Top 50 most impactful publications on massive rotator cuff tears.

Background: Bibliometric analysis is a useful tool for measuring the scholarly impact of a topic and its more and less heavily studied aspects. The purpose of this study is to use bibliometric analysis to comprehensively analyze the 50 articles with the highest citation indices in studies evaluating the treatment and outcomes of massive rotator cuff tears (mRCTs). Methods: This cross-sectional study identified articles within the Scopus database published through December 2022. Keywords used were "massive rotator cuff tear." Articles were sorted in chronological order. The year published and number of citations were recorded. A citation index (CI) was calculated for each article by dividing the number of citations by number of years published [1 citation/1 year published (2021) = CI of 1]. Of these, the 50 articles with the highest CIs were carried forward for evaluation. Frequencies and distributions were assessed for data of each variable collected. Results: These search methods produced 625 articles regarding mRCT research (ranging from January 1986 to December 2022). Four of the top 10 most impactful articles were published in the 2010s. The level of evidence (LOE) published with the greatest frequency was level of evidence 4 (41%). The journal Arthroscopy published the highest number within the top 50 (26%) followed by the Journal of Bone and Joint Surgery and the American Journal of Sports Medicine (20% each). Clinical studies composed 88% of the top 50. Case series (38%) predominated, while systematic reviews (20%) and randomized control trials (8%) were less prevalent. The majority of studies concentrated on the clinical outcomes of certain interventions (62%), mainly comparing multiple interventions. Conclusion: Despite the relatively high prevalence of mRCTs (40% of all tears), this topic comprises only a small proportion of all rotator cuff research. This analysis has identified gaps within and limitations of the findings concerning mRCTs for researchers to propose research questions targeting understudied topics and influence the future treatment and outcomes of this clinically difficult diagnosis.

Promotion of Joint Degeneration and Chondrocyte Metabolic Dysfunction by Excessive Growth Hormone in Mice.

OBJECTIVE: Many patients with acromegaly, a hormonal disorder with excessive growth hormone (GH) production, report pain in joints. We undertook this study to characterize the joint pathology of mice with overexpression of bovine GH (bGH) or a GH receptor antagonist (GHa) and to investigate the effect of GH on regulation of chondrocyte cellular metabolism. METHODS: Knee joints from mice overexpressing bGH or GHa and wild-type (WT) control mice were examined using histology and micro-computed tomography for osteoarthritic (OA) pathologies. Additionally, cartilage from bGH mice was used for metabolomics analysis. Mouse primary chondrocytes from bGH and WT mice, with or without pegvisomant treatment, were used for quantitative polymerase chain reaction and Seahorse respirometry analyses. RESULTS: Both male and female bGH mice at ~13 months of age had increased knee joint degeneration, which was characterized by loss of cartilage structure, expansion of hypertrophic chondrocytes, synovitis, and subchondral plate thinning. The joint pathologies were also demonstrated by significantly higher Osteoarthritis Research Society International and Mankin scores in bGH mice compared to WT control mice. Metabolomics analysis revealed changes in a wide range of metabolic pathways in bGH mice, including beta-alanine metabolism, tryptophan metabolism, lysine degradation, and ascorbate and aldarate metabolism. Also, bGH chondrocytes up-regulated fatty acid oxidation and increased expression of Col10a. Joints of GHa mice were remarkably protected from developing age-associated joint degeneration, with smooth articular joint surface. CONCLUSION: This study showed that an excessive amount of GH promotes joint degeneration in mice, which was associated with chondrocyte metabolic dysfunction and hypertrophic changes, whereas antagonizing GH action through a GHa protects mice from OA development.