Arthroscopy: The Journal of Arthroscopic & Related Surgery
Original articleInflammatory Cytokine Profiles Associated With Chondral Damage in the Anterior Cruciate Ligament–Deficient Knee
Section snippets
Methods
This study included a consecutive series of patients who met the study inclusion criteria. Patients had to be between the age of 18 and 45 years and sign an Institutional Review Board–approved consent form. All patients had a diagnosed ACL tear on clinical examination that was verified at arthroscopy in order to complete the enrollment. Patients were excluded from the study if meniscal pathology or other ligament pathology was identified at arthroscopy. All patients were surveyed regarding date
Articular Surface Grading
Two patients were grade 0 with intact articular surfaces and no signs of pathology. Eight patients were Outerbridge grade I with softening of the articular surface. Seven patients had partial-thickness defects less than 1.5 cm and were graded Outerbridge II. Twelve patients were grade III with partial-thickness defects greater than 1.5 cm, and 2 patients had full-thickness defects down to bone and were classified as Outerbridge IV.
Chondral Damage Versus Time From Index ACL Injury
For patients with grade 0 chondral damage, the mean time from
Discussion
To better understand the natural history of cartilage loss in the ACL-deficient knee, this study measured cytokine levels in the chronic ACL-deficient knee. Our results showed that the concentrations of chondrodestructive cytokine, IL-1β, and TNF-α were elevated in injured knees. The level of chondroprotective IL-1ra also increased; however, the increase was much less than the corresponding increases in chondrodestructive cytokines. Differences in cytokine concentrations were also seen based on
Conclusions
In this study, we found an elevation of both chondrodestructive and chondroprotective cytokines in the ACL-deficient knee. Chondrodestructive cytokines are more markedly increased than their inhibitors. This suggests a possible imbalance between cartilage-damaging and cartilage-preserving factors in favor of the cartilage-damaging cytokines. This imbalance may result in progressive cartilage loss over time. Continued work in this area may identify disease-modulating cytokines that may be able
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