Latarjet procedure (transfer of coracoid process to the anterior glenoid rim) has been widely used for severe anterior shoulder instability. The purpose of the present study was to investigate the intraarticular stress distribution after this procedure to clarify the pathomechanism of its postoperative complications. CT-DICOM data of the contralateral healthy shoulder in 10 patients with unilateral anterior shoulder instability (9 males and 1 female, age: 17–49) was used for the present study. Three-dimensional finite element models of the glenohumeral joint was developed using software, Mechanical Finder (RCCM, Japan). In each shoulder, a 25% bony defect was created in the anterior glenoid cavity, where coracoid process was transferred using two half-threaded screws. The arm position was determined as 0-degree and 90-degree abduction. While medial margin of the scapula was completely constrained, a standard compressive load (50 N) toward the centre of the glenoid was applied to the lateral wall of the greater tuberosity. A tensile load (20N) was also applied to the tip of coracoid process along the direction of conjoint tendon. Then, elastic analysis was performed, and the distribution pattern of Drucker-Prager equivalent stress was investigated in each model. The proximal half of the coracoid represented significantly lower equivalent stress than the distal half (p < 0.05). In particular, the lowest mean equivalent stress was seen in its proximal-medial-superficial part. On the other hand, a high stress concentration newly appeared in the antero-inferior aspect of the humeral head exactly on the site of coracoid bone graft. We assumed that the reduction of mean equivalent stress in the proximal half of the coracoid was caused by the stress shielding, which may constitute one of the pathogenetic factors of its osteolysis. A high stress concentration in the humeral head may eventually lead shoulder joint to osteoarthritis.

In the pubertal growth plate, sex hormones play important roles for the regulation of the proliferation, differentiation, maturation and programmed death of chondrocytes. Many studies have been reported on the regulation of oestrogen in long bone growth, however, some of the mechanisms have remained unclarified to date including its role for cell kinetics in the growth plate chondrocytes. The aim of this study was to clarify the effect of the deficiency of oestrogen on growth plate chondrocytes.

We obtained the growth plates of femoral head from the normal and ovariectomized Japanese white rabbits at 10, 15, 20 and 25 weeks. Ovariectomy was performed at 8 weeks. The cell kinetics of chondrocytes as defined by the numbers of proliferating and programmed dying cells was investigated using immunohistological methods.

The lengths of the femur were almost same both in the ovariectomised and normal rabbits. The height of the growth plate was larger in the former. The total number of chondrocytes in the ovariectomised rabbits was less than that of normal rabbits of the same age. Immunostaining of proliferating cell nucleous antigen (PCNA) showed a decrease number of proliferating chondrocytes and that of caspase-3 indicated a little increased number of apoptotic chondrocytes.

Oestrogen regulates endochondral bone formation through several pathways. It directly binds oestrogen receptor alpha and beta, and the former accelerates longitudinal bone growth whereas the latter represses it. Another pathway is through the GH-IGF-I axis: it closely interacts with GH and IGF-I for the control of longitudinal bone growth. In addition, there might be other mediators including transforming growth factor-beta, other IGFs and still unknown paracrine or auto-crine factors as IHH PTHrP. Our study suggests that in the rabbit growth plate during puberty, oestrogen mainly acts through the GH-IGF-I axis since its defi-ciency declined the proliferating ability of chondrocytes, which led the decrease of the number of chondrocytes.

Sex hormones play important roles in the regulation of the proliferation, maturation and death of chondrocytes in the epiphyseal growth plate. We have investigated the effects of male castration on the cell kinetics of chondrocytes as defined by the numbers of proliferating and dying cells. The growth plates of normal rabbits and animals castrated at eight weeks of age were obtained at 10, 15, 20 and 25 weeks of age.

Our study suggested that castration led to an increase in apoptosis and a decrease in the proliferation of chondrocytes in the growth plate. In addition, the number of chondrocytes in the castrated rabbits was less than that of normal animals of the same age.