Orthodontic tooth movement: The biology and clinical implications

Abstract Orthodontic tooth movement relies on coordinated tissue resorption and formation in the surrounding bone and periodontal ligament. Tooth loading causes local hypoxia and fluid flow, initiating an aseptic inflammatory cascade culminating in osteoclast resorption in areas of compression and osteoblast deposition in areas of tension. Compression and tension are associated with particular signaling factors, establishing local gradients to regulate remodeling of the bone and periodontal ligament for tooth displacement. Key regulators of inflammation and tissue turnover include secreted factors like RANK ligand and osteoprotegerin, transcription factors such as RUNX2 and hypoxia-inducible factor, cytokines, prostaglandins, tissue necrosis factors, and proteases, among others. Inflammation occurred during tooth movement needs to be well controlled, as dysregulated inflammation leads to tissue destruction manifested in orthodontic-induced root resorption and periodontal disease. Understanding the biology has profound clinical implications especially in the area of accelerating orthodontic tooth movement. Surgical, pharmacological, and physical interventions are being tested to move teeth faster to reduce treatment times and time-dependent adverse outcomes. Future developments in acceleratory technology and custom appliances will allow orthodontic tooth movement to occur more efficiently and safely.