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Adhesive capsulitis of the shoulder involves loss of passive range of motion with associated pain and can develop spontaneously, with no obvious injury or inciting event. The pathomechanism of this disorder remains to be elucidated, but known risk factors for adhesive capsulitis include diabetes, female sex, and thyroid dysfunction. Additionally, transcriptional profiling and pedigree analyses have suggested a role for genetics. Identification of elements of genetic risk for adhesive capsulitis using population-based techniques can provide the basis for guiding both the personalized treatment of patients based on their genetic profiles and the development of new treatments by identification of the pathomechanism.A genome-wide association study (GWAS) was conducted using the U.K. Biobank (a collection of approximately 500,000 patients with genetic data and associated ICD-10 [International Classification of Diseases, 10th Revision] codes), comparing 2,142 patients with the ICD-10 code for adhesive capsulitis (M750) to those without. Separate GWASs were conducted controlling for 2 of the known risk factors of adhesive capsulitis-hypothyroidism and diabetes. Logistic regression analysis was conducted controlling for factors including sex, thyroid dysfunction, diabetes, shoulder dislocation, smoking, and genetics.Three loci of significance were identified: rs34315830 (in WNT7B; odds ratio [OR] = 1.28; 95% confidence interval [CI], 1.22 to 1.39), rs2965196 (in MAU2; OR = 1.67; 95% CI, 1.39 to 2.00), and rs1912256 (in POU1F1; OR = 1.22; 95% CI, 1.14 to 1.31). These loci retained significance when controlling for thyroid dysfunction and diabetes. The OR for total genetic risk was 5.81 (95% CI, 4.08 to 8.31), compared with 1.70 (95% CI, 1.18 to 2.36) for hypothyroidism and 4.23 (95% CI, 2.32 to 7.05) for diabetes.The total genetic risk associated with adhesive capsulitis was significant and similar to the risks associated with hypothyroidism and diabetes. Identification of WNT7B, POU1F1, and MAU2 implicates the Wnt pathway and cell proliferation response in the pathomechanism of adhesive capsulitis.Prognostic Level III . See Instructions for Authors for a complete description of levels of evidence.

End-stage knee osteoarthritis (OA) is a highly debilitating disease for which total knee arthroplasty (TKA) serves as an effective treatment option. Although a genetic component to OA in general has been described, evaluation of the genetic contribution to end-stage OA of the knee is limited. To this end, we present a genome-wide association study involving patients undergoing TKA for primary knee OA to characterize the genetic features of severe disease on a population level.Individuals with the diagnosis of knee OA who underwent primary TKA were identified in the U.K. Biobank using administrative codes. The U.K. Biobank is a data repository containing prospectively collected clinical and genomic data for500,000 patients. A genome-wide association analysis was performed using the REGENIE software package. Logistic regression was also used to compare the total genetic risk between subgroups stratified by age and body mass index (BMI).A total of 16,032 patients with end-stage knee OA who underwent primary TKA were identified. Seven genetic loci were found to be significantly associated with end-stage knee OA. The odds ratio (OR) for developing end-stage knee OA attributable to genetics was 1.12 (95% confidence interval [CI], 1.10 to 1.14), which was lower than the OR associated with BMI (OR = 1.81; 95% CI, 1.78 to 1.83) and age (OR = 2.38; 95% CI, 2.32 to 2.45). The magnitude of the OR for developing end-stage knee OA attributable to genetics was greater in patients60 years old than in patients ≥60 years old (p = 0.002).This population-level genome-wide association study of end-stage knee OA treated with primary TKA was notable for identifying multiple significant genetic variants. These loci involve genes responsible for cartilage development, cartilage homeostasis, cell signaling, and metabolism. Age and BMI appear to have a greater impact on the risk of developing end-stage disease compared with genetic factors. The genetic contribution to the development of severe disease is greater in younger patients.Prognostic Level III . See Instructions for Authors for a complete description of levels of evidence.

