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Osteoarthritis Cartilage. 2017 Sep;25(9):1551-1562. doi: 10.1016/j.joca.2017.05.007. Epub 2017 May 19.

Matrix replenishing by BMSCs is beneficial for osteoarthritic temporomandibular joint cartilage.

Author information

1
State Key Laboratory of Military Stomatology, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center for Oral Diseases, Department of Oral Anatomy and Physiology and TMD, School of Stomatology, The Fourth Military Medical University, 145 Changle West Road, Xi'an, China.
2
Department of Biology, The Fourth Military Medical University, 17 Changle West Road, Xi'an, China.
3
Department of Biology, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China; Department of Biochemistry, Rush University Medical Center, Chicago, IL 60612, USA.
4
State Key Laboratory of Military Stomatology, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center for Oral Diseases, Department of Oral Anatomy and Physiology and TMD, School of Stomatology, The Fourth Military Medical University, 145 Changle West Road, Xi'an, China. Electronic address: mqwang@fmmu.edu.cn.

Abstract

OBJECTIVES:

The present goal was to explore whether matrix replenishment is the primary requirement for osteoarthritic (OA) cartilage.

METHODS:

Cells isolated from the superficial and deep zone cartilage of a pig temporomandibular joint (TMJ) were exposed to fluid flow shear stress (FFSS). Differences in matrix production and cellular differentiation were detected. Unilateral anterior crossbite (UAC) was applied to C57BL/6J female mice. Green fluorescent protein-labeled exogenous bone marrow stromal cells (GFP-BMSCs) were injected weekly into TMJs, starting from 3 weeks of UAC stimulation and continuing for 4-, 8- and 12-weeks. Another GFP-BMSCs injection UAC group stopped receiving injections for 4-weeks after 8-weeks of injections. Assessments were focused on morphological alterations in UAC mouse TMJ cartilage, the expression levels of DAP3, an anoikis marker, CD163, a scavenger receptor family member, and ki67, a proliferation indicator.

RESULTS:

FFSS down-regulated type-II collagen expression but stimulated terminal differentiation in cells isolated from deep zone cartilage. It down-regulated aggrecan expression but up-regulated type I collagen in cells isolated from both superficial and deep zones. UAC caused matrix loss and anoikis and enhanced scavenging activity in deep zone chondrocytes without affecting cell proliferation. Superficial fibrillation was obvious in the late stage. Weekly injections of BMSCs largely restored these changes. The implanted BMSCs expressed a high level of CD163 protein but did not show remarkable cell proliferation. Terminating the supply of exogenous BMSCs reversed the restorative effects.

CONCLUSIONS:

Scavenging the degraded matrix and replenishing the fibrosis-developmental matrix are the primary requirements for the repair of OA cartilage.

KEYWORDS:

Bone marrow mesenchymal stem cells; CD163; Cartilage; Osteoarthritis; Temporomandibular joint

PMID:
28532603
DOI:
10.1016/j.joca.2017.05.007
[Indexed for MEDLINE]
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