Page 849 - Adams and Stashak's Lameness in Horses, 7th Edition

Principles of Musculoskeletal Disease 815

of a tissue. Regeneration may be considered a special reported that large defects were less likely to heal.
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form of repair in which the cells replace lost or damaged A more recent study distinguished between large (15 mm )
VetBooks.ir suggested that with the exception of bone fractures, bearing and non‐weight‐bearing areas of the antebra­
tissue with a tissue identical to the original. It has been
and small (5 mm ) full‐thickness lesions in weight‐
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most injuries and diseases of the musculoskeletal tissues
chiocarpal (radiocarpal), middle carpal (intercarpal),
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do not stimulate regeneration of the original tissue. 8 and femoropatellar joints. At 1 month, small defects
The limited potential of articular cartilage for regen­ were filled with poorly organized fibrovascular repair
eration and healing has been appreciated for more tissue; by 4 months, repair was limited to an increase in
than two centuries. In 1743, Hunter stated, “From the amount of organization of this fibrous tissue, and
Hippocrates to the present age, it is universally allowed by 5 months, small radiocarpal and femoropatellar
that ulcerated cartilage is a troublesome thing and that lesions were hardly detectable because of combinations
when once destroyed it is not repaired.” There are a of matrix flow and extrinsic repair mechanisms.
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limited response of cartilage to tissue damage and an Large lesions showed good initial repair, but at
inability of natural repair responses from adjacent 5 months, perilesional and intralesional subchondral
tissues to produce tissue with the morphologic, bio­ clefts developed.
chemical, and biomechanical properties of articular The repair tissue that forms after full‐thickness injury
cartilage. to hyaline cartilage or as a natural repair process in joints
The major limiting factor in the successful rehabilita­ with OA is primarily composed of type I rather than
tion of any joint after injury or disease is the failure of type II collagen, at least at 4 months. 9,13 Identification
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osteochondral defects to heal. Three mechanisms have of type II collagen is the critical biochemical factor dis­
been recognized as possible contributors to articular car­ tinguishing hyaline cartilage from repaired fibrous tissue
tilage repair. Intrinsic repair (from within the cartilage) and fibrocartilage. It is thought that the presence of an
relies on the limited mitotic capability of the chondrocyte abnormal subchondral bone plate and the absence of a
and a somewhat ineffective increase in collagen and tide mark reforming may create a stiffness gradient and
proteoglycan production. Extrinsic repair comes from that shear stresses of the junction of the repair tissue and
mesenchymal elements from the subchondral bone par­ underlying bone develop. The propagation of such shear
ticipating in the formation of new connective tissue that stresses would lead to the degradation of repair fibrocar­
may undergo some metaplastic change to form cartilage tilage and exposure of the bone. This mechanical failure
elements. The third phenomenon, known as matrix flow, has been observed experimentally and clinically in the
may contribute to equine articular cartilage repair by horse. 39,67
forming lips of cartilage from the perimeter of the lesion In a study looking at the long‐term effectiveness of
that migrate toward the center of the defect. 38,39 sternal cartilage grafting, the repair tissue in the non‐
The depth of the injury (full or partial thickness), size grafted defects at 12 months consisted of fibrocartilagi­
of defect, location and relation to weight‐bearing or nous tissue with fibrous tissue in the surface layers, as
non‐weight‐bearing areas, and age of the animal influ­ was seen in control defects at 4 months. However, on
ence the repair and remodeling of an injured joint biochemical analysis, the repair tissue of the non‐grafted
surface. 9,13,62 defects had a mean type II collagen percentage of 79%,
With a partial‐thickness defect, some repair occurs compared with being non‐detectable at 4 months. 112,113
with increased GAG synthesis and increased collagen On the other hand, the GAG content expressed as mil­
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synthesis. However, the repair process is never com­ ligrams of total hexosamine per gram of dried tissue
pletely effective. In humans, complete repair of chondro­ was 20.6 ± 1.85 mg/g, compared with 26.4 ± 3.1 mg/g at
malacia of the patella has been reported to occur if 4 months and 41.8 ± 4.3 mg/g DW in normal equine
matrical depletion and surface breakdown are minimal. articular cartilage. 112,113
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However, more recent work with arthroscopic debride­ The fibrocartilaginous repair seen in normal full‐thick­
ment of partial‐thickness defects in humans questions ness defects is therefore biomechanically unsuitable as a
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any actual regeneration. In addition, superficial defects replacement‐bearing surface and has been shown to
are not necessarily progressive and do not necessarily undergo mechanical failure with use. The lack of durabil­
compromise joint function. ity may be related to faulty biochemical composition of
With full‐thickness defects, the response from the the old matrix and incomplete remodeling of the interface
adjacent articular cartilage varies little from that after between old and repaired cartilage or to increased stress
superficial lesions and provides only the limited repair in the regenerated cartilage because of abnormal remod­
necessary to replace dead cells and damaged matrix at eling of the subchondral bone plate and calcified cartilage
the margins of the wound. These defects heal by layer. Although recent work implies that it may be possi­
ingrowth of subchondral fibrous tissue that may or may ble to reconstitute the normal collagen type in equine
not undergo metaplasia to fibrocartilage. 13,30,39,54,113 articular cartilage, clearly there is continued deteriora­
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Subchondral bone defects either heal with bone that tion of GAG content, and these are important compo­
grows up into the defect or fill in with fibrocartilaginous nents in the overall composition of the cartilage matrix.
ingrowth. Duplication of the tide mark in the calcified The presence of a cartilage defect may not represent
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cartilage layer is rare, and adherence of the repair tissue clinical compromise. In the equine carpus, loss of up to
to surrounding noninjured cartilage is often 30% of articular surface of an individual bone may not
incomplete. 30,54 compromise the successful return of a horse to racing.
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A number of equine studies demonstrate that the However, loss of 50% of the articular surface or severe
size and location of articular defects significantly affect loss of subchondral bone leads to a significantly worse
the degree of healing achieved. Convery et al. first prognosis.