Osteoarthrosis (OA) is the most common disease and major cause of disability in middle-aged and elderly people, seriously affecting patients’ quality of life and social productivity. With the process of population aging, numerous countries have entered the aging society. The current number of people over 60 years old in China is over 130 million, and it is expected that the total number of people over 60 years old will exceed 200 million by 2015. According to WHO estimates, 10% of the world’s population over the age of 60 suffers from OA, 80% of OA patients have mobility problems, and 25% are unable to perform daily activities. The prevalence of OA in the 20-year-old age group is reported to be only 20 percent, while the 70-year-old age group is 85 percent. Statistics show that about 40 million adults in the United States suffer from arthritis, of which OA accounts for 43%, 90% of women and 80% of men over 65 years of age suffer from this disease. With the increasing aging of the world’s population, the incidence of OA is on the rise globally, and degenerative joint diseases have become one of the most important topics of medical research today. Strengthening research on age-related osteoarthritis is conducive to improving the quality of life of the elderly, promoting social and economic development, and improving the health of the nation.
Section I. Etiology of osteoarthritis Osteoarthritis (OA for short), first proposed by Garrod in 1890, when it was believed that such diseases were defined as functional changes in the bone joints due to inflammatory processes in the bone joints.
Osteoarthritis is a chronic degenerative bone and joint disease of the elderly, characterized by degenerative changes in articular cartilage with meniscal and synovial lesions. the exact cause of OA remains unclear. It is thought to be related to age, mechanical wear and tear, and impingement factors, and has been found to be related to immune response, free radicals, increased intraosseous pressure and cytokines, which are still under further study.
The age factor is an important factor in OA because degeneration of articular cartilage will be inevitable with age, as the water content decreases, viscoelasticity decreases, and resistance to impact and wear decreases.
Most scholars now believe that although articular cartilage is more resistant to wear and tear, it is less resistant to impact. Physiological degeneration of articular cartilage is only a potential causative factor for the occurrence of OA, not a decisive factor. Articular cartilage damage is proportional to age and exercise, and the older the age, the more cumulative damage, the more severe the degeneration of articular cartilage. After cartilage injury, the resistance to mechanical, cumulative, repeated small impact decreases, which can aggravate the degeneration of articular cartilage, resulting in cartilage surface or deep damage, thus forming a vicious circle to further aggravate the injury.
It has been proposed that OA is associated with increased intraosseous pressure. Some studies have shown that OA patients with increased subchondral bone pressure, bone tissue can be necrotic under the action of excessive internal pressure, necrotic bone trabeculae in the process of absorption and reconstruction, so that the sclerotic gradient of subchondral bone increases, the ability to absorb oscillations decreases, so that the cartilage is unevenly stressed, the local pressure is high, resulting in or aggravating cartilage damage.
The immune response is a new doctrine proposed in recent years. In the study of OA, it was found that when mechanical factors were removed, the progression of OA did not stop, and OA patients had recurrent clinical symptoms that were difficult to explain by purely mechanical trauma causes. The recurrent swelling and synovitis of the patient’s joints were obvious, and it was hypothesized that the occurrence of OA might be related to the immune response.
Donohue’s “hidden antigen” theory suggests that the injured cartilage exposes components of the body’s autoimmune surveillance system that are normally isolated from the body and act as antigenic stimuli for autoimmune reactions. The “immune etiology theory” is more convincing.
Free radicals are molecules, atoms, atomic groups and ions with unpaired electrons, and Pelletier et al. showed that debris from damaged articular cartilage stimulates phagocytes in the synovial membrane to produce large amounts of oxygen radicals. Oxygen free radicals can attack the chondrocyte membrane, causing morphological changes and functional impairment of chondrocytes, blocking the synthesis and secretion of proteoglycans and collagen, and causing physiological functional variation of the cartilage matrix.
The relationship between cytokines and OA is currently a hot topic of research in the etiology of OA. In 1983, Wood et al. first reported that high levels of IL-1 were detected in the synovial fluid of patients with osteoarthritis and rheumatoid arthritis, and IL-1 was mainly secreted by the lining cells of synovial tissue and chondrocytes. It was found by immunohistochemical methods that under normal conditions, only a few chondrocytes located in the superficial layer of cartilage showed positive reactions for IL-1 secretion, while the middle and upper layer cells and the stroma of OA cartilage tissue showed strong positive reactions for IL-1. In addition, IL-l mRNA expression was also found in intra-membranous osteogenesis-related osteoblasts in OA bone tissue, suggesting that IL-l may be directly involved in the pathological process of osteoarthritis.
