For the treatment of temporomandibular joint disorder patients are often confused and unable to find the way, and after seeing some doctors are really frightened by the terminal development of the disease, they are determined to operate. So how exactly should this disease be treated, let’s see what two authorities in this area of treatment at the North University Hospital have to say. The indications for surgery are described in detail, and I hope to give you a reference for patients who are eager to have surgery and those who are hesitant to have surgery. This article is for reference only, or to combine the actual situation of individuals, does not have the main basis for guiding the actual treatment of patients. In the mid to late 1950s, oral and maxillofacial surgery was born and grew in China. As an oral and maxillofacial surgeon, there is nothing better than to be able to master open techniques, such as mandibular resection, maxillary resection, facial nerve dissection parotid superficial lobe resection and other surgeries at that time. There was little interest in temporomandibular disorders (TMD). It was at this time that Prof. Zhang Zhenkang began his research on the treatment of TMD, which has been conducted for nearly half a century. Over the decades, we have grown with the progress of TMD research. After treating thousands of TMD patients, we have been thinking hard about what the cause of TMD is, what the pathogenesis is, what the essence of TMD is, which treatment works best, why this patient has recurrent attacks while another patient has long-term stability, whether a cure can be found or why a cure cannot be found yet. We have used almost all of the dozens of treatments available in China and abroad, and the patients have left us with invaluable experience, insight and inspiration for the treatment of TMD. We have experienced an extremely important moment in our clinical research, when arthrography began to be used in China in the 1960s and 1970s, and played an important role in clinical diagnosis, but many of these imaging images were difficult to interpret; the surgical exploration clarified these incomprehensible arthrographic images, and made it possible to visualize all kinds of displacement of the articular disc, perforation or rupture of the articular disc, etc. In cases of long-term non-healing and organic damage, the pain disappeared completely after surgery. These advances encouraged us to perform one procedure after another, and the indications now seem to have definitely expanded. In this way, we have reached the first peak period of surgery on TMD. In fact it was a repetition of the surgical peak that had occurred in the history of TMD research abroad. However, it did not last long, and after a few years of follow-up, it was found that about 20% of the patients did not have satisfactory postoperative results and had to be redirected to conservative treatment. It appeared that surgical treatment was neither effective nor curative for TMD. In the early 1980s, in the United States, as in China, arthrography was fully diagnostic of disc displacement, rupture, and perforation, so oral and maxillofacial surgeons had a “reason” to perform disc perforation repair and disc rupture silicone disc replacement. This type of surgery is performed in the operating room almost every day. At that time, it was believed that the ruptured disc could be repaired, the displaced disc could be repositioned, and even if the ruptured disc could not be repaired, it could be replaced artificially, which made sense. In 1983, the author brought back from abroad the necessary equipment for arthroplasty and immediately performed arthroplasty, arthroplasty repair and arthroplasty with removal of silicone discs in patients with painful displaced, perforated or ruptured arthroplasty discs. Since then, the Peking University School of Stomatology has carried out a large number of surgical treatments, and now it seems that the indications have definitely been expanded, so that we have been introduced to the peak of TMD surgical treatment once again. Unfortunately, still, as with previous surgical treatments, about 20% of patients do not resolve their symptoms after surgery. It seems that this type of surgery is still neither effective nor curative, and thus there is a shift back to conservative treatment. In a significant number of patients with TMD we have treated, although we have exhausted all the therapies at our disposal, including surgical treatment, they continue to have varying degrees of pain and limited opening in the temporomandibular joint and masticatory muscle groups. Some patients apparently had felt that they could only tolerate such a condition and did not return to the clinic. Interestingly, some years later, these patients would come to the hospital for dental treatment and, because they were our “regular patients”, would stop by to see us and tell us that his TMD was now healed. When we asked what treatment he had undergone afterwards, the patient replied that he had followed the precautions we had instructed him to take and that he had not been treated again and had slowly recovered. This reminded us of the term “self2limiting” in the literature. It seems that TMD does have the characteristic of self-limiting. Recently, a number of international literature and follow-up reports have reported that after simple treatment, 60% to 90% of patients with symptoms disappeared or significantly reduced after 6 months to 7 years of follow-up; 76% of patients with irreducible disc displacement had disappeared or improved after 25 years of follow-up; 90% of patients with irreducible disc displacement had significantly improved after 18 months of follow-up; and 30% of patients with disc displacement