Monday, July 9, 2018

Can "biologics" help rotator cuff repairs heal?

Biologic Therapies as Adjunctive Treatments in Rotator Cuff Repair

These authors point out that despite the application of new surgical techniques, failures of cuff repair continue to pose a challenge for orthopaedic surgeons and their patients.

They suggest that a poor biologic environment imay be partly responsible for the inadequate tissue healing associated with rotator cuff tear repairs. This has motivated a search for strategies involving the use of adjunctive biologic therapies, such as platelet-rich plasma (PRP), patches and scaffolds mesenchymal stem cells (MSCs), and cytokines.

However they conclude that the degree of short-term and long-term benefits of these therapies reported in the literature has varied and the indications for use of these approaches have not been established.

This review does not include the costs of these different approaches so it is not possible to determine their incremental value to the patient (i.e. the improvement in clinical outcomes divided by the increase in cost).

Comment: Healing of a failed rotator cuff tendon insertion is a huge challenge. Usually the cuff tear presents with residual tendon that lacks normal quality and quantity. In other words the tissue has less material strength and the normal tendon length is lost. To make matters worse, the cuff tear is bathed in joint fluid containing enzymes that interfere with scar tissue formation, the tendon is relatively avascular, and the loads on the attempted repair are large. And to top it off, the reconstruction of a physiologically and mechanically normal tendon attachment (see below) is highly unlikely in spite of good surgery and whatever biologics may be used. Thus the high rates of failure of cuff repairs are not unexpected.

Assembly, maturation, and degradation of the supraspinatus enthesis

The 4 zones of the normal enthesis: The tendon zone consists of elongated tenocytes. At the border to the fibrocartilaginous zone, the cells change from elongated fibroblasts to round chondrocytes, stacked in columns. The cells enlarge during the transition  from unmineralized to mineralized fibrocartilage. These hypertrophic cells are large cells imbedded in the mineralized matrix, gradually mineralizing the matrix. The mineralized fibrocartilage firmly anchors into the underlying trabecular bone tissue. The tidemark separates the 2 fibrocartilaginous zones.

These authors summarize the current knowledge about development and age-related degradation of the supraspinatus enthesis. Healing and repair of an injured and degenerated supraspinatus enthesis is a challenge, as the original graded transitional tissue of the fibrocartilaginous insertion is not re-created after the tendon is surgically reattached to bone.Instead, mechanically inferior and disorganized tissue forms at the healing site because of scar tissue formation. Consequently, the enthesis never reaches mechanical properties comparable to those of the native enthesis. So far, no novel biologic healing approach has been successful in enhancing healing of the injured enthesis.

Comment: Nature's design for the insertion of the supraspinatus tendon is a marvel of engineering. It provides a smooth mechanical transition from flexible tendon to stiff bone through the intermediate zones of unmineralized and then mineralized fibrocartilage. This structure is analogous to that of a modern electrical plug with transition from the flexible cord to the stiff metal blades.
This graduated transition is designed to prevent the failures associated with a sharp change from flexible to stiff seen in the old plug design.

When we try to repair a rotator cuff detachment, we are taking the degenerated edge of the tendon and attaching it directly to the stiff bone of the tuberosity.

The normal transition through unmineralized and mineralized fibrocartilage is lost and replaced by what the authors call "mechanically inferior and disorganized tissue at the healing site" resulting from scar tissue formation".

Given that we are attempting a repair because of failure of the original tendon insertion to bone, it is not surprising that the inferior tissue at the healing site is at risk for failure as well.

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