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Commentary and Perspective

Make No Bones About It—Rotator Cuff Repair Healing Is Not Just About the Tendon

Commentary on an article by Shivam A. Shah, PhD, et al.: “Sclerostin Antibody Treatment Enhances Rotator Cuff Tendon-to-Bone Healing in an Animal Model”

Werner, Brian C. MD*

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The Journal of Bone and Joint Surgery: May 17, 2017 - Volume 99 - Issue 10 - p e52
doi: 10.2106/JBJS.16.01602
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Commentary

Rotator cuff tears are the most common musculoskeletal injury in the shoulder. Even with recent advances in repair techniques, there remains a high rate of tendon healing failure. Numerous factors have been correlated with failure to heal after rotator cuff repair, including patient and surgeon-related variables1.

As rotator cuff repair techniques have improved, failure of the tendon to heal is less likely to occur from weak fixation. More likely causes of failure include biologic factors such as lack of vascularity to the repaired tendon, fatty infiltration or atrophy of the muscle, intrinsic degeneration of the tendon, or decreased bone quality at the repair site2. Methods of biologic augmentation or enhancement have been increasingly the subject of recent investigations.

While a majority of studies in this area focus on improving the general biologic milieu through the use of platelet rich plasma, mesenchymal stem cells, or growth factors; improving the biomechanical qualities of the repaired tissue through the use of biologic scaffolds; or improving tendon tissue quality and healing, Shah et al. sought to improve the healing process by biologically mitigating bone loss at the rotator cuff repair site.

The authors should be commended for furthering the science of biologic augmentation of rotator cuff repair by investigating the less frequently discussed aspect of rotator cuff repair healing: the bone at the enthesis. In a rat model, the authors confirmed the findings from previous studies that rotator cuff injury and repair led to a reduction in bone mineral density (BMD) at the repair site up to 4 weeks postoperatively. Treatment with sclerostin antibody improved BMD at the repair site, which resulted in improved strength, construct stiffness, and integration of tendon to the bone by 8 weeks. Gene expression analysis demonstrated that this result appeared to be due to changes specific to the bone, rather than tendon.

The etiology of bone loss in the setting of rotator cuff injury and repair is likely multifactorial, potentially due to mechanical unloading after a tear occurs and to high osteoclast activity during the immediate postrepair period3,4. A previous approach to this problem has been to suppress osteoclast activity using bisphosphonate treatment. While this improved the mechanical properties of repair constructs, use of systemic bisphosphonates has been associated with several complications that may limit the clinical applicability of this approach.

The authors utilized a different approach, administering sclerostin antibodies to block sclerostin, a negative regulator of bone formation. The findings of the study are important, as they emphasize the importance of bone quality in healing after rotator cuff repair, and provide a novel potential avenue to modify this variable, which would be of particular use in aging patients or in more chronic rotator cuff tears.

There are limitations of this study that should be noted, mostly related to the ability to translate this approach clinically. As previously noted, bisphosphonates may not be appropriate for this problem because of systemic side effects. This study does not provide data on the systemic clearance of sclerostin antibody, or the potential systemic side effects of this treatment on remote locations other than at the repair site. The authors note that recent human clinical trials with sclerostin antibody have not demonstrated any deleterious effects. Lastly, the authors only assessed the effect of sclerostin antibody on early repair after an acute rotator cuff tear; further studies are needed to investigate this effect in a more chronic rotator cuff tear. In this scenario, the biology is typically more compromised, with greater demineralization at the enthesis, which may result in an even greater effect from sclerostin antibody treatment.

*Disclosure: The author indicated that no external funding was received for any aspect of this work. The Disclosure of Potential Conflicts of Interest form is provided with the online version of the article (https://links.lww.com/JBJS/D276).

References

1. Deprés-Tremblay G, Chevrier A, Snow M, Hurtig MB, Rodeo S, Buschmann MD. Rotator cuff repair: a review of surgical techniques, animal models, and new technologies under development. J Shoulder Elbow Surg. 2016 Dec;25(12):2078-85. Epub 2016 Aug 20.
2. Edwards SL, Lynch TS, Saltzman MD, Terry MA, Nuber GW. Biologic and pharmacologic augmentation of rotator cuff repairs. J Am Acad Orthop Surg. 2011 Oct;19(10):583-9.
3. Silva MJ, Ritty TM, Ditsios K, Burns ME, Boyer MI, Gelberman RH. Tendon injury response: assessment of biomechanical properties, tissue morphology and viability following flexor digitorum profundus tendon transection. J Orthop Res. 2004 Sep;22(5):990-7.
4. Killian ML, Cavinatto L, Shah SA, Sato EJ, Ward SR, Havlioglu N, Galatz LM, Thomopoulos S. The effects of chronic unloading and gap formation on tendon-to-bone healing in a rat model of massive rotator cuff tears. J Orthop Res. 2014 Mar;32(3):439-47. Epub 2013 Nov 14.

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