were asymptomatic. These reports are fully consistent with our clinical experience. The above experience led us directly to reflect on the indications for surgery during the two peak surgical periods in the 1960s and 1980s. The indications for surgery did expand at that time. This gradually shaped our view of the indications for surgery, suggesting that the indications for surgery for TMD should be: (1) confirmation of displacement, perforation, rupture, or destruction of other joint structures, resulting in severe functional impairment; (2) confirmation that the patient’s signs and symptoms are the result of the above-mentioned lesions; (3) that the above-mentioned lesions have failed after six months of reasonable, procedural, comprehensive conservative treatment; (4) that the above-mentioned lesions have prevented the patient from living and working normally; (5) both the doctor and the patient have fully considered that psychological2 social factors, nocturnal molar disorder, mandibular parafunction, and bad habits may affect the outcome of the surgery; (6) the patient urgently requested the surgery, fully informed about the surgery and agreed to the surgery despite the fact that it is not guaranteed to be necessarily effective. Therefore, the current indications for TMD surgery have been significantly narrowed, and surgical treatment is quite limited, including open surgery and endoscopic surgery of the joint. The concept that surgery is not the primary treatment for TMD has been accepted by most TMD specialists internationally. The cost and risk to the patient for surgical treatment is always greater than for those treated conservatively. Any treatment has a cost to the patient in terms of time, money, enduring pain and emotional stress, side effects, complications, sequelae, tissue or organ damage and loss, and various accidents. When a physician chooses any kind of treatment, he or she always hopes that it will lead to improvement, improvement, cure or even eradication of the patient’s disease. Therefore, a good physician must choose the treatment that gives the patient the least possible benefit and the greatest possible result. The greater the ratio, the better the choice. The concept of maximizing efficacy is the golden rule of any treatment choice, including the choice of TMD treatment. What exactly is the etiology and nature of TMD? Let’s use the exclusion method of categorizing the etiology of thousands of human diseases discovered so far to think: TMD is not an infectious disease caused by pathogens; TMD is not a disease caused by trauma; TMD is not a tumor or tumor-like disease; TMD is not a disease caused by a single factor; TMD is not a congenital disease; TMD is not even an infectious disease seems to be none of them. Let us analyze the following information again. 1. Analysis of the incidence of TMD: Agerberg (1975) surveyed 1106 people and the prevalence of TMD was 40%; Solberg (1979) surveyed 739 people and the prevalence was 76%; Weiborowicz and Makaworowa surveyed 4229 people and the prevalence ranged from 55% to 80%; Xu Sakurahua ( (1985) investigated 1321 people, and the prevalence of positive symptoms was 13%, and the prevalence of positive objective signs was 75178%. Deng Yumeng (1992) surveyed 3105 children and adolescents aged 3-19 years, and the prevalence of TMD was 1413% in the period of milk teeth, 2012% in the period of replacement teeth, and 2119% in the period of permanent teeth. The results of the survey showed that as many as 80% to 90% of the adults had signs of TMD, but most of them had no conscious symptoms and therefore did not seek medical attention. Only 30% of them have symptoms, but even if they feel symptoms, most of them have no significant functional impairment. As a result, only about 5% of these people end up being seen for dysfunction. In other words, is it fair to say that the vast majority of TMD patients only have symptoms or signs that are transient, a transient functional maladjustment that does not constitute a disease. Westesson (1989) showed that about 30% of asymptomatic individuals had anterior displacement of the articular disc. Ma Xuchen, Zou Zhaoyu, Zhang Zhenkang et al. (1983) also showed that most cases of TMD remained stable for a longer period of time, including cases of perforated discs. Kuita (1998) found that 43% of 40 patients with irreducible anterior disc displacement were asymptomatic, 33% had reduced symptoms, and only 25% had no improvement in symptoms or required treatment after 25 years of follow-up without treatment. In 44 cases of irreducible anterior displacement of the disc without treatment, the follow-up results were a significant reduction in pain after 6 months, a significant improvement in the degree of opening after 12 months, and only 2 cases (911%) with joint compression after 18 months. Similarly, Lundh (1999) performed arthroscopic surgery in 26 patients with irreducible anterior disc displacement without treatment at 12 months of follow-up, with one third of the patients having reduced pain and only 16% of the patients having worsened symptoms. The results were excellent in 28 cases (68%), good in 11 cases (27%), and only 2 cases (5%) still had significant symptoms. Among the 28 asymptomatic cases examined by MR I at the time of review, only 1 case had a repositioned disc, only 1 case had a partial reposition, 1 case had a reversible disc displacement, and the remaining 25 cases still had an irreversible disc displacement. The above case data show that: (1) the proportion of disc displacement is higher in healthy people; (2) the proportion of disc displacement increases with age; (3) although there are symptoms of disc displacement, most of them can be alleviated and disappear on their own; (4) the disappearance of symptoms does not indicate that the joint disc has been reset, and most of them are still not reset. 