| The knee was the most frequent sites where osteoarthritis happened. Osteoarthritis was a common disease,frequently-occurring disease in the elderly population, which mainly destroyed articular cartilage, bone and synovial tissues, leading to joint pain, deformity and dysfunction,Thus it affected the patient's move. As the age increased,the incidence of osteoarthritis increased. However, the age of onset of osteoarthritis was getting progressively younger,along with the frequency and intensity of modern people,s activities increasing. The incidence rates in female were higher than in men, a higher incidence in the post-menopausal women. China was a populous country, only over the age of 60 more than 100 million, and it wsa estimated that patients with osteoarthritis were approximately more than 50 million.It was estimated that the next largest group of patients with osteoarthritis would be in China.The most basic pathological changes in osteoarthritis is change of articular cartilage,including articular cartilage fibrosis,splitting,ulcers,stripping,which was caused by variety of reasons. Under normal circumstances, it was in balace between articular synthesis and degradation of cartilage collagen. When the articular cartilage was destroyed, cartilage cells can produce new cartilage extracellular matrix, which did not act to injury. When the injury of articular cartilage did not involve the subchondral bone, the adjacent cartilage cells were only caused to produce a slight reaction,and the cartilage cells can hardly regenerate ,the surrounding stromal cells no increase; When the damage of articular cartilage did not reach the subchondral bone, the articular cartilage surface appears only inflammatory healing response. After the cartilage chondrocytes was damaged, the number of enzymes in extracellular matrix which was produced by the cartilage chondrocytes changed, and the surrounding environment of cells was damaged , leading to further cartilage damage, finally resulting in the occurrence of osteoarthritis. When cartilage was injury, a large number of matrix metalloproteinase appeared in the cartilage matrix, which had the role of degradation of prostaglandins and collagen fibers , cellular and humoral immune aggravated cartilage damage, which was caused by a large number of degraded prostaglandins and collagen fragments , and nitric oxide produced due to stimulation of inflammatory factors.nitric oxide and its products made chondrocyte apoptosis, inhibiting the synthesis of proteoglycan and collagen and promoting its decomposition. The lack of collagen and proteoglycan made cartilage elasticity fall ,and cartilage was damaged after the role of confrontation was reduced.Pain was a common symptom of knee osteoarthritis. Since there was not nerve distribution in articular cartilage, it was not direct relationship between cartilage damage and pain. However,there was rich nerves in subchondral bone, periosteum, synovium, ligaments and joint , and those parts of the nerve endings were stimulated directly or indirectly due to cartilage degeneration ,which was the origin of pain. Nociceptors was also nerve endings, which was found around blood vessels as the interstitial, lying in fat pad of the joint capsule, synovium and joint. Receptors had usually non-active, which was activated only after the highly enhanced joint tension or chemical stimuli direct stimulation. Pain mechanism of knee osteoarthritis was currently considered to be three main areas including Synovitis, bone pain and the syndrome around joints. When the synovial inflammatory response occurs, the release of neuropeptides in the inflammatory response could sensitize nerve endings (nociceptors). These chemicals could reduce the excitement threshold of nociceptor,and could also directly stimulate and activate nociceptors. Neurogenic inflammation could be caused,as the neuropeptides had the role in the blood vessels of the synovium and joint capsule. With the progression of knee osteoarthritis, joint space was becaming narrow,and line of force changed. Causing the Varus,valgus deformity to varying degree, the joint capsule and synovial being stimulated due to joint weight-bearing on and causing an increase in the number of neuropeptides ,directly activating pain receptors in the synovial tissue to produce pain-induced effects. Inflammatory mediators activated cartilage cells the release of protease,the release of fibroblast collagenase,and these enzymes into the joint fluid directly stimulated nociceptor to produce pain. Subchondral bone exposed or increased internal pressure in bone also caused pain. After cartilage was exposed , blood vessels, nerves of subchondral bone and marrow was exposed. The synovial cells was under the action of neuropeptides, releasing substances into the joint cavity such as prostaglandins and collagenase, which could increase cartilage destruction and could cause a vicious circle, in addition to causing pain; Neuropeptides, inflammatory mediators, cytokines and other substances in Joint fluid could stimulate the sensory nerve endings of the subchondral bone marrow cavity to cause pain.It could not be ignored for the impact of knee osteoarthritis on quality of life and social public health, which had attracted wide attention from the international community. a threat to humanity in knee osteoarthritis is rapidly increasing. The pathogenesis of the pain mechanism was not entirely clear, to be further studied. But It was an important aspect to improve the quality of life by effective prevention and treatment.At present there were many method of treatment. Arthroscopic treatment of knee osteoarthritis arised a surgical technique in the last two or three decades. The basic arthroscopic surgical techniques included irrigation, cleaning and drilling or grinding, and the diagnosis could be confirmed by microscopy. There were the advantages in arthroscopy which had a comprehensive, intuitive, taking into account of the treatment diagnostic, but the arthroscopic technique was not still generalizable. Most patients could not be the system of early treatment, and the patient treatment was late, the related inspection fees expensive. There is no simple and effective way to determine the extent of their lesions.The aim of the study was that associated analytica between pain and arthroscopic cartilage degeneration at patients with knee osteoarthritis. Aim to explore whether the extent of the pain of knee osteoarthritis could be as a indicator to determine the extent of an disease, which provided a scientific basis for the choice of clinical treatment. Objective: To explore the clinical significance and the correlation between cartilage degeneration and the degree of pain of knee arthroscopic under knee arthroscopy.Methods: Analysis of unilateral knee osteoarthritis in different levels using knee arthroscopy examination and treatment from March 2008 to August 2009,there was 56 patients ,man 28,woman 38.The average age was 52 year old(42 to 58). The pain was assessed before surgery, using arthroscopic to assess the extent of cartilage degeneration,and the relevance of the two assessments were analyzed.Reasult: It had no statistically significant between cartilage degeneration of knee osteoarthritis and the degree of pain of visual analog scale assessment (P> 0.05); It had significance between cartilage degeneration of knee osteoarthritis and the degree of pain of the WOMAC questionnaire assessment ( P <0.05).Conclution: Correlation between the degree of cartilage degeneration with the degree of pain is not yet entirely clear in the attemptive study of knee osteoarthritis. Visual analog scale assessment of pain intensity reacted to the pain within 48 hours or when the situation is not yet the pain response to the recent situation. WOMAC pain section describes the summary of the recent pain, for those with chronic knee pain in osteoarthritis. This has important clinical between significance of pain and knee osteoarthritis cartilage degeneration.
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