Abstract
Articular cartilage is composed of chondrons within a territorial matrix surrounded by a highly organized extracellular matrix comprising collagen II fibrils, proteoglycans, glycosaminoglycans, and non-collagenous proteins. Damaged articular cartilage has a limited potential for healing and untreated defects often progress to osteoarthritis. High hopes have been pinned on regenerative medicine strategies to meet the challenge of preventing progress to late osteoarthritis. One such strategy, autologous chondrocyte implantation (ACI), was first reported in 1994 as a treatment for deep focal articular cartilage defects. ACI has since evolved to become a worldwide well-established surgical technique. For ACI, chondrocytes are harvested from the lesser weight bearing edge of the joint by arthroscopy, their numbers expanded in monolayer culture for at least four weeks, and then re-implanted in the damaged region under a natural or synthetic membrane via an open joint procedure. We consider the evolution of ACI to become an established cell therapy, its current limitations, and on-going strategies to improve its efficacy. The most promising developments involving cells and natural or synthetic biomaterials will be highlighted.
Highlights
Articular cartilage acts as a cellular cushion, ensuring that our joints withstand the physical and mechanical demands of everyday life
Each chondrocyte is surrounded by a 2–4 μm thick collagen VI-rich pericellular matrix (PCM) forming a chondron [1,2]
Chondrons are surrounded by a territorial matrix and a highly organized extracellular matrix (ECM) comprising collagens, proteoglycans, glycosaminoglycans (GAGs), and non-collagenous proteins [6,7]
Summary
Articular cartilage acts as a cellular cushion, ensuring that our joints withstand the physical and mechanical demands of everyday life. Each chondrocyte is surrounded by a 2–4 μm thick collagen VI-rich pericellular matrix (PCM) forming a chondron [1,2]. With increasing depth from the articular surface, there are four architectural zones (Figure 1) with striking variations in both chondrocytes and their surrounding ECM [8]. The amounts of proteoglycans and GAGs vary with depth; their concentrations greatest in the middle to deep zones [9,10]. 3. TSehveeSraulrsguicraglicSatlraatpepgrioesacfhoersTerxeiasttintog rCeapratiirladgaemInagjuerdyarticular cartilage (Table 1) with variable outcomes due to factors associated with the individual’s demographics, the injury, and any previous surgicaSl epvreorcaeldsuurregsic[1a4l,a1p5]p.rWoahcehnescheoxiosstintog rtehpeasiur rdgaicmaal gaepdpraoraticchu,liatriscaimrtiplaogreta(nTtafbolreth1)ewsuitrhgevoanritaoble conosuitdceormthese dinudeivtoidfuacatlonreseadsssoocfiathteedpwatiitehntt,hwe iinthdrivesidpuecatl’tsodtehme ojoginratpthhaictsi,sthafefeinctjuedrya,nadndthaenpyaptireenvti’osus hosbubrigeiscaalnpdrloicfeesdtuyrlee.s C[1o4n,1s5e]q. What works for one patient, may lead to a different outcome in another
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