Traumatic temporomandibular joint ankylosis refers to fibrous or bony fusion between the condyle and the glenoid fossa. It can cause problems with mouth- opening limitations, mastication difficulties, obstructive sleep apnea and hypopnea syndrome. When traumatic temporomandibular joint ankylosis occurs during childhood, it can cause facial asymmetry, micrognathia, and malocclusion, which significantly affect the physical and mental health. Once temporomandibular joint ankylosis occurs, it will be refractory and recurrent. The pathogenesis of temporomandibular joint ankylosis has not been completely elucidated and has always been a research hotspot in the oral and maxillofacial fields. In this paper, worldwide research was conducted, and the pathogenesis of traumatic temporomandibular joint ankylosis was clarified, such as“damage of condyle”“, disc displacement or rupture”“, damage to the glenoid fossa”and “lateral pterygoid muscle distraction”. The relative pathogenesis hypotheses were summarized, such as“hematoma organization”and“lateral pterygoid muscle distraction osteogenesis”. The related pathogenesis of traumatic temporomandibular joint ankylosis was discussed based on the latest cytology and molecular biology research.

Periodontitis and periapical periodontitis have a high incidence rate and often result in the progressive absorption of alveolar bone. This is one of the main causes of tooth loosening and loss. Prolonged local inflammation leads to the proliferation of capillaries, fibroblasts, and inflammatory cells such as neutrophils and lymphocytes. This process results in the replacement of surrounding bone tissue with inflammatory granulation tissue. Traditionally, it has been advocated that inflammatory granulation tissue is pathological and should be completely removed from the extraction socket to avoid complications such as bleeding, infection, and poor bone healing after tooth extraction. Although the regenerative capacity of inflammatory granulation tissue is reduced, it can be enhanced by increasing the body’s immunity or by eliminating pathogenic stimuli (such as tooth extraction and root canal treatment). As a result, the fibrous components in the inflammatory granulation tissue gradually increase, while infiltrating inflammatory cells gradually decrease. Ultimately, this transformation leads to the formation of reparative granulation tissue, followed by ossification. Furthermore, the use of granulation tissue from the tooth extraction socket for immediate implantation to facilitate wound closure or soft tissue reconstruction has yielded favorable clinical outcomes, and histological studies simultaneously confirmed the presence of mesenchymal stem cells within the inflammatory granulation tissue. Therefore, it is necessary to reconsider the traditional belief that inflammatory granulation tissue must be completely removed. Given the potential of inflammatory granulation tissue to undergo osteogenic transformation under appropriate interventions, regulating the transformation of inflammatory granulation tissue into reparative granulation tissue with osteogenic potential represents a novel strategy for the regenerative treatment of dental alveolar inflammatory lesions. This approach holds broad clinical application prospects and is an important research direction for the future. Reactive oxygen species, NOD-like receptor protein 3, and matrix metalloproteinase K are key regulatory factors involved in the transformation of inflammatory granulation tissue into reparative granulation tissue. Furthermore, bone morphogenetic protein 2 and vascular endothelial growth factor are key regulatory factors involved in the osteogenic regeneration of reparative granulation tissue. However, the molecular mechanisms of these regulatory factors remain unclear; therefore, elucidating their molecular mechanisms will help identify suitable targets for promoting the regeneration of dental alveolar inflammatory lesions. Furthermore, this will contribute to the development of related biological treatment technologies and drugs, which may ultimately provide a more minimally invasive and effective treatment for inflammatory lesions of alveolar bone. However, it is important to note that research in this field is still in its early stages. There is still considerable progress to be made before clinical translation and application can be achieved.