3. Analysis of the alteration of the bilabial area: In 1999, Goldstein mentioned in a literature review that adaptive alterations occurred in the bilabial area after joint disc displacement, so it did not necessarily lead to TMD or only transient TMD symptoms. 2001 to 2003, Gu Zhiyuan et al. conducted an experimental study on the alteration of the bilabial area after joint disc displacement and observed that after experimental anterior joint disc displacement, the bilabial area had class They observed disc-like tissue alterations in the bilabial region after experimental anterior displacement of the joint disc, and therefore came to the same conclusion as Goldstein. Wang Meiqing also observed this change and directly referred to it as the “4th band of the articular disc”. Under normal conditions, the bilaminar zone of the articular disc is composed of loose connective tissue, rich in blood vessels, collagen fibers and elastic fibers, and it is not as load-bearing as fibrocartilage. When the articular disc is displaced anteriorly, the posterior band of the articular disc moves forward and so does the bilaminar area. In other words, the bilabial zone gradually enters the loading zone of the joint. The greater the shift, the greater the load. Once the bilabial zone is loaded, two major types of alterations may occur: one type of destructive change in the bilabial zone tissue occurs, i.e. degenerative changes in the bilabial zone, collagen fibers and elastic fibers break down and disappear. In some cases, inflammatory reactions occur, and finally the bilaminar area becomes thin and even perforated, losing its function, and clinically, TMD symptoms appear. Another type of adaptive alteration of the bilaminar area occurs, as reported in the above experiments, i.e., the transformation of loose connective tissue to fibrocartilage, which is a component of the articular disc and can withstand pressure and shear forces. If this alteration is sufficient and there is enough fibrocartilage that resembles the native tissue of the articular disc, the bilaminar region of the articular disc also becomes part of the native component of the articular disc. It can also be said that the lengthening of the body part of the articular disc is more adaptable to the sliding motion of the condyle, so that the range of pressure that the condyle can withstand when it slides back and forth is expanded. The symptoms may disappear clinically. The severity of clinical symptoms is likely to be related to the degree of successful adaptation of the articular disc. In conclusion, in the course of human evolution, the jaw bone shrinks, the tooth volume shrinks, and the reduction in tooth volume is less than the reduction in bone volume, resulting in more tooth volume than bone volume, causing wisdom teeth obstruction, especially in the lower jaw, and malocclusion. The degree of malocclusion occurs differently in each individual and the malocclusion varies. In mild cases, there is no functional impairment and it cannot be called a disease and does not require orthodontic treatment. If orthodontic treatment is required, it is only because the patient wants to align the teeth and make them more aesthetically pleasing. In severe cases, dysfunction occurs, resulting in disease and requiring treatment. In the studies of TMD over the last hundred years, the search for why the incidence of TMD is so high seems to be similar to the phenomenon of wisdom teeth blockage and malocclusion, i.e., during the evolution of human evolution, uprightness changed the horizontal suspension of the head to a vertical position. During the mouth opening movement, the posterior swing of the mandible is obstructed by the cervical spine and its corresponding soft tissues, whereupon the mandibular movement becomes compensated and the sliding movement of the temporomandibular joint occurs. Only when the condyle slides forward, i.e. during the open mouth movement, it can be unobstructed by the cervical spine and its corresponding soft tissues. The evolution of modern humans has resulted in smaller and weaker structures of the masticatory organs and a corresponding weakening of the ligamentous muscle groups of the temporomandibular joint. This change accommodates the flexibility of TMJ movement, but at the same time this joint instability is sometimes a potential threat of injury to the TMJ. Although the masticatory organ no longer functions as a foraging and defensive weapon, ancient human movements such as yawning and gnawing food with a wide open mouth are still the extreme movements of the open mouth movement, and the range of forward sliding of the condyle and articular disc will be the greatest, thus causing damage to the weakest anatomical link of the disc 2 condyle complex, resulting in anterior displacement of the articular disc and subsequently a series of changes. If the patient is asymptomatic and has no functional impairment after adaptation by alteration, then treatment is not necessary. In patients with TMD with subluxation and reversible anterior displacement of the joint disc, if there is no functional impairment, then sclerotherapy and arthroscopic suturing are not necessary, and there is no need for capsular reduction. If a patient with TMD who has bony changes of the condyle on radiographs is diagnosed with osteoarthrosis on radiographs, but if there are no symptoms and no functional impairment, then arthroscopic surgery is not necessary, let alone open surgical treatment. We present these views in order to discuss the nature of TMD with our colleagues and to understand the modern concepts and principles of TMD prevention and treatment.