Tooth eruption represents a dynamic, multi-step biological process driven by coordinated molecular and cellular interactions that allow the tooth to migrate through surrounding tissues. As development progresses, the stratum intermedium is replaced by the papillary layer within the enamel organ. Earlier work identified intercellular adhesion molecule-1 (ICAM-1) in this papillary region, which later gives rise to ICAM-1–positive junctional epithelium. Since ICAM-1 production can be stimulated by inflammatory cytokines such as interleukin-1 and tumor necrosis factor, both known to mediate tissue breakdown, this study explored whether inflammatory events are part of the eruption mechanism. Reverse transcription–polymerase chain reaction (RT-PCR) results showed sequential activation of hypoxia-inducible factor-1α, interleukin-1β, and chemotactic mediators like keratinocyte-derived chemokine (KC) and macrophage inflammatory protein-2 (MIP-2) during the eruption stage. Immunohistochemistry further demonstrated KC and MIP-2 presence within papillary layer cells of maturing enamel organs. Numerous macrophages and neutrophils were also observed within the connective tissue between the developing tooth and oral epithelium. These patterns indicate that inflammatory pathways contribute to the removal of tissue above erupting teeth, potentially triggered by local hypoxia resulting from reduced vascular supply. The data suggest this process is sterile and governed by innate inflammatory regulation rather than bacterial infection.
