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Nicotine Delays Tendon-to-Bone Healing in a Rat Shoulder Model
L.M. Galatz, MD1; M.J. Silva, PhD1; S.Y. Rothermich, MA1; M.A. Zaegel, BS1; N. Havlioglu, MD1; S. Thomopoulos, PhD1
1 Department of Orthopaedic Research, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8233, St. Louis, MO 63110. E-mail address for L.M. Galatz: galatzl@wustl.edu
View Disclosures and Other Information
In support of their research for or preparation of this manuscript, one or more of the authors received grants or outside funding (Zimmer/OREF Career Development Award). None of the authors received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.
Investigation performed at the Department of Orthopaedic Surgery, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, Missouri

The Journal of Bone and Joint Surgery, Incorporated
J Bone Joint Surg Am, 2006 Sep 01;88(9):2027-2034. doi: 10.2106/JBJS.E.00899
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Abstract

Background: Many studies have shown that nicotine negatively impacts fracture healing and bone fusion processes. However, very little is known about its effect on tendon and ligament healing. The goal of the present study was to evaluate the effect of nicotine on tendon-to-bone healing.

Methods: Supraspinatus tendons in both shoulders of seventy-two rats were transected and repaired to the humeral head. Osmotic pumps were implanted subcutaneously, and nicotine or saline solution was delivered for ten, twenty-eight, or fifty-six days. Cell morphology was evaluated with use of histologic sections. Cells were counted, and proliferating cell nuclear antigen (PCNA) immunohistochemistry was performed to assess cellular proliferation. In situ hybridization was performed to measure type-I collagen mRNA expression. Biomechanical and geometric properties were assessed.

Results: Inflammation persisted longer in the nicotine group than in the saline solution group. Cellular proliferation was higher in the saline solution group than in the nicotine group at the early time-points. Type-I collagen expression was higher in the saline solution group at twenty-eight days. Mechanical properties increased over time in both groups. Maximum stress was significantly lower in the nicotine group than in the saline solution group at ten days. Maximum force was significantly lower in the nicotine group than in the saline solution group at twenty-eight days. Maximum force was significantly higher in the nicotine group than in the saline solution group at fifty-six days. Stiffness was not different between the groups at any time-point.

Conclusions: Nicotine caused a delay in tendon-to-bone healing in a rat rotator cuff animal model. Mechanical properties increased over time in both groups, but the properties in the nicotine group lagged behind those in the saline solution group. Chronic inflammation and decreased cell proliferation may partly explain the inferior biomechanical properties in the nicotine group as compared with the saline solution group.

Clinical Relevance: Failure of rotator cuff repair is a major clinical problem. The adverse effect of nicotine on rotator cuff healing noted in this clinically appropriate animal model may be an important clinical consideration.

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    Accreditation Statement
    These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Orthopaedic Surgeons and The Journal of Bone and Joint Surgery, Inc. The American Academy of Orthopaedic Surgeons is accredited by the ACCME to provide continuing medical education for physicians.
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