We know that healing of a tendon wound takes place by an invasion of fibreblasts
from the surrounding tissues; the tendon itself has no intrinsic healing
capacity. lt was Potenza (1962) who proved that a traumatic suture of the tendons
within their sheath is followed by disintegration of the synovia and the
formation of granulation tissue. The tissue invades the tendon at those places
where its surface is wounded and forms new collagen which restores its continuity.
As soon as this scar tissue matures, the adhesions become looser and
the integrity of the sheath is repaired. Potenza (1963) also observed that when
contact between the tendon and its sheath is made impossible by the introduction
of polyethylene tubes or millipore, healing of the tendon wound is postponed
until granulation tissue has invaded the tube from its end and reached
the wound along the surface of the tendon. However, trauma is not always
restricted to a loss of continuity; circulatory loss may also occur and the consequences
of deprivation of a tendon's blood supply force us to study the role
of its circulation during healing