The ultrastructural changes in OA articular cartilage are complex, with chondrocyte consolidation, fragmentation, and necrosis, as well as increased metabolic activity of some chondrocytes, as evidenced by the appearance of intracellular rough endoplasmic reticulum, Golgi apparatus, and a large number of microfilaments, disorganized collagen fibers in the cartilage matrix, and deposition of calcium salt crystalline particles.The degeneration of OA articular cartilage not only causes changes in its own biological and mechanical properties, but also inevitably affects the cartilage. also inevitably affects the subchondral bone. The subchondral bone tissue is subjected to high compressive stress conduction and microfracture, followed by trabecular necrosis and formation of bone cystic degeneration. During the process of bone tissue repair and remodeling, subchondral bone will form bone redundancy when repairing its own damage and cartilage defects. The destruction of cartilage and bone may in turn form microscopic free bodies in the joint, which stimulate inflammation of the synovium.
The clinical diagnosis of osteoarthritis includes a thorough history taking, physical examination, and overall assessment of the condition. The first question should be about the duration and severity of the lesion. Pain symptoms are usually insidious when they begin, and they tend to persist for several months before the patient sees a physician. Patients often experience discomfort from prolonged standing, walking or running, and symptoms usually resolve after rest. As the extent of the lesion increases, daily activities and sleep can be affected. In addition to pain, there is a grinding sensation and popping in the joint. Injury to the cartilage, meniscus or free bodies can cause “locking” symptoms, often affecting joint flexion and squatting activities. The medial, lateral, and anterior compartments of the knee are further identified by physical examination. Internal knee malalignment is more common than external knee malalignment, and changes in the line of force and flexion deformity of the lower extremity in the standing position often indicate severe knee involvement. Joint line gap tenderness and McMurray’s test generally elicits discomfort in the involved compartment. Most patients have stable ligaments, but it is important to rule out underlying ligament instability.
Pain is predominant in the patellofemoral and tibiofemoral joints in a weight-bearing state, especially when walking, walking up and down stairs, squatting and standing, and can be sudden, tender-legged or fallen during walking. Cartilage exfoliation and subchondral bone exposure are stimulated by pressure leading to reflexive and spasmodic tension of the quadriceps muscle, and symptoms of strangulation may occur due to meniscal wear and cartilage damage. Due to cartilage wear of the patella, the subchondral bone is exposed and reflexively causes spasticity of the quadriceps muscle, so the patellar nudge activity is restricted and the patellar grind test is positive. As a result of synovial hypertrophy, congestion and edema, the synovial tissue is embedded in the joint space and swelling, pain and functional limitation of the joint cavity may occur. In obese patients, the knee is often associated with inversion and valgus deformity and patellar subluxation, with narrowing of the joint space on the stress side in standing X-rays and sclerosis or hyperplasia of the subchondral bone.
On examination, we found inversion or valgus deformity of the knee, standing flexion deformity, palpable rubbing sensation or twisting or tearing rubbing sound in knee flexion and extension, pressure pain in the joint space and patellar rim, limited patellar pushing activity, positive patellar grinding test, and positive knee floating patella test. In patients with long-term physiotherapy, the skin around the knee joint changes in color and patches, and the skin shows leopard skin-like changes. It is very difficult to get up from a squat and requires two hands on the ground for support.
Imaging of the knee joint helps in clinical diagnosis and understanding to determine the extent of articular cartilage lesions. In the early stages of cartilage lesions, x-rays include anterior-posterior (PA) orthopantomographs of the knee in weight-bearing position and x-rays of the knee in 20°-30° of flexion in weight-bearing position, which clearly show narrowing of the joint space, unequal width on both sides, sharp tibial spines, flattening of the joint edges, subchondral bone sclerosis or cystic changes, inversion or valgus of the knee, and subchondral deformities. Force lines of the tibia and femur are assessed by weight-bearing x-ray of the knee, but assessment of the mechanical axis requires a full-length x-ray of the lower extremity.
Magnetic resonance imaging (MRI) is noninvasive and MRI clearly demonstrates cartilage changes when the radiographs do not show joint space narrowing changes before, i.e., early stages of articular cartilage lesions, proton density fat-saturated fast spin echo (PDFSE) as well as three-dimensional gradient echo (3D SPGR) scans.
