Connective tissue ageing is accelerated by the progressive accumulation of advanced glycation end products (AGEs). The formation of AGEs is characteristic for diabetes mellitus (DM) progression and affects only specific proteins with relatively long half-lives. This is the case of fibrillar collagens that are highly susceptible to glycation. While collagen provides a framework for plenty of organs, the local homeostasis of specific tissues is indirectly affected by glycation. Among the many age- and diabetes-related morphological changes affecting human connective tissues, there is concurrently reduced healing capacity, flexibility, and quality among ligaments, tendons, bones, and skin. Although DM provokes a wide range of known clinical disorders, the exact mechanisms of connective tissue alteration are still being investigated. Most of them rely on animal models in order to conclude the patterns of damage. Further research and more well-designed large-cohort studies need to be conducted in order to answer the issue concerning the involvement of ligaments in diabetes-related complications. In the following manuscript, we present the results from experiments discovering specific molecules that are engaged in the degenerative process of connective tissue alteration. This review is intended to provide the report and sum up the investigations described in the literature concerning the topic of ligament alteration in DM, which, even though significantly decreasing the quality of life, do not play a major role in research.
Keywords: AGEs; ROS; comorbidities; connective tissue; diabetes ligaments; diabetes mellitus; diabetes mellitus complications; ligaments alteration; orthopaedic surgery.