While impaired wound healing associated with Type I diabetes mellitus has been well-studied in skin tissue, the influence of this metabolic disorder on tendon healing and recovery has not been extensively investigated. Because tendons are known to have limited repair potential, we studied the tendon-healing process using a diabetic rat tendinitis model. We tested the hypothesis that diabetes influences the inflammatoryresponse, cell proliferation, and angiogenesis in injured Achilles tendons. Diabetes was induced by injecting streptozotocin at 45mg/kg of body weight. Non-diabetic rats as well as diabetic and insulin-treated diabetic animals were then injected with collagenase. The accumulation of inflammatory cells was quantified in transversal sections of Achilles tendon using immunohistochemical staining at days 0, 1, 3, 7, 14, and 28 post-trauma. The number of proliferative cells and the extent of neovascularization was also quantified in the paratenon and the core of the tendon at days 0, 3, 7, 14, and 28 post-trauma. Relative to non-diabetic and insulin-treated diabetic animals, the numbers of accumulated neutrophils and ED1⁺ and ED2⁺ macrophages in diabetic rats decreased by 46%, 43% and 52%, respectively, in the first 3 days post-injury compared to levels in non-diabetic and insulin-treated diabetic animals. The density of newly formed blood vessels decreased by 35% and 29% in the paratenon and the core of tendon, respectively, at days 3 and 7 post-injury. Lastly, the concentration of proliferative cells decreased by 34% in the paratenon at day 7 post-trauma in injured tendons from diabetic rats relative to non-diabetic rats. These results indicate that alterations in inflammatory, angiogenic, and proliferative processes occurred in the diabetic state which might eventually perturb tendon healing and remodeling.