BACKGROUND INFORMATION Tendon injuries are extremely common and encountered frequently in all manual medicine settings, including chiropractic offices. Many years ago, the pain in chronic tendon overuse injuries was believed to be the direct result of a chronic inflammatory process, but because inflammatory cells could be consistently demonstrated in damaged tendons, the opinion changed from inflammation (implied by the older term ‘‘tendinitis’’) to degeneration (represented by the newer terms ‘‘tendinosis’’ or “tendinopathy”). There is controversy, however – although most histologic findings in tendinopathy represent chronic degeneration, regeneration, and microtears of the tendinous tissue, newer studies using immunohistochemistry and flow cytometry have shown inflammatory cells. The goal of this review paper was to discuss these findings in the framework of a new continuum pathology model for load-induced tendinopathies. General Considerations In general, tendon injuries can occur in the mid-tendon or at the attachment of the tendon to the bone, also called the enthesis. Although the mid-portion and insertion sites of tendons are structurally different when normal, the onset of pathology creates cell and matrix alterations that are virtually indistinguishable. That being said, the reader should be reminded that in some regions (specifically the Achilles) – insertional and mid-portion tendinopathies respond differently to the same treatment intervention. Despite the obvious importance of load in tendon injuries, it is rarely considered when implementing treatment – the authors propose that their model will take this into account and assist the clinician to tailor treatment to the pathology. The authors propose the following pathological continuum model that has three phases:j 1. Reactive Tendinopathy 2. Tendon Disrepair (failed healing) 3. Degenerative Tendinopathy CONCLUSIONS AND PRACTICAL APPLICATIONS The authors of this paper have presented a simple and succinct model for load-induced tendinopathy that appropriately includes contemporary, multidisciplinary literature on this topic. The authors wisely reiterate that this is merely a model of pathology, and that clinicians should remember that load tolerance and soft tissue healing are individual factors with wide variability. That being said, they have provided an excellent and simple framework for us to work with. They also emphasize the need for more research on early-stage tendon pathology, the area that is currently most lacking. •