Background Periodontitis is an infectious disease initiated by plaque. However, the role of peripheral nerves in the progression of periodontitis remains unclear.

Objective To study the effect of capsaicin-sensitive neurons on the progression of experimental periodontitis in mice.

Methods Twenty male C57BL/6 mice were randomly divided into ablation group (Cap) and non-ablation group (Veh), 10 mice in each group. The Cap group received injections of high-concentration capsaicin (5 μg/mL) into the ocular/maxillary region of bilateral trigeminal nerves to ablate capsaicin-sensitive neurons, while the Veh group received injections of a vehicle containing 1% DMSO and 10% Tween-80 phosphate-buffered saline. One week later, a ligature was tied around the left maxillary second molar of each mouse, the right maxillary second molar was untreated as a control. The mice were then divided into four groups: non-ablative control (Veh/Con), ablative control (Cap/Con), non-ablative periodontitis (Veh/Lig), and ablative periodontitis (Cap/Lig). One week later, the maxilla was examined by micro-CT to observe the reduction of alveolar bone. After decalcification, the HE staining and the TRAP staining were performed to observe soft and hard tissue destruction and osteoclast formation. Quantitative real-time polymerase chain reaction (RT-qPCR) was employed to detect expression levels of inflammatory factors TNF-α and IL-1β in gum tissue.

Results The results of micro-CT showed that compared with the Veh/Lig group, alveolar bone resorption was decreased in the Cap/Lig group (P < 0.05). HE staining and TRAP staining showed that compared with the Veh/Lig group, damage to soft and hard tissues was reduced in the Cap/Lig group; furthermore, there was also a decrease in the number of osteoclasts around the alveolar bone (P < 0.05). RT-qPCR results indicated that expression levels of inflammatory factors TNF-α and IL-1β were lower in the Cap/Lig group than those in the Veh /Lig group (P < 0.05).

Conclusion Capsaicin-sensitive neurons can promote bone resorption in periodontitis, which may be related to osteoclast differentiation and local tissue inflammation.