Treatment of malocclusion with fixed orthodontic appliances takes about 2-3 years is a burden for the patient. Acceleration of orthodontic tooth movement (OTM) by accelerating bone remodeling is still a challenge in orthodontics. One of the efforts to accelerate alveolar bone remodeling is to increase cellular and molecular interactions related to Danger Associated Molecular Pattern (DAMP) and Resolution Associated Molecular Pattern (RAMP) during orthodontic tooth movement. To describe the role of DAMP and RAMP on alveolar bone remodeling during OTM. OTM force initiating sterile inflammation associated with the presence of DAMPs which are defined as endogenous molecules that are specifically and rapidly released upon cellular stress, injury or necrosis, conditions that induce inflammation of host tissues. OTM resulting an inflammatory response, many endogenous molecules such as deoxyribonucleic acid (DNA), and reactive oxygen species (ROS). DAMPs are released from infected or suppressed host cells resulting in the subsequent release of cytokines and chemokines, including interleukin (IL) IL-1, IL-6 and Tumor Necrosis Factor-α (TNF-α). DAMPs are known alarmins such as heat shock protein (HSP), high mobility group box 1 (HMGB-1), IL-1α, and IL-33. RAMPs are released during cellular stress that help offset the inflammatory effects of DAMP. HSP10 and HSP27 are molecules that play a role in the RAMP mechanism. RAMPs inhibit macrophage activity resulting in resolution of inflammation, either through direct antagonism through HSP10 or by induction of IL-10. Inflammatory regulation can increase osteogenic-related molecules thereby accelerating alveolar bone remodeling. DAMP and RAMP have an important role in alveolar bone remodeling during OTM.