The Role of Mechanobiology in the Attachment of Tendon to Bone - Structural Interfaces and Attachments in Biology - page 238

tissue that forms at the interface has a larger volume than the native tissue, but is
functionally inferior. This may be explained by the dramatic decrease in the amount
of underlying bone and the loss of collagen fiber organization [ 125 - 128 ]. These
factors are compounded in the case of a chronic rupture, which is typically
accompanied by significant degeneration prior to injury, increasing the difficulty
of repair and the risk of re-rupture. While many factors contribute to the observed
decrease in tissue functional behavior, the main distinction between a healing and a
normal insertion is the near complete loss of transitional tissue in the enthesis.
11.5.2 Precise Control of Loading Is Needed
to Improve Healing
Immobilization of the limb or joint after a repair is often utilized to prevent disruption
of the recently reattached tissues during the early stages of healing. As previously
described, immobilization can have undesired effects on the nearby uninjured muscu-
loskeletal tissues, which require precisely defined loading conditions to maintain their
structure and composition. Due to this, a delicate balance between periods of immo-
bilization and controlled remobilization must be used to maximize healing while
reducing unwanted damage to nearby musculoskeletal tissues.
The role of cast immobilization in tendon-to-bone healing has been investigated
in a series of studies using a rat rotator cuff tendon model [ 7 , 130 - 132 ]. Tendons
were surgically transected and reattached to the bony insertion, then assigned cast
immobilization, cage activity, or treadmill exercise for post-operative recovery. All
interfaces healed by a fibrovascular scar without evidence of a functionally graded
transitional tissue and an increased tendon cross-sectional area compared to normal
uninjured controls. The exercised group had a significantly larger cross-sectional
area compared to the cast immobilized group. Acute injury and repair diminished
the functional biomechanical performance of the bone tendon interface for all
injury groups compared to controls. The exercise group had less favorable mechan-
ical properties, collagen fiber alignment, and matrix composition than the cast
immobilized group. Furthermore, the increased joint stiffness due to post-operative
immobilization was eventually resolved [ 132 ]. Finally, passive motion after surgery
instead of exercise also increases joint stiffness [ 131 ]. The results of these studies
suggest that exercise is detrimental to healing in a rat rotator cuff, as it results in
more material accumulation at the healing interface with less desirable structural
and mechanical properties.
A possible mechanism for the poor healing observed with exercise has recently
been suggested by studies using a rat model of ACL reconstruction [ 133 - 135 ].
Cytokines produced by macrophages have been implicated in tendon-to-bone
healing and reducing the number of macrophages improves the biomechanical
behavior of the interface. Furthermore, immobilization seems to also block macro-
phage recruitment, thus contributing to improved interface healing [ 133 ].