Cartilage defects of the patellofemoral joint are commonly found in association with patellar instability owing to abnormal biomechanics. Strategies to address chondral defects of the patellofemoral joint secondary to instability should first address causes of recurrent instability. Most patellofemoral chondral defects associated with instability are less than 2 cm2 and do not generally require intervention beyond chondroplasty. Larger defects of the patella and/or the trochlea can be repaired with osteochondral or surface cartilage repair.

SUMMARY In this article, we present a novel patella fixation technique using a low-profile highly contoured dorsal mini-fragment locking plate. This procedure is ideally indicated in patients with fracture patterns that are transverse without significant comminution. Long-term clinical studies are being performed to evaluate the effectiveness of this surgical technique.

To use computed tomography (CT) to determine a reproducible method of coracoid measurement to compare the ability of the classic Latarjet technique and the congruent arc modification (CAM) to restore native glenoid diameter and to develop a preoperative planning algorithm for glenoid restoration with a goal of achieving an on-track shoulder.Coracoid dimensions were measured on multiplanar reconstructed shoulder CT scans of patients aged 18 to 45 years obtained between December 1, 2019, and March 13, 2020. Patients were excluded if CT demonstrated osteophyte formation, glenoid dysplasia, coracoid fracture, or tumor. The proportion of glenoid diameter able to be restored using classic Latarjet technique and CAM were calculated. A treatment algorithm was proposed considering the amount of bone loss present and coracoid dimensions.Coracoid dimensions of 117 consecutive patients were measured and varied considerably (length: 17.5-31.8 mm, width: 9.1-20.5 mm, thickness: 6.1-15.7 mm). While most patients had harvestable coracoid length ≥20 mm (male: 96.3% vs female: 94.4%, P = .65), only 27.8% of female patients had coracoid thickness ≥10 mm. When comparing Latarjet techniques, there was no difference in the proportion of patients in whom 30% glenoid diameter could be fully restored, but CAM was able to restore at least 35% in more male and female patients (98.8% vs 79.0% and 100% vs 61.1%, respectively, P = .00001). Intra- and inter-rater reliability was excellent ( intraclass correlation coefficient ≥0.950 for all dimensions).We describe a reliable method of measuring coracoid dimensions for preoperative planning of glenoid restoration. The classic Latarjet technique reliably restores the glenoid anteroposterior diameter with bone loss of up to 30%. The majority of female patients have coracoid thickness10 mm, which may increase the risk of graft fracture when using CAM. The decision to use the classic Latarjet technique or CAM considers each individual's glenoid and coracoid dimensions with a goal of achieving an on-track shoulder.Our reliable method of coracoid measurement demonstrated the differing abilities of the classic Latarjet and CAM to restore the native glenoid diameter. An evidence-based algorithm using these measurements was developed to assist in preoperative planning for glenohumeral instability in the setting of bone loss, with a goal of achieving an on-track shoulder. Alternative techniques may be considered if an on-track shoulder cannot be achieved with Latarjet.

Bone has well documented natural healing capacity that normally is sufficient to repair fractures and other common injuries. However, the properties of bone change throughout life, and aging is accompanied by increased incidence of bone diseases and compromised fracture healing capacity, which necessitate effective therapies capable of enhancing bone regeneration. The therapeutic potential of adult mesenchymal stem cells (MSCs) for bone repair has been long proposed and examined. Actions of MSCs may include direct differentiation to become bone cells, attraction and recruitment of other cells, or creation of a regenerative environment via production of trophic growth factors. With systemic aging, MSCs also undergo functional decline, which has been well investigated in a number of recent studies. In this review, we first describe the changes in MSCs during aging and discuss how these alterations can affect bone regeneration. We next review current research findings on bone tissue engineering, which is considered a promising and viable therapeutic solution for structural and functional restoration of bone. In particular, the importance of MSCs and bioscaffolds is highlighted. Finally, potential approaches for the prevention of MSC aging and the rejuvenation of aged MSC are discussed.