Implantation of autologous chondrocyte cultures for cartilage restoration has required research into the biochemistry of cartilage tissue. It is currently understood that the key to successful cartilage defect repair is the reversibility of collagen production using autologous chondrocyte cultures. Mature cartilage chondrocytes retain the ability to change the type of collagen they produce. When tissue is harvested from the donor site, chondrocytes produce type II collagen. During culture, their properties change. If chondrocytes form a monolayer culture, they begin to produce type I collagen. After this culture is placed into the defect on the articular surface, type II collagen production resumes. Chondrocytes lack type X collagen, which is an indicator of chondrocyte hypertrophy and possible bone formation. This suggests that adult chondrocytes are mature cells that cannot further differentiate into bone cells. After implantation, chondrocytes from the implanted culture are located along the periphery of the cartilage defect and adhere to each other, eventually fully integrating with the host cartilage. Chondrocytes, labeled with beta-galactosidase for 6 months, form a cartilaginous covering, which in some cases resembles hyaline cartilage. Currently, this is the most effective technique for replacing defects in the cartilaginous surface of articular bone ends. (Barone L. Genzyme Tissue Repair, Cambridge, Massachusetts. Cultured autologous chondrocyte implantation for cartilage repair. July, 1997). Brittberg M. et al. were among the first to apply the chondrocyte transplantation technique to patients and shared the first clinical results. The authors had extensive experience with subchondral bone tunneling, abrasion, and spongification. These surgeries resulted in cartilage with a disorganized structure containing type I collagen fibers. The biomechanical properties of the new cartilage were clearly insufficient to withstand the loads imposed on the joint in vivo. Transplantation of periosteal and perichondrial grafts yielded inconsistent results. This led to the development of new approaches to treating cartilage defects based on chondrocyte culture. In the author's presentation, the treatment technology took the following form. During arthroscopy of the affected joint, a 300-500 mg sample of intact cartilage is removed from a non-load-bearing area near the medial condyle. The cartilage is transferred to a special vessel containing sodium chloride. Cells are separated over the course of 2 to 5 hours. The cartilage is crushed and washed three times with a HEPAS buffer containing gentamicin, amphotericin, and ascorbic acid. The crushed cartilage is transferred to a vessel containing clostridial collagenase and deoxyribonuclease. The cells are filtered using a 25-micron nylon filter, washed, and mixed with the patient's serum. The cells are counted and then transferred to Costar culture medium, where they are grown. The medium is changed twice a week, with mandatory bacteriological testing. The chondrocyte suspension is treated with trypsin and then washed three times in the patient's serum. After the final centrifugation, a suspension of 50 to 100 microliters is formed, containing 2 to 5 million cells. The chondrocyte suspension is ready for cartilage defect closure 2 to 3 weeks after cartilage collection. The authors performed autologous chondrocyte transplantation in 23 patients with isolated knee cartilage lesions resulting from trauma or osteochondritis dissecans. Sixteen patients were examined after three years, and joint function was restored in 14 cases. These patients developed new hyaline cartilage. The unsatisfactory results can be explained by joint instability due to ligamentous insufficiency. Of the seven patients with patellar cartilage defects, five improved to satisfactory condition, while only two achieved good condition. This is likely due to the patellar defects being caused by incongruence between the patella and the femoral condyles. To prevent infection and tissue incompatibility, chondrocyte culture was performed in the patient's own serum. Chondrocyte production during culture increases 10-20-fold. Currently, the mechanism of native cartilage restoration in the defect area remains unknown. Histological examination revealed that newly formed cartilage forms close to the underlying bone but differs from the native cartilage covering. Three explanations for the cartilage restoration process are possible. 1) Cells transplanted into the defect area produce a new cartilage matrix. 2) The periosteum stimulates the formation of new chondrocytes. 3) The periosteum and transplanted cells stimulate chondrocytes from surrounding tissues to grow and close the defect. Conclusion: Chondrocyte transplantation into the cartilage defect located on the femoral condyles results in the formation of new hyaline-like cartilage containing type II collagen, which helps restore knee joint function. (Brittberg M., Lindahl A., Nilsson A., et al. Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N. Eng. J. Med., 1994, 331, 889-895). Currently, experience with cartilage transplantation in different age groups is accumulating. This experience was shared by Minas T. According to the author, primary or idiopathic osteoarthritis of one joint occurs in 5% of people under 25 years of age and in 80% of people over 75 years of age. Radiographic changes characteristic of moderate to severe osteoarthritis occur in people under 45 years of age in less than 5% of cases, and in more than 40% of cases in people over 75 years of age. In young people, damage to joint cartilage is most often associated with sports. Although full-thickness cartilage damage is considered a cause of degeneration and the development of osteoarthritis, criteria for assessing the severity of damage and predicting progression have not yet been developed. An analysis of 31,516 arthroscopies performed over a 4-year period revealed 53,569 cases of hyaline cartilage damage in 19,827 patients. Of these, 5% of arthroscopies performed in individuals under 40 years of age revealed an Outerbridge stage 4 cartilage defect. These patients had full-thickness damage to the cartilage covering, which is an indication for cartilage grafting to prevent the progression of degeneration. With stage 4 cartilage damage, radiographic signs of osteoarthritis eventually appear. If the cartilage covering defect in the knee joint exceeds 1 square cm, joint space narrowing is observed in 50% of patients. These patients underwent joint debridement as a therapeutic procedure. In the presence of osteophytes and subchondral bone sclerosis, 57% of patients experienced progression over time. In patients with a half-narrowing of the joint space, progression of the process was observed in 61% of cases and no progression in 39% of cases. This suggests that as the degree of degeneration increases, the tendency of the process to progress is relatively more pronounced. (Minas T. Nonarthroplasty management of knee arthritis in the young individual. Curr. Opin. Orthop., 1998, 9, 46-54). The Swedish orthopedist L. Peterson has the most extensive experience with corticel. According to the author, in Sweden, experience with transplanting autologous chondrocytes to patients with knee joint pathology exceeds 500 people; however, as of the beginning of 1998, long-term results from 2 to 10 years have been analyzed for only 219 people. The long-term condition of these patients was assessed using various methods: clinical (Lysholm, Tegner-Wahlgren, Cincinnati scales, visual analogue scale), arthroscopic, biomechanical, and histological. The patients had the following types of pathology: isolated femoral condyle defect, condyle defect with anterior cruciate ligament injury, osteochondritis dissecans, patellar cartilage injury, intercondylar area defect, and multiple defects. The treatment outcomes for patients in different groups were as follows (mean figures for the studied parameters are shown): — Isolated femoral condyle defect. The patient’s age was 39 years, the defect size was 4.2 cm2, ranging from 1.3 to 12 cm2, the average follow-up was 4 years. The preoperative score was 2.4 points, and the postoperative score was 8.4 points. — Femoral condyle defect and anterior cruciate ligament injury. The patient was 30 years old, the defect size was 3.9 square cm, its borders ranged from 1.5 to 14 square cm, and the follow-up period was 4.3 years. The preoperative score was 2.2, while the postoperative score was 7.0. Relatively worse results were observed in patients with joint instability and delayed ligament reconstruction. — Osteochondritis dissecans. The patient was 25 years old, the defect size was 5.3 square cm, its borders ranged from 1.5 to 16.0 square cm, and the follow-up period was 3.9 years. The preoperative score was 1.9, while the postoperative score was 7.9. — Arthroscopy. A repeat examination of the joint was performed in 46 patients. The following factors were assessed: the degree of defect closure with newly formed cartilage, the condition of the cartilaginous covering, and the macroscopic appearance of the transplanted cartilage. — Biomechanical studies. Cartilage hardness was determined during arthroscopy using an electronic sensor (Kiviranta I). Normal hardness ranged from 3.6 to 6.1 N, hyaline-like cartilage 2.7 N, fibrous cartilage 1.2 N. Mechanical properties correlated with the histological picture. — Histological examination. A needle biopsy of 2 mm of tissue was performed. Cartilage grading was made according to 4 types: hyaline-like, hyaline-like with fibrous coating, a combination of hyaline and fibrous cartilage, fibrocartilage. The histological picture correlated with the clinical