The Effect of Vascularization on Avian Flexor Tendon Repair

Cc, Kain; Je, Russell; Burri, R; Dunlap, Janet; McCarthy, John A.; Pr, Manske

doi:10.1097/00003086-198808000-00036

Cited by 13 publications

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“…These results are in contrast to those previously reported for tendon explants cultured with serum (23,35). Kain and associates (15), however, reported a reduction in tendon collagen content during the first 3 weeks of flexor tendon healing in vivo.…”

Section: Discussioncontrasting

confidence: 99%

“…This was the result of a combined decrease in absolute collagen synthesis and an increase in absolute NCP synthesis. A decrease in relative collagen synthesis was reported during flexor tendon repair in vivo (15). With time in culture, fibroblasts lose their ability to maintain high levels of collagen production, which has been suggested to illustrate "normal" development of tendons (34).…”

Section: Discussionmentioning

confidence: 96%

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Long‐term explant culture of rabbit flexor tendon: Effects of recombinant human insulin‐like growth factor‐I and serum on matrix metabolism

Abrahamsson

Lundborg

Lohmander

1991

Journal Orthopaedic Research

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Summary:The effects of human recombinant insulin-like growth factor-I (rhIGF-I, 50 ng/ml) on matrix metabolism in the deep flexor tendon from the tendon sheath region of the rabbit were studied in explants cultured for 3 weeks. Tendon segments cultured in medium supplemented with fetal calf serum (FCS) exhibited proliferation of the superficial cell layers. Synthesis of proteoglycan and non-collagen protein (NCP) increased threefold during the first week and remained elevated during the next 2 weeks of culture in medium supplemented with rhIGF-I or FCS, but not in medium without supplements (bovine serum albumin, BSA). The estimated halflife (t%) for elimination of newly labeled proteoglycans from the tendon explants ranged from 5.1 to 8.5 days and from 4.9 to 6.8 days for NCP in supplemented medium. Presence of rhIGF-I or FCS did not affect degradation of matrix as compared with BSA. The total hexosamine content per tendon segment was stable during the culture period, but the non-collagen protein content decreased by 25%. Collagen synthesis decreased to 10% of the initial level after 3 weeks in supplemented medium, but to 3% in unsupplemented medium. There was no measurable turnover of collagen in explants cultured in either medium, and the collagen content remained unchanged. Our results suggest that rhIGF-I, as well as FCS, stimulates matrix synthesis but does not influence matrix turnover in rabbit flexor tendon explants in long-term culture as compared with medium without supplements. We conclude that rhIGF-I may be used as a defined growthpromoting factor in serum-free media and may be of importance in tendon healing. Key Words: Recombinant human insulin-like growth factorTendon-Proteogly can-Collagen-Turnover.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 96%

Long‐term explant culture of rabbit flexor tendon: Effects of recombinant human insulin‐like growth factor‐I and serum on matrix metabolism

Abrahamsson

Lundborg

Lohmander

1991

Journal Orthopaedic Research

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“…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 - 7 ]. A large number of in vitro studies on animal and human tendon have also been performed [ 1 , 2 , 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Untitled

2002

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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...

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“…An environment enriched in HA has been associated with cell migration in developing and remodelling tissues (Toole, 1991), indicating a role for HA during development and tissue repair. Like other tissues, healing tendons contain increased amount of HA during the ®rst week after repair (Kain et al, 1988). Exogenous application of hyaluronic acid has also been proposed to decrease the formation of adhesions after tendon surgery (Amiel et al, 1989;Hagberg and Gerdin 1992;St Onge et al, 1980;Thomas et al, 1986;Weiss et al, 1987), but the anti-adhesive eects of HA have been questioned by others (Green et al, 1986;Hagberg 1992;Meyers et al, 1989).…”

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confidence: 99%

Hyaluronic Acid Modulates Cell Proliferation Unequally in Intrasynovial and Extrasynovial Rabbit Tendons In Vitro

Wiig

Abrahamsson

2000

Journal of Hand Surgery

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As tendons differ in biochemical composition and cellular capacities, we have compared dose response effects of hyaluronic acid on cell proliferation and synthesis of matrix components in intermediate and proximal segments of intrasynovial deep flexor tendons and extrasynovial peroneus rabbit tendons in vitro. Compared with matched control tendons, hyaluronic acid inhibited cell proliferation in intermediate and proximal intrasynovial flexor tendon segments at the concentrations of 0.1-2.0 mg/ml and 0.5-2.0 mg/ml respectively, but in extrasynovial tendon segments only at the concentration of 0.5 mg/ml. Hyaluronic acid did not affect synthesis of proteoglycan, collagen and non-collagen protein in either type of tendon. These results show that hyaluronic acid modulates cell proliferation unequally in intra- and extrasynovial tendons without affecting the synthesis of matrix components in the two types of tendons, indicating differential hyaluronic acid sensitivity and a possible mechanism of action.

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The Effect of Vascularization on Avian Flexor Tendon Repair

Cited by 13 publications

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Long‐term explant culture of rabbit flexor tendon: Effects of recombinant human insulin‐like growth factor‐I and serum on matrix metabolism

Long‐term explant culture of rabbit flexor tendon: Effects of recombinant human insulin‐like growth factor‐I and serum on matrix metabolism

Untitled

Hyaluronic Acid Modulates Cell Proliferation Unequally in Intrasynovial and Extrasynovial Rabbit Tendons In Vitro

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