Section 3 Selective limited arthroscopic clearance for osteoarthritis Treatment of osteoarthritis is divided into conservative and surgical therapies. Conservative treatment is based on systemic medication and intra-articular local medication. In patients with early OA, oral anti-inflammatory and analgesic drugs or drugs that activate blood circulation and resolve blood stasis can be given symptomatically to improve symptoms and quality of life. Intra-articular injection of hyaluronic acid, a joint cartilage protector, has certain effect.
For OA patients with significant joint pain, swelling, walking dysfunction, MRI showing cartilage destruction, intra-articular free bodies, bone growth or with meniscal damage, they should resort to surgery. Surgical methods for the treatment of OA include arthroscopic cleanup, drilling and decompression microfracture in the area of total cartilage damage, high tibial osteotomy with corrective force lines, and artificial joint replacement. The application of chondrocyte transplantation, growth factors and gel carriers are in the research and trial stage.
Arthroscopic cleanup can be performed with epidural anesthesia or local anesthesia. Local anesthesia is applied with 2% lidocaine 20ml + saline 40mm + 0.1% epinephrine solution 0.1ml as a mixture, which is injected into the surgical entrance and joint cavity respectively for local infiltration anesthesia, and the procedure can be performed after 10 minutes. To maintain a clear intraoperative view, saline 3000ml + 0.1% epinephrine injection 1ml as perfusion solution can be dispensed with for surgery under tourniquet control. Arthroscopic examination was performed sequentially to obtain a comprehensive understanding of the intra-articular lesion and to perform arthroscopic surgery.
Arthroscopy reveals intra-articular as suspended granules, hyperplastic and hypertrophic patellofemoral synovial tissue, cartilage fragmentation, white elongated fibrous villi in some of the suprapatellar capsule, tortuous and congested synovial vessels, edematous synovial tissue in fusiform, grape-like and other abnormal synovial changes. The intercondylar fossa of the femur is narrowed, the cartilage is exfoliated, the subchondral bone is exposed and uneven, and the meniscus in the corresponding part of the cartilage injury is worn. Meniscal injury in turn can aggravate cartilage wear, and the degree of meniscal injury is proportional to the degree of cartilage injury. Cartilage and meniscal injury are causal and affect each other. The meniscus wears out and becomes thin and fibrous, and the free edge is crenulated, which can stimulate synovial hyperplasia and cause knee pain or locking symptoms. The intercondylar fossa or suprapatellar capsule has a different morphology of free bodies, which is a common cause of symptoms of colic.
There are more arthroscopic cleanup methods, generally radiofrequency gasification or planar grinding is used to treat the free edge of meniscal injury and trim its stump. The anterior horn of the meniscus has relatively good blood flow and the possibility of healing, so in principle, it is preserved as much as possible and resection is avoided as much as possible. In some cases, the anterior horn of the meniscus is louver-like or fascicled fiber-like injury, but the body and posterior horn of the meniscus are normal, radiofrequency wrinkling can be used to flatten the injury wound, while the torn anterior horn of the meniscus is sutured from the inside out, and the postoperative brake is applied for 4-6 weeks. Preservation of the meniscus plays an important role in preventing cartilage injury.
Articular cartilage degeneration, especially in the weight-bearing areas of the patella, femoral condyle, and tibial plateau, is characterized by wrinkled swollen augmentation, cartilage cracking, patchy exfoliation, and exposure of subchondral bone. The uneven trajectory of the femoral and tibial articular surfaces is often secondary to or exacerbates meniscal wear. Removal or revision of the ruptured meniscus, grinding of the bony blockage affecting joint motion, and release of joint strangulation factors and functional disorders are of great value in interrupting the vicious cycle of inflammatory process and improving clinical symptoms.
Full-layer cartilage damage less than 2 cm in extent can be applied by subchondral bone drilling, which can form fibrocartilage. If there is extensive cartilage degeneration, there is no good strategy to save it, only the unstable free edge can be cleaned and repaired, not extensive scraping or cleaning, otherwise the clinical symptoms are bound to increase and it is difficult to restore normal.
