Maturational alterations in gap junction expression and associated collagen synthesis in response to tendon function

The Pathogenesis of Tendon Microdamage in Athletes: the Horse as a Natural Model for Basic Cellular Research

“…In both the SDFT and CDET, the cellularity reduces significantly during maturation (up to approximately 2 years of age) and then more gradually during ageing; in all age groups the SDFT is significantly more cellular than the CDET (Stanley et al, 2007;Young et al, 2009). Similarly in man, the adult AT is more cellular than the ATT (Birch, 2007).…”

Achilles Tendon Injuries in Elite Athletes: Lessons in Pathophysiology from Their Equine Counterparts

“…significantly more tenocytes (tendon fibroblasts; Figure 3) per unit area than the CDET (Stanley et al 2007). Although both tendons reduce collagen turnover with age, the CDET consistently maintains the higher level (Birch, Worboys, et al 2008); in adult tendons, the level of procollagen type I aminopropeptide (cleaved during collagen synthesis) is higher per square millimeter in the less cellular CDET (Young et al 2009). This is, of course, relative because tendons in general have extremely slow collagenous matrix metabolism; the half-life of collagen in the SDFT and CDET has been estimated at 197.5 and 34.0 years, respectively (Thorpe et al 2010).…”

“…This is, of course, relative because tendons in general have extremely slow collagenous matrix metabolism; the half-life of collagen in the SDFT and CDET has been estimated at 197.5 and 34.0 years, respectively (Thorpe et al 2010). Reductions in gap junction expression and communication have also been measured with maturation in the SDFT, suggesting a reduced capacity of the tenocyte network to coordinate matrix control (Young et al 2009). Measurement of retention of carbon-14 in people (those alive in the years 1955-1963 when nuclear bombs were tested) demonstrated almost no collagen turnover in the adult AT (Heinemeier et al 2013).…”

“…Responses of bone to exercise in both horses and people is relatively well understood, and significant data have been generated on possible positive effects of weight-bearing exercise during musculoskeletal development (defined as enhancement of bone mineral accretion and/or bone size) (Brama et al 2009;Firth et al 2011;Hind and Burrows 2007). Controlled studies of treadmillexercised foals and young adult horses have indicated that the situation in tendon tissue is significantly different, with little (if any) adaptation shown by the SDFT, even though the tenocytes are more synthetically active in immature tendon (Birch, Wilson, et al 2008;Moffat et al 2008;Young et al 2009). Acceleration of SDFT growth has been noted in exercised foals, but this normalizes by the time they reach maturity (Cherdchutham, Meershoek, et al 2001;Kasashima et al 2002).…”

“…Adult tendons are not highly cellular structures, with only 200 to 400 tenocytes per square millimeter in the SDFT (Stanley et al 2007). Additionally, the tenocytes are not active in turning over the extracellular collagenous matrix, and their linkage by gap junction communication reduces significantly with maturation (Young et al 2009). Given that this sparse cellular network must monitor and maintain very large amounts of extracellular matrix and that both are frequently subjected to mechanical conditions likely to cause fibrillar rupture (because of the need to stretch sufficiently to store enough elastic energy), the dysfunction and/or loss of even small numbers of tenocytes is likely to have a significant effect on repair ability.…”