Chemokine receptor-2 deficiency induced mild experimental periapical lesion in mice

Macrophages are considered to play an important role in the development of chronic apical periodontitis (CAP). However the function of tissue resident macrophages in CAP is unclear. This study aims to investigate the potential role of macrophages of different origins in CAP.

Chemokine receptor-2 deficiency (CCR2^-/-) mice and C57BL/6N mice (control group, WT mice) were used to induce apical periodontitis. The pulp of mandibular first molars of both sides were exposed to the oral environment. After 0, 7, 21, 28 days of pulp explosion, animals were sacrificed, the mandibular bones were collected and scanned with micro-CT, further processed for HE & IHC Staining to analyze the development of CAP, as well as the expression of surface markers of macrophages.

Both CCR2^-/- and WT mice exhibited CCR2 negative macrophages in normal periapical area, which indicated the presence of tissue resident macrophages. CCR2 deficiency decreased the number of macrophages in periapical lesions, the M1 type macrophages' number as well as osteoclasts around the edge of the lesion decreased compared to wild type. Meanwhile CCR2 deficiency decreased the volume of periapical lesion significantly compared to wild type, but did not inhibite and disappeare the lesion thoroughly.

Monocyte-macrophage system derived macrophages promote the progression of periapical lesions, while tissue resident macrophages in periodontal ligament might also be involved in the progression of periapical lesion.