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Abstract

252 ACL = anterior cruciate ligament; bFGF = basic fibroblast growth factor; FDP = flexor digitorum profundus; TGF = transforming growth factor; VEGF = vascular endothelial growth factor; VEGFR = vascular endothelial growth factor receptor. Arthritis Research Vol 4 No 4 Fenwick et al. IntroductionEvidence exists that tendon repair can occur either intrinsically via the resident tenocytes [1,2] or via extrinsic mechanisms, whereby cells from the surrounding sheath or synovium invade the tissue [3]. It seems likely that both mechanisms occur, although the involvement of external cells depends on the site of injury and vascular perfusion. Many in vivo animal studies have been performed on the ability of tendon to repair following laceration, transection and other models of injury [4][5][6][7]. A large number of in vitro studies on animal and human tendon have also been performed [1,2,8,9]. The roles of many factors in tendon repair have been examined, including cell proliferation and DNA synthesis [10,11], collagen [11], noncollagenous protein [12] and proteoglycan synthesis [13]. Intratendinous degenerative change is strongly associated with both chronic tendinopathies and spontaneous tendon rupture [14][15][16][17].Degeneration and subsequent rupture of tendons has been associated with hypovascularity of specific regions within certain tendons [18,19]. A permanent disruption of the central blood vessels to normal tendons has been shown to cause cellular death and disintegration of collagen bundles [20]. Contradictory to this, however, would appear to be the finding that in many cases of chronic tendinopathy that have been examined histologically, there is an 'angiofibroblastic' response, and the presence of many large blood vessels [21][22][23]. The presence of blood vessels was not considered to be an indication of tissue repair [22]. What then is the role of a proliferative vasculature in the damaged tendon?The aim of this review is to discuss the importance of the vasculature in tendon damage and repair, and what is known about factors that regulate changes in the vasculature of what is normally a sparsely vascularised tissue. Tendon vasculatureDuring development, tendons are highly cellular and metabolically active, and are thus supplied with a rich capillary network [20]. Mature tendons, however, are poorly vascularised [24][25][26]; tendon nutrition is more reliant on synovial fluid diffusion than vascular perfusion [27], although they do have more blood vessels than is commonly accepted. Like any other connective tissue, tendon does not undergo neovascularisation under normal circum- ReviewThe vasculature and its role in the damaged and healing tendon AbstractTendon pathology has many manifestations, from spontaneous rupture to chronic tendinitis or tendinosis; the etiology and pathology of each are very different, and poorly understood. Tendon is a comparatively poorly vascularised tissue that relies heavily upon synovial fluid diffusion to provide nutrition. During tendon injury, as with damage to any t...

Effects of Neuromobilization on Tendinopathy: Part I

“…15 Neovascularization is the proliferation of blood vessels to the tendon, not associated with tendon repair. 15 Researchers have theorized that neovascularization of the paratenon leads to a disturbance in blood supply to the tendon, causing ischemic pain during exercise. 15 Without appropriate testing, a clinician cannot diagnose a pathological tendon with neovascularization based on patient symptoms.…”

“…16 The vascular theory may account for potential causative factors for degeneration of a tendon but fails to address other tendinopathy issues, such as why adolescents would be predisposed to neovascularization in a growing tendon 11 despite an abundance of cellular and metabolic activity. 15 The neural theory includes several components that may lead to tendon pathology. 11 Increased stresses and tension on nerves will result in altered or ceased blood flow to the nerve, which will influence blood supply to the tendon.…”

“…15 Researchers have theorized that neovascularization of the paratenon leads to a disturbance in blood supply to the tendon, causing ischemic pain during exercise. 15 Without appropriate testing, a clinician cannot diagnose a pathological tendon with neovascularization based on patient symptoms. For example, patients that present with pain and stiffness in a tendon are likely to have a diagnosis of tendinopathy without diagnostic testing being performed; therefore, a clinical diagnosis of neovascularization could not be determined.…”

“…11 The natural disposition of the vascular system may predispose specific portions of the tendons to degeneration. 15 For instance, a mature Achilles tendon has poor vascular supply to the distal portion of the tendon (i.e., two to six centimeters above the insertion). 15 Neovascularization is the proliferation of blood vessels to the tendon, not associated with tendon repair.…”

“…15 For instance, a mature Achilles tendon has poor vascular supply to the distal portion of the tendon (i.e., two to six centimeters above the insertion). 15 Neovascularization is the proliferation of blood vessels to the tendon, not associated with tendon repair. 15 Researchers have theorized that neovascularization of the paratenon leads to a disturbance in blood supply to the tendon, causing ischemic pain during exercise.…”