Stenosis of the intercondylar fossa of the femur and impingement of the hyperplastic tibial intercondylar spine can affect the knee extension function. The clinical manifestation is knee flexion deformity, standing knee can not be completely straight, the knee joint is arched bridge-like, accompanied by knee inversion or valgus deformity. The posterior meniscal horn and femoral condyle cartilage wear were aggravated by the negative focus and stress posterior shift of the knee joint. Arthroscopic dynamic examination revealed that the tibial tuberosity was impinging on the intercondylar fossa, and the ACL was degenerated by the impingement and wear of the tuberosity in the intercondylar fossa, losing its luster, deforming and thinning, and spreading out in a bundle. The femoral intercondylar fossa was enlarged by occlusion or grinding of the enlarged bone, and the intercondylar fossa space was enlarged until the impingement disappeared and the knee extension function improved significantly, and the ACL was not worn out. We found a corresponding improvement in inversion or valgus deformity of the knee after enlargement of the intercondylar fossa of the femur and resection of the tibial tuberosity, which may be related to the offset of the impingement point formed after the enlargement of the intercondylar fossa and the tibial tuberosity, resulting in a change in the line of force that aggravates or induces inversion or valgus deformity of the knee.
It has been suggested that in osteoarthritis of the knee, tension of the lateral patellar support band restricts the normal movement of the patella in the patellofemoral trajectory, further increasing the pressure on the patellofemoral joint, leading to wear of the patellofemoral cartilage and worsening the clinical symptoms.Merchant (1974), first reported the release of the lateral patellar support band, and Breitenfelder (1987) performed a long-term Fulkson et al. (1986) suggested that the selection of lateral patellar support band release was based on knee symptoms, patellar tilt on X-ray, and lateral patellar bone formation. He found that the patellar tilt test was the most important sign affecting the final treatment outcome, followed by the patellar internal displacement test, and the results of X-ray examination had little effect on the treatment outcome. The author believes that for younger patients with less severe articular cartilage wear, early release of the lateral patellar support band is an effective method to relieve pain and reduce articular cartilage wear due to increased pressure on the lateral patella. However, if the patient is elderly, has considerable cartilage wear, and has developed a significant motion trajectory, lateral patellar support band release, which may aggravate clinical symptoms and be detrimental to functional recovery, should not be performed as a routine and should be determined on a case-by-case basis.
Friedman et al. reported the efficacy of arthroscopic cleanup for osteoarthritis, with functional improvement achieved in 60% of cases. They found that patient age had a direct effect on the efficacy of the procedure, with 86% of those under 40 years of age achieving improvement, while only 53% improved over 40 years of age. Bert reported an excellent rate of 50% to 76% for arthroscopic cleanup. OA is an age-related, degenerative change, and no method can stop aging. The so-called arthroscopic debridement is only relative and cannot reverse the degeneration that has developed in the joint. Cleaning and repairing unstable cartilage trauma, unblocking and impinging motion trajectories, and removing intra-articular pain-causing factors, cartilage degradation particles, macromolecular components, debris and microcrystals from worn out articular cartilage, inflammatory factors and pain-causing substances facilitate functional recovery.
The factors of poor postoperative efficacy are not only the heavy degeneration of articular cartilage at advanced age, but also the change of force line in the lower limb of internal and external knee deformity, which is directly related to the size of surgical trauma. Therefore, we advocate selective and limited minimally invasive cleanup under local anesthesia arthroscopy without excessive interference with intra-articular tissues.
To facilitate microscopic observation, the hypertrophied synovial tissue that obscures the field of view can be shaved without extensive removal. Excise the intercondylar fossa of femur and intercondylar de tibial bone hyperplasia and release the intercondylar fossa stenosis; trim the worn meniscus and cartilage defect area, remove the exfoliated separated and unstable cartilage fragments in the joint, remove the free body, grind the bony obstruction that affects the joint activity with high and low level, remove the pain-causing substances in the joint, and flush with plenty of physiological saline. If there are abnormal changes in the force lines of the lower extremity, the damaged joint surface can be relieved by osteotomy to reduce the stress on the joint surface, such as high tibial osteotomy.
Postoperative ice packs applied cold to the affected knee for 24 to 48 hours can achieve hemostasis and pain relief. Post-operative swelling should be aspirated to remove blood and fluid accumulation in the joint cavity, and intra-articular injection of sodium hyaluronate 7-10 days later. Postoperative functional exercises for the quadriceps muscle of the knee are beneficial for functional recovery.