Resumo: Objetivo Avaliar a influência de polimorfismos nos genes que codificam o colágeno tipo I e a suscetibilidade genética da tendinopatia. Metodologia Estudo caso-controle envolvendo 242 atletas brasileiros de diferentes modalidades esportivas (55 casos de tendinopatia e 187 controles). Os polimorfismos COL1A1 (rs1107946) e COL1A2 (rs412777, rs42524 e rs2621215) foram analisados pelo sistema TaqMan. As razões de chance (OR) com seus intervalos de confiança (IC) de 95% foram calculadas usando um modelo de regressão logística não-condicional. Resultados A média de idade foi de 24,0 ± 5,6 anos e 65,3% eram homens. Dos 55 casos de tendinopatia, 25,4% apresentaram mais de um tendão acometido, sendo os mais frequentes o patelar (56,3%), o manguito rotador (30,9%) e o do cotovelo ou flexores das mãos (30,9%). A idade e o tempo de prática esportiva foram associados a uma maior chance de apresentar tendinopatia (5 e 8 vezes, respectivamente). A frequência dos alelos variantes nos controles e casos, respectivamente, foi: COL1A1 rs1107946 24,0 e 29,6%; COL1A2 rs412777 36,1 e 27,8%; rs42524 17,5 e 25,9%; e rs2621215 21,3 e 27,8%. Após ajuste pelos fatores de confundimento (idade e anos de práticas esportiva), os polimorfismos COL1A2 rs42524 e rs2621215 foram associados a um risco aumentado de tendinopatia (OR = 5,5; IC95% = 1,2–24,6 e OR = 3,9; IC95% = 1,1–13,5, respectivamente). O haplótipo COL1A2 CGT foi associado a um baixo risco para desenvolvimento da doença (OR = 0,5; IC95% = 0,3–0,9). Conclusão A idade (≥ 25 anos), o tempo de prática esportiva (≥ 6 anos) e polimorfismos no gene COL1A2 aumentaram o risco de desenvolvimento da tendinopatia.

Background/Objectives: Tendon structure is predominantly composed of the extracellular matrix (ECM), and genetic variants in non-collagenous ECM components may influence susceptibility to tendinopathy. We investigated the potential influence of single nucleotide polymorphisms (SNPs) in fibrillin-2 (FBN2), tenascin-C (TNC), and matrix metalloproteinase-3 (MMP3) on the tendon regeneration failure phenotype and impact on the susceptibility to tendinopathy in Brazilian high-performance athletes. Methods: This case–control study was conducted with 397 high-performance athletes from different sports modalities (197 tendinopathy cases and 200 controls), and they were analyzed by validated TaqMan^TM SNP genotyping assays of the SNPs FBN2 (rs331079), TNC (rs2104772), and MMP3 (rs591058). Results: Out of the 197 tendinopathy cases, 63% suffered from chronic tendon pain and 22% experienced more than three episodes of disease manifestation. The TNC-rs2104772-A allele was significantly associated with tendinopathy (OR: 1.4; 95% CI: 1.1–1.8), while athletes carrying the MMP3-rs591058-T allele were linked to an increased risk of more episodes of disease manifestation (OR: 1.7; 95% CI: 1.1–2.8). The TNC-MMP3 tendon regeneration failure phenotype (TNC-A/MMP3-T) was associated with an increased risk of tendinopathy (OR: 1.4; 95% CI: 1.1–2.0) and episodes of disease manifestation (OR: 2.0; 95% CI: 1.2–3.5). Athletes with tendinopathy who had the TNC-A/MMP3-T interaction were more prone to experiencing more than three disease exacerbations (OR: 4.3; 95% CI: 1.8–10.5) compared to TNC-A/TNC-C. Conclusions: This study suggests that rs2104772 and rs591058 SNPs could be involved in the tendon regeneration failure phenotype and may influence the molecular mechanism related to the regulation of the tendon ECM during training workload.

Describe the results of proximal humeral fractures surgically treated with the Philos locking plate system. Between March 2003 and October 2004 we prospectively reviewed 24 of 26 patients with proximal humerus fractures treated with a Philos plate. The mean follow-up time was 12 months and the mean age of patients was 57 years. Six patients had four-part proximal humerus fractures, 11 patients had three-part proximal humerus fractures, and nine patients had two-part proximal humerus fractures. Clinical evaluation was performed using the University of California at Los Angeles (UCLA) criteria. The mean UCLA score was 30 points (17-34). All fractures showed union. Three patients showed fracture union at varus position. The mean UCLA score for these patients was 27 points. Osteosynthesis with Philos plate provides a stable fixation method with good functional outcome.

Maximal oxygen uptake ($\stackrel{.}{\mathrm{V}}$O₂max) assesses athletic performance; however, its values are inconsistent in post-COVID-19 athletes. This study aimed to analyze the dynamics of $\stackrel{.}{\mathrm{V}}$O₂max in post-COVID-19 athletes. Observational studies were identified by screening the PubMed database published up to 17 July 2023. The initial electronic search found 320 studies. Of these, 26 employing the cardiopulmonary exercise test (CPET) to assess aerobic fitness were selected. Of the 2625 pooled athletes, 1464 were infected and considered as the post-COVID-19 group, either asymptomatic or symptomatic, while the remaining 1161, who were uninfected or had $\stackrel{.}{\mathrm{V}}$O₂max results prior to infection, were defined as the infection-free group. Age and $\stackrel{.}{\mathrm{V}}$O₂max were differently distributed between post-COVID-19 athletes and those without infection (p = 0.03 in both). Persistent symptoms athletes had 8 mL/Kg/min lower $\stackrel{.}{\mathrm{V}}$O₂max than those without infection (p = 0.04). In addition, post-infected athletes who underwent CPET after 12 weeks showed a significant reduction of 2.9 mL/Kg/min in $\stackrel{.}{\mathrm{V}}$O₂max according to the increase in body mass index (BMI). The pooled analysis showed that aerobic fitness was reduced in athletes post-COVID-19. $\stackrel{.}{\mathrm{V}}$O₂max was negatively correlated with BMI in those who underwent CPET at 12 weeks, suggesting that symptoms persist beyond 12 weeks, affecting return-to-play.