Tendon

A tendon is a highly specialized anatomical structure composed of dense regular connective tissue that facilitates movement by connecting skeletal muscle to bone. Its primary biological function is the transmission of mechanical forces generated by muscle contraction to the skeletal system, while also serving as a resilient energy reservoir that protects muscles from damage (StatPearls, 2023). Structurally, tendons are dominated by a densely packed extracellular matrix consisting largely of Type I collagen fibers, which provide exceptional tensile strength. Although not a single molecular target like a receptor or enzyme, the tendon is a clinically significant site of drug-induced adverse effects and therapeutic focus. Certain classes of drugs, most notably fluoroquinolone antibiotics and corticosteroids, can compromise tendon integrity by disrupting tenocyte metabolism and promoting the activity of degradative enzymes (NIH, 2024). Pathological conditions such as tendinopathy involve a failure of the homeostatic repair process, characterized by collagen disorganization and hypervascularization, requiring treatments that aim to restore the mechanical and biochemical environment of the tissue.

Other names

SinewDense regular connective tissueTendo

Drugs affecting tendons typically modulate the extracellular matrix (ECM) turnover or inflammatory signaling within tenocytes. Fluoroquinolones are associated with increased expression of matrix metalloproteinases (MMPs) and reduced tenocyte proliferation, leading to matrix degradation (Kim et al., 2014). Corticosteroids provide short-term anti-inflammatory effects by inhibiting phospholipase A2 and pro-inflammatory cytokines, but they can impair collagen synthesis and reduce the mechanical integrity of the tendon with chronic use (Nichols et al., 2018). NSAIDs inhibit cyclooxygenase (COX) enzymes to reduce prostaglandin-mediated pain and inflammation during the acute phase of tendon injury (Bordoni & Varacallo, 2023).