Copyright © 2006 by The Journal of Bone and Joint Surgery, Inc.
Commentary & Perspective
Commentary & Perspective by
Theodore I. Malinin, MS, MD*,
Department of Orthopaedics and Rehabilitation, University of Miami, Miami, Florida
The trauma of surgery leads one to marvel at the
recuperative capacity of the human body. Soft tissues are burned, compressed, drilled, cut, reamed, rendered ischemic, and subjected to many
other insults, yet eventually heal with minimal sequelae. However, as with any
biological phenomena, there are always exceptions. In orthopaedic surgery,
cartilage is such an exception. Cartilage is different. It is a complex structure
with complex dynamics1. A cut in the articular cartilage, be it
inflicted with a knife or a cautery, will not heal and will persist through the
life of the individual. Articular cartilage will heal only if subchondral bone
is involved, but, even then, the defect will be filled with fibrocartilage2.
The matter is further complicated by the intimate relationship between
cartilage and subchondral bone; if contact between subchondral bone and
articular cartilage is interrupted, the cartilage will die with time3.
Borazjani and colleagues provide another clear-cut example
of the vulnerability of articular cartilage. Fresh osteochondral cylindrical
autografts and allografts were used to fill osteochondral defects and were
subjected to high compression forces during insertion. The impact forces
resulted in cell death in all zones of articular cartilage. However, the damage
was most severe in the superficial layer. The authors postulate that the cell
death occurred by apoptosis, followed by DNA fragmentation.
As interesting and instructive as their study is, it has
some limitations. One of the most serious limitations is the selection of the
material to be tested. The osteochondral plugs used in this study were obtained
from six human cadavers with a postmortem interval of up to seventy-two hours.
This is at variance with clinical practice. For the purpose of clinical
transplantation, osteochondral allografts are excised within a twenty-four-hour
postmortem interval. It is possible that the additional postmortem degradation
had rendered these chondrocytes more susceptible to injury than their fresh
counterparts were. The rate of creep and recovery vary depending on
permeability and the rate of increase of deformation4. Cartilage
that is removed seventy-two hours postmortem has likely been subjected to fluid
inhibition. The second problem is, of course, the in vitro nature of the
experiments. It would be interesting to compare in animals the results obtained
with osteochondral allografts inserted with and without application of
compressive force. The similarity between human and monkey cartilage makes the
nonhuman primate models attractive for these purposes4,5.
Even with these limitations, the study is still an
instructive one. It has direct clinical relevance because it clearly points to
the vulnerability of cartilage and the necessity for careful handling of this
tissue during surgical procedures. To this end, it might be advisable to
reevaluate the use of tamps in the insertion of osteochondral grafts and to
devise more benign methods for their insertion.
*The author did not receive grants or outside funding in
support of his research for or preparation of this manuscript. He did not
receive 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 author is affiliated or associated.
References
1. Malinin GI, Malinin TI. Microscopic and histochemical manifestations of hyaline cartilage dynamics. Prog Histochem Cytochem. 1999;34:163-242.
2. Buckwalter JA, Mow VC. Cartilage repair in osteoarthritis. In: Moskowitz RW, Howell DS, Goldberg VM, Mankin HJ, editors. Osteoarthritis: diagnosis and medical/surgical management. 2nd ed. Philadelphia: WB Saunders; 1992. p 71-107.
3. Malinin T, Ouellette EA. Articular cartilage nutrition is mediated by subchondral bone: a long-term autograft study in baboons. Osteoarthritis Cartilage. 2000;8:483-91.
4. Athanasiou KA, Rosenwasser MP, Buckwalter JA, Malinin TI, Mow VC. Interspecies comparisons of in situ intrinsic mechanical properties of distal femoral cartilage. J Orthop Res. 1991;9:330-40.
5. Malinin T, Temple HT, Buck BE. Transplantation of osteochondral allografts after cold storage. J Bone Joint Surg Am. 2006;88:762-70.
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