assessment. Conclusion: Within 2 years or more after cartilage transplantation, improvement in the condition was noted in 80% of patients. Cartilage transplantation can be used both in patients with isolated defects of the cartilaginous coating and in combined lesions of the cartilage and cruciate ligaments, as well as in dissecting osteochondritis. When the integrity of the cartilaginous covering of the patella is compromised, good results are achieved relatively rarely. After chondrocyte transplantation, the newly formed cartilage integrates with the cartilage at the edge of the defect. There is a direct relationship between the type of restored cartilage and the assessment of the patient's clinical condition. The result obtained was maintained for 10 years. Transplantation of autologous chondrocytes is a safe procedure that can be used to replace cartilage defects. (Peterson L. Autologous chondrocyte transplantation: 2-10 year follow-up in 219 patients. Amer. Acad. Orthop. Surg., 1998 Annual Meeting, New Orleans). There are publications in which the effectiveness of transplantation was assessed based on a large number of clinical observations. Mandelbaum B. et al. in 1998 summarized the results of an international study of chondrocyte autotransplantation. Remote results of chondrocyte autotransplantation were assessed in two groups of patients. In the first group of 249 patients, the follow-up period was 12 months. In the second group of 50 patients, the follow-up period reached 24 months. According to the registry data, as of December 1997, a total of 891 autologous chondrocyte transplantations were performed worldwide. These operations were performed by 410 surgeons. The age of the patients ranged from 15 to 55 years, with an average of 36 years. There were 67.2% men and 32.8% women. Acute joint injury was in the anamnesis of 67.2% of patients. The average size of the cartilage defect was 4.4 square cm. Cartilage defects of the medial femoral condyle were observed in 60.8%, lateral femoral condyle in 18.2%, and in the remaining cases there were defects of the patella and tibial plateau. In 27.6% of cases, the injury was related to sports. 76% of patients had at least one medical procedure in their medical history. The clinical condition of the patients was assessed using the Cincinnati scale. It was found that after transplantation, 779 patients (87.4%) experienced a decrease in pain, joint swelling, and crunching sensation in the joint during movement. They had no complications of the procedure. In 112 patients, or 12.6%, 132 cases of complaints were observed. Of these, 101 patients (11.3%) were found to have complications during the clinical examination. In 11 patients (1.2%), there were complaints that were rejected as having no clinical significance. In 47 patients (5.3%), complications were recognized as clinically significant and, possibly, associated with the chondrocyte implantation procedure. Violation of the implantation process technique was found in 18 patients, which amounted to 2%. Repeat surgery was performed in 88 patients, which amounted to 9.9%. In 58 cases (6.5%), arthroscopic joint debridement, shaving, lavage, and chondroplasty were performed. Adhesion release was performed in 21 cases (2.4%), and patellar arthroplasty was performed in 14 cases (1.6%). Complications included adhesions and joint fibrosis in 28 cases (3.1%), tissue hypertrophy at the defect site in 21 cases (2.4%), and delamination and fraying of the cartilage cover in 16 cases (1.8%). Analysis of the chondrocyte transplantation results allowed the authors to draw the following conclusion: Chondrocyte transplantation is the most effective procedure for cartilage defects in the femoral condyles, a less effective procedure for the patella, and the least effective intervention for the tibial plateau. 24 months after the procedure, patients demonstrated a significant improvement in their condition. Chondrocyte transplantation is a safe manipulation. The authors of the study identified key principles that should be considered during cartilage transplantation. Joint injury triggers the release of cytokines and the enzyme stromelysin in the synovial fluid, which promote cartilage degeneration more than its restoration. Partial cartilage damage does not heal. Partial damage may remain unchanged for a long time because the regeneration mechanism is inactive. Full-thickness cartilage damage is replaced by fibrocartilage, whose mechanical properties are insufficient to withstand normal joint loads. A cartilage defect smaller than 2 square cm may be asymptomatic and not progress. This defect has the most favorable prognosis. Cartilage defects larger than 2 square cm have a poor prognosis and are prone to progression, leading to synovitis, pain, and loss of joint function. — The incorrect relationship of the segments forming the joint