Tendons are designed to transmit the force of muscle contraction to bone, but they can also be positional or power structures. A sheath, where present and a surface paratenon are repositories for blood vessels and nerves. These structures penetrate inward to the epitenon, then endotenon and finally fascicle bundles. Each anatomic layer is replete with a tenocyte population distinct from the other group (Banes et al., 1998). Tenocyte surface cells (TSCs) differ from internal tenocytes (TIFs) that integrate with collagen fibrils and fascicles. TSCs are more stellate and spread, secrete fibronectin and PG4 (lubricin) and, as determined by gene array, have a different transcriptome from TIFs (Banes et al., 2004). TIFs are more spindle shaped, make collagen and are intimate with fibrils. Biomarkers for tendon are few compared to those for bone and cartilage, but recently, scleraxis (Scx), a basic helix-loop-helix transcription factor, and tenomodulin (TNMD), driven by Scx, have been identified with tendon development (Schweitzer et al., 2001). No concordance on TNMD function has been reached, but mature as well as developing TSCs and TIFs express TNMD. A TNMD KO mouse showed a mild collagen phenotype with larger, but less well organized fibrils, decreased cell proliferation, but no other problems (Docheva et al., 2005).

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