of obtaining optimal base plate declination in reverse shoulder arthroplasty.

BACKGROUND: Reverse total shoulder arthroplasty has shown promising early and midterm results; however, complication rates remain a concern. Glenoid loosening and notching, for example, can be deleterious to the long-term success. A 15° inferior inclination angle has been shown to offer the most uniform compressive forces across the base plate and the least micromotion at the base plate-glenoid interface. The inferior inclination angle may also avoid scapular notching. The purpose of this study was to determine the accuracy of obtaining 15° of inferior inclination of the base plate. METHODS: The radiographs of 138 reverse total shoulder patients were included. Overall, glenoid inclination and change in inclination from preoperative radiographs were measured using a previously described standardized method. Measurements were obtained by 2 orthopedic surgeons, who repeated all measurements 3 weeks apart. The final angle and change in inclination were averaged. RESULTS: Seventy-two patients had pre- and postoperative radiographs of sufficient quality to accurately measure inclination. Average pre- and postoperative inclination measured -4.8° (-27.2° to 28.1°) and -13.3° (-22.8° to 43.6°), respectively. The average change in inclination was -8.5° (-53.7(o) to 34.6(o)). No scapular notching was observed, which may relate to the lateralized center of rotation of the implant used in this study. DISCUSSION: Overall, the average decrease in inclination was very close to the intended target value using the standard guide. However, patients with preoperative superior glenoid erosion from advanced rotator cuff tear arthropathy appeared to be consistently tilted superiorly, suggesting the standard guide may be inadequate in these patients.

Greater tuberosity osteotomy and teres minor transfer for irreparable superior rotator cuff tears.

The purpose of this study was to evaluate the mid- to long- term objective, subjective and radiographic results of patients who underwent anterior-superior transfer of remaining infraspinatus tendon and teres minor tendon for irreparable superior rotator cuff tears. Thirteen patients were identified who underwent infraspinatus tendon transfer to a more superior position on the humeral head between January 1, 1990 and December 31, 2001. Nine shoulders in eight patients were available for clinical examination, radiographs and questionnaire follow-up at an average of 83.5 +/- 31.4 months. Radiographic examination revealed 1 fibrous union and 6 united tuberosity osteotomies. Samilson-Prieto grading of radiographs revealed 4 shoulders with mild, and 4 shoulders with moderate, OA. Seven of the patients were satisfied with their shoulder. There were two poor outcomes. Local antero-superior teres minor and residual infraspinatus transfer provides a viable option for irreparable rotator cuff defects. Mid- to long-term satisfactory outcome was achieved in 7 out of 9 shoulders.

Metabolic alteration of the N-glycan structure of a protein from patients with a heterozygous protein deficiency.

Glycosylation, an important post-translation modification, could alter biological activity or influence the clearance rates of glycoproteins. We report here the first example of a heterozygous protein deficiency leading to metabolic alteration of N-glycan structures in residual secreted protein. Analysis of C1 esterase inhibitor (C1INH) glycans from normal individuals and patients with hereditary deficiency of C1INH demonstrated identical O-glycan structures but the N-glycans of patients with a heterozygous genetic deficiency were small, highly charged and lacked sialidase releasable N-acetylneuraminic acid. Structural studies indicate that the charge character of these aberrant N-glycan structures may result from the presence of mannose-6-phosphate residues. These residues might facilitate secretion of C1INH through an alternate lysosomal pathway, possibly serving as a compensatory mechanism to enhance plasma levels of C1INH in these deficient patients.