or joint instability should be corrected simultaneously with the procedure of cartilage defect replacement. — Articular cartilage replacement should be an effective and safe procedure. Efficiency means that the following changes should occur as a result of the procedure: a) the defect is replaced with hyaline, not fibrous cartilage, b) the patient's pain, synovitis and movement impairment disappear, c) the patient's physical activity is restored. Safety means a decrease in the number of possible complications associated with both the surgical intervention itself (cartilage damage, inflammation, thrombosis, etc.) and the general impact on the body (allergic reaction). (Mandelbaum B., Browne J., Fu F., et al. Articular cartilage lesions of the knee. Am. J. Sport. Med., 1998, 26, 6, 853-860). The International Society for Articular Cartilage Repair developed a program and proposed a document entitled "Unified Standard Approach to Assessing Articular Cartilage Repair." The standard includes 12 key points. Each point includes an explanatory section and several questions that the physician performing chondrocyte transplantation must answer. 1. Etiology of the process. Is the cartilage defect acute or chronic? Did the cartilage defect develop as a result of acute trauma or chronic overload? Typically, the formation of a cartilage defect is characterized by the interaction of a combination of factors. 2. Depth of the defect. How deep is the cartilage defect? ??The most acceptable method for determining the depth of a cartilage defect is the Outerbridge classification, which includes four degrees of damage. 0) нормальный хрящ, 1) размягчение хряща, 2) складчатость хряща, 3) неполная трещина хряща, 4) полное нарушение хрящевого покрытия и обнажение кости. Стадии 1 и 2 рассматриваются, как частичное поражение, а стадии 3 и 4, как полное. Для оценки степени поражения следует учитывать наличие асептического некроза подлежащей кости или инфаркта костной ткани. 3. Размер дефекта. Размер дефекта измеряется в квадратных сантиметрах, обычно с помощью артроскопического зонда. Дефект размером до 2 квадратных см считается малым, от 2 до 10 квадратных см считается средним и размером более 10 квадратных см определяется, как большой. 4. Степень устойчивости краев дефекта. Устойчивы края хрящевого дефекта или нет? Правильно очерченный дефект с плотными краями способен выдерживать нагрузку. Если края хряща разволокнены или истончены, то дефект способен к распространнию и прогрессированию. В таком случае на рентгенограмме определяется сужение суставной щели. 5. Локализация дефекта. Где расположен дефект хряща? Имеется ли одиночный дефект или дефекты носят множественный характер? Данные о локализации оказывают влияние на прогноз заболевания. 6. Состояние связок сустава. Сохранена ли целостность крестообразных связок или имеется их частичное, либо полное повреждение? Какова стабильность коленного сустава? Была ли в анамнезе операция по стабилизации сустава? 7. Состояние менисков. Сохранена ли целостность менисков? Была ли частичная, или субтотальная резекция менисков, либо восстановление менисков путем их сшивания? 8. Соотношение бедра и голени. Расположены ли бедро и голень на одной оси? Если между ними есть угол, то это варусная или вальгусная деформация? Какова величина угла? Была ли в анамнезе операция корригирующая остеотомия? Если да, то какая? Следует обратить внимание на состояние пателло-феморального сочленения. Есть ли необходимость в исправлении положения надколенника? 9. Предшествующее лечение. Было ли в анамнезе оперативное или консервативное лечение? Если да, то какое? Дебридемент, туннелизация, трансплантация и т.д.? 10. Данные рентгенологического исследования. Необходима рентгенограмма сустава в передне-задней проекции под нагрузкой. Основными признаками являются степень сужения суставной щели, наличие остеофитов и костных кист. 11. Данные магнитно-резонансной томографии. Определение состояния хрящевого покрытия и субхондральной кости. Оценка глубины дефекта, обнажения кости, наличие расслаивающего остеохондрита или асептического некроза кости. 12. Анамнез жизни, семейный анамнез. а) Исключение специфического ревматоидного процесса, артрита, системной красной волчанки, положительной реакции на антиген HLA В-27. б) Состояние эндокринной системы, патология щитовидной железы, диабет, ожирение. в) Наличие семейных формы остеоартроза, наследственной патологии коллагена, типа синдрома Элерса-Данлоса или Марфана. (International Cartilage Repair Society Documentation and Classification System. Freiburg, Switzerland, Newsletter 1, March, 1998, 5-8). Выводы: В нашем исследовании показано, что ручное пособие сокращает время операции по сравнению с трансперитонеальным и ретроперитонеальным доступами, но чаще осложняется грыжами. При трансперитонеальном доступе больные раньше покидают стационар и возвращаются к активной деятельности.