Abstract
A study was made of collagen fibril populations in healing tendon using a window lesion in rat extensor tendon. Two environments were thus created. One (the lesion area) where stress levels were reduced; the other (the non-lesion area) where stress levels were increased. In both areas a population of small diameter (<50nm) collagen fibrils were synthesized. Lesion area fibrils increased their diameter only slowly. Non-lesion area fibrils added to a population which increased its diameter distribution comparatively rapidly. It is suggested that in the lesion area fibrils were synthesized in response to tissue damage and low levels of stress. These may be of type III collagen. In the non-lesion area fibrils were synthesized in response to raised levels of stress. These may be of type I collagen. Implications of these events, especially as they might relate to gap formation in flexor tendon surgery are discussed.
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