Periodontitis is a chronic periodontal disease with a high incidence, and chronic obstructive pulmonary disease (COPD) is considered to be a chronic airway inflammatory disease. In recent years, many studies have observed that there is a potential relationship between periodontitis and COPD. The periodontal condition of patients with COPD is relatively poor, and the composition of their oral microbiome is different from that of healthy people. The inflammation “spillage”and hypoxia may induce the occurrence and development of periodontal disease. At the same time, the risk of COPD in periodontitis patients may be related to the inhalation of periodontal pathogens and inflammatory factors. Regular periodontal sequence therapy can reduce the risk of acute exacerbation of the disease to a certain extent. Since periodontitis and COPD are both chronic progressive diseases characterized by chronic inflammation and accompanied by proteolytic destruction of connective tissue, they may share a common pathophysiological process and may be intrinsically linked. This article reviews the latest research progress on the relationship between chronic periodontitis and COPD, and possible interaction mechanism, in order to provide insight for further study on the interaction between the two conditions.

AIM:To elucidate the possible biological mechanism of silica-induced acute lung injury in rats.METHODS:Sixteen Male Sprague-Dawley rats were divided into control and acute silicosis model groups,and instilled intratracheally with 1 mL of normal saline and 50 g/L silica suspension,respectively.After 7 d,the rats were sacrificed for collection of lung tissue and serum.The serum levels of interleukin-1β(IL-1β),IL-18 and tumor necrosis factor-α(TNF-α)were measured by using ELISA.The protein expression levels of nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)and gasdermin D(GSDMD)were measured by immunohistochemistry.Bacterial DNA was ex-tracted from the lung tissue for 16S ribosomal RNA gene sequencing to characterize changes in the composition of lung flo-ra.The differences in the structure of bacterial flora between control and model groups were analyzed by bioinformatic analy-ses.RESULTS:Immunohistochemical analysis showed that the protein expression levels of NLRP3 and GSDMD were higher in the lungs of the rats in model group.In addition,serum cytokine profiling showed that IL-1β,IL-18 and TNF-α levels were significantly higher in model group.The most abundant bacterial genera in the lung flora of the rats in model group were Bifidobacterium,Clostridium sensu stricto 1,and Parasutterella.The NLRP3 and GSDMD levels in the lung tissue and IL-1β and TNF-α levels in serum were positively correlated with the abundance of Parasutterella.CONCLU-SION:The alterations in lung flora structure and increased inflammation levels may be the actual biological mechanisms underlying silica-induced acute lung injury.The modulation of lung flora may provide a basis for the prevention and treat-ment of silica-induced acute lung injury.