Adipose tissue releases several bioactive peptides and hormones, like adipokines that promote a low inflammatory systemic state. Inflammation, affecting the tendon homeostasis, could play a role in tendon disease development as well as in the healing process. Obese patients show a dysregulated level of adipokines and considering the higher mechanical demand, this relates to higher incidence of tendinopathies among these subjects.

A systematic review was performed searching PubMed, Embase and Cochrane Library databases. Inclusion criteria were studies of any level of evidence published in peer-reviewed journals reporting clinical or preclinical results. Evaluated data were extracted and critically analysed. PRISMA guidelines were applied, and risk of bias was assessed, as was the methodological quality of the included studies. We excluded all the articles with high risk of bias and/or low quality after the assessment.

After applying the previously described criteria, we included 12 articles assessed as medium or high quality. Leptin, others adipokines and in general changes in the hormones delicate equilibrium affect the tendon either qualitatively and/or quantitatively. The evidence still lacks consensus on their role which is probably involved in both anabolic and catabolic pathways.

The role of adipokines in the structure and healing of tendons is still debated. Further studies are needed to clarify the relation between deregulated levels of adipokines and the development of tendinopathy. A better understanding of the molecular interactions could allow us to individuate future therapeutic targets.

Obese patients show a higher incidence of tendon-related pathologies. These patients present a low inflammatory systemic environment and a higher mechanical demand which can affect the tendons. In addition, inflammation might have a role in the progression of the disease as well as in the healing process.

A systematic review was performed by searching PubMed, Embase and Cochrane Library databases. Inclusion criteria were studies of any level of evidence published in peer-reviewed journals reporting clinical or preclinical results. Evaluated data were extracted and critically analysed. PRISMA guidelines were applied, and risk of bias was assessed, as well as the methodological quality of the included studies. We excluded all the articles with high risk of bias and/or low quality after the assessment. Due to the high heterogeneity present among the studies, a metanalysis could not be done. Thus, a descriptive analysis was performed.

After applying the previously described criteria, thirty articles were included, assessed as medium or high quality. We analysed the data of 50865 subjects, 6096 of which were obese (BMI over 30 accordingly to the WHO criteria). The overall risk of re-tear after surgery is about the 10% more than normal BMI subjects. The rupture risk fluctuates in the studies without showing a significant trend.

Obese subjects have a higher risk to develop tendinopathy and a worse outcome after surgery as confirmed in several human studies. The obesity influence on tendon structure and mechanical properties may rely on the fat tissue endocrine proprieties and on hormonal imbalance.

Clinicians should consider obesity as a predisposing factor for the development of tendinopathies and for a higher risk of complications in patients who underwent surgical repair of tendons.