The Leydig cell is the primary source of testosterone in males. Levels of testosterone in circulation are determined by the steroidogenic capacities of individual Leydig cells and the total numbers of Leydig cells per testis. Stress-induced increases in serum glucocorticoid concentrations inhibit testosterone-biosynthetic enzyme activity, leading to decreased rates of testosterone secretion. It is unclear, however, whether the excessive glucocorticoid stimulation also affects total Leydig cell numbers through induction of apoptosis and thereby contributes to the stress-induced suppression of androgen levels. Exposure of Leydig cells to high concentrations of corticosterone (CORT, the endogenously secreted glucocorticoid in rodents) increases their frequency of apoptosis. Studies of immobilization stress indicate that stress-induced increases in CORT are directly responsible for Leydig cell apoptosis. Access to glucocorticoid receptors in Leydig cells is modulated by oxidative inactivation of glucocorticoid by 11 beta-hydroxysteroid dehydrogenase (11 betaHSD). Under basal levels of glucocorticoid, sufficient levels of glucocorticoid metabolism occur and there is likely to be minimal binding of the glucocorticoid receptor. We have established that Leydig cells express type 1 11 betaHSD, an oxidoreductase, and type 2, a unidirectional oxidase. Generation of redox potential through synthesis of the enzyme cofactor NADPH, a byproduct of glucocorticoid metabolism by 11 betaHSD-1, may potentiate testosterone biosynthesis, as NADPH is the cofactor used by steroidogenic enzymes such as type 3 17beta-hydroxysteroid dehydrogenase. In this scenario, inhibition of steroidogenesis will only occur under stressful conditions when high input amounts of CORT exceed the capacity of oxidative inaction by 11 betaHSD. Changes in autonomic catecholaminergic activity may contribute to suppressed Leydig cell function during stress, and may explain the rapid onset of inhibition. However, recent analysis of glucocorticoid action in Leydig cells indicates the presence of a fast, non-genomic pathway that will merit further investigation.

Purpose This study aimed to evaluate the safety and efficacy of fusiform capsulectomy of posterior capsule in correcting severe flexion contracture during total knee arthroplasty (TKA). Methods A retrospective analysis was performed in the patients who had preoperative severe flexion contracture (> 30 degrees) prior to TKA and received fusiform capsulectomy of posterior capsule during TKA between December 2013 and November 2018. Range of motion (ROM), knee functional score, forgotten joint score (FJS), post-operative complications, and radiographic results were collected and evaluated. Result Twenty patients (32 knees) were enrolled in this study. The mean duration of follow-up was 27.19 ± 15.92 months. The flexion contracture improved from pre-operative 37.69 ± 11.79°to post-operative 5.78 ± 4.44°( p < 0.001), and ROM increased from pre-operative 63.50 ± 21.74°to post-operative 97.88 ± 13.20°(p < 0.001). KSS clinical score increased from pre-operative 32.94 ± 11.03 to post-operative 82.34 ± 10.73 (p < 0.001), and KSS function score increased from pre-operative 28.97 ± 18.43 to post-operative 68.75 ± 15.96 (p < 0.001). The postoperative FJS was 76.08 ± 2.14. There was no implant loosening, infection, obvious haematoma formation, resultant instability, neurovascular complications, or revision for any reasons in the cohort until the last follow-up. Conclusions The technique of fusiform capsulectomy of posterior capsule to correct the severe flexion contracture during primary TKA is safe and effective and could provide good short-term results.

Background The purpose of this study was to examine whether surgeon handedness could affect cup positioning in manual total hip arthroplasty (THA), and whether robot could diminish or eliminate the impact of surgeon handedness on cup positioning in robot-assisted THA.Methods Fifty-three patients who underwent bilateral robot-assisted THA and sixty-two patients who underwent bilateral manual THA between August 2018 and July 2019 in our institute were respectively analyzed in this study. When the difference between the bilateral anteversion or inclination was greater than 5°, the patient was regarded as having different cup positioning between bilateral THA. Their demographics, orientation of acetabular cup and postoperative 3 month Harris hip score (HHS) were recorded for analysis.Results There were no significant difference in the gender, age, BMI, diagnosis's composition, preoperative and postoperative HHS between the robotic and manual group. Two left hips dislocated in the manual group. The anteversion of left hip was significantly larger than that of right hip (24.77±10.44 vs 22.44±8.67, p=0.043) in the manual group. There were no significant difference of cup positioning between bilateral robot-assisted THA. The patients in manual group were significantly more likely to have different cup positioning between bilateral hips than those in robotic group (77% vs 45%, p=0.000).Conclusions Surgeon's handedness had adverse impact on anteversion of the non-dominant side in manual THA and right-handed surgeons were more likely to place the left cup in larger anteversion. Robot could help surgeon eliminate the adverse impact caused by personal innate handedness.

The last couple of decades have seen brilliant progress in stem cell therapies, including native, genetically modified, and engineered stem cells, for osteonecrosis of the femoral head (ONFH). In vitro studies evaluate the effect of endogenous or exogenous factor or gene regulation on osteogenic phenotype maintenance and/or differentiation towards osteogenic lineage. The preclinical and clinical outcomes accelerate the clinical translation. Bone marrow mesenchymal stem cells and adipose-derived stem cells have demonstrated better effects in the treatment of femoral head necrosis. Various materials have been used widely in the ONFH treatment in both preclinical and clinical trials. In a word, in vivo and multiscale efforts are expected to overcome obstacles in the approaches for treating ONFH and provide clinical relevance and commercial strategies in the future. Therefore, we will discuss the above aspects in this paper and present our opinions.

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