## 4 Discussion
Regarding the average length of hospitalization (29.7 days), as reported in the literature, this cost would increase by an additional PLN 11,820 (which is an additional 146% of the original cost) and would amount to PLN 19,920. Each repeated arthroscopic debridement would increase the cost of treatment by another PLN 2100. For comparison, the cost of arthroscopic ACL-R in Poland is PLN 4500 (data from the Polish National Health Insurance Fund). The etiology of OA after SA following ACL-R is multivariable [24; 25; 26; 31; 32]. An overlooked aspect of its etiopathogenesis is the effect of infection on the content of meniscus proteoglycans. Experimental studies have shown that a 1% decrease in their content causes a 1.35% decrease in the biomechanical properties of the meniscus [25]. Moreover, a 1% decrease in the elasticity of the meniscus results in a 0.77% decrease in the elasticity of the underlying medial tibial condyle cartilage. These data indicate that the degradation of 1% of the extracellular matrix proteoglycans of the meniscus results in a total decrease in the shock-absorbing capacity of the meniscus and cartilage together by 2% (1.35% + 0.77%). Assuming a similar decrease in the femoral condyle cartilage, this value approaches 3%. Moreover, experimental studies indicate that a 15% decrease in proteoglycans in the meniscus leads to irreversible changes in cartilage in the form of chondrocyte apoptosis [25; 46; 47]. Thus, the development of OA post-SA after ACL-R may have a threefold cause: (1) infection that causes degradation of proteoglycans, leading to a decrease in the shock-absorbing capacity of the meniscus and cartilage; (2) damage to the ACL which, despite reconstruction, is associated with the development of degenerative changes at 10 years follow-up; and (3) co-occurrence of pathologies of the meniscus and cartilage. Based on the results presented in this study, it can be concluded that the method we adopted protects the meniscus and articular cartilage from loss of proteoglycans, causing a decrease in the viscoelastic properties of both structures, which has a key effect on the development of degenerative changes. Apart from the applied treatment of SA after ACL-R, we believe that an extremely important factor in the prevention of knee degenerative changes was convincing the patients to give up competitive sports. This is particularly supported by the correlation of the KT-1000 results with the MRI images. The observation period (mean 18.1 years) is one of the longest in the current literature. Moreover, our study is prospective because the clinical evaluation of knees after infection was performed twice, at a mean of 10.9 years and a mean of 18.1 years. The clinical results obtained from our patients were similar to those of previous publications [6; 16; 17; 48]. [PERSON] et al. recently published a study assessing the functional outcomes of 15 patients at a mean of 39.3 months after SA following ACL-R. The prevalence of SA was 1.8%. They obtained a mean Lysholm score of 77.7 and an IKDC score of 70.4, and the KT-1000 compared to the non-injured contralateral knee showed a mean difference of 1.3 mm [48]. The Ladman test was positive in four patients and the pivot-shift test in three patients. They also observed early signs of radiographic degeneration (Fairbank grade I) in three patients. In addition to arthroscopic debridement and intravenous, and later oral, antibiotic therapy, ambulatory irrigation of the knee for 4 h/day for an average of 2 days using two spinal needles was used [48]. A similar incidence of SA following ACL-R (1.7%) was observed in her notes by [PERSON] [6]. She obtained a mean Lysholm score of 74.9, IKDC score of B-5 patients, C-3 patients, D-2 patients, and a KT-1000 mean difference of 1.4 mm after 3 years follow-up. In the one-leg hop test, seven patients achieved at least 90% motor skill of the contralateral limb, one with 80%, and two who were unable to perform a jump with the reconstructed leg at all.