Shoulder:Rotator Cuff Pathology/Biology of Rotator Cuff Healing
Bullet Points
Despite advances in surgical reconstruction of chronic rotator cuff tears leading to improved clinical outcomes, failure rates of 13-94% have been reported. Reasons for this rather high failure rate include compromised healing at the bone-tendon interface, as well as the musculotendinous changes that occur after RC tears, namely retraction and muscle atrophy, as well as fatty infiltration. It is important to note that instead of a physiological enthesis, an abundance of scar tissue is formed during healing process. Even though cytokines have demonstrated the potential to improve rotator cuff healing in animal models, there is little information about the correct concentration and timing of the more than 1500 cytokines that interact during the healing process. There is only minimal evidence that platelet concentrates may lead to improvement in radiographic, but not clinical outcome. Using stem cells to biologically augment the reconstruction of the tears might have a great potential since these cells can differentiate into various cell types that are integral for healing.
Key Words
Biological augmentation, Rotator cuff healing, Stem cells, Growth factors, Scaffolds, Shoulder surgery, Platelet rich fibrin, Platelet concentrates, Mesenchymal stem cells, Fatty infiltration, Atrophy, Retraction.
Introduction
Pathologies of the rotator cuff are by far the most common cause of shoulder dysfunction and pain. In the presence of full thickness rotator cuff tears, rotator cuff reconstruction is a commonly performed surgical solution. Even though rotator cuff repair results in improved clinical outcome, several studies report failure of healing in up to 94% of patients.[1]
The reason for these high failure rates may be due to intrinsic degenerative changes of the musculotendinous unit. Subsequent to a tear, the muscle retracts, but this muscular retraction is significantly less then the degree of tendon retraction that occurs at later stages.[2][3]
In the tendon low cellularity, degenerative changes and poor blood supply of the enthesis are significant in the findings. Whilst in the muscle, there is significant migration of inflammatory cells within the first few days of a tear and the muscle fibers undergo apoptosis. In the ensuing weeks to months, this early response leads to muscular retraction, degeneration and atrophy. The progressive loss of muscle volume is due to a loss of sarcomeres in series that is associated with an increase in pennation angle which causes an enlargement of the inter- and intramyofibrillar spaces. If the muscle remains unloaded and retracted, the myogenic precursor cells may be reprogrammed into the adipogenic pathway, with mature adipocytes infiltrating the free inter- and intramyofibrillar spaces. This phenomenon is termed fatty infiltration.[4]
- ↑ Galatz LM, Ball CM, Teefey SA, Middleton WD, Yamaguchi K. The outcome and repair integrity of completely arthroscopically repaired large and massive rotator cuff tears. J bone Joint Surg Am 2004;86-A(2):219-24.
- ↑ Kuenzler MB, Nuss K, Karol A, Schär MO, Hottiger M, Raniga S, Kenkel D, von Rechenberg B, Zumstein MA. Neer Award 2016: reduced muscle degeneration and decreased fatty infiltration after rotator cuff tear in a poly(ADP-ribose) polymerase 1 (PARP-1) knock-out mouse model. J Shoulder Elbow Surg. 2017 May;26(5):733-744
- ↑ Lädermann A, Zumstein M, Kolo F, Grosclaude M, Koglin L, Schwitzguebel A. In Vivo Clinical and Radiological Effects of Platelet-rich Plasma on Interstitial Supraspinatus Lesion: Case Series. Orthop Traumatol Surg Res. 2016 Dec;102(8):977-982.
- ↑ Lundgreen K, Lian OB, Engebretsen L, Scott A. Tenocyte apoptosis in the torn rotator cuff: a primary or secondary pathological event? Br J Sports Med. 2011;45(13):1035-9.
