Periodontal disease burden is related to economic level. The burden of periodontal disease in Europe and the Western Pacific, which have higher economic levels, is lower than that in Africa and Southeast Asia. The burden of periodontal disease is mostly concentrated in people over 65 years of age. China currently has the heaviest burden of oral disease in the world; the country’s disability adjusted life years account for 18.69%. There are regional differences in the distribution of periodontal conditions that are related to socioeconomic conditions, dietary habits, and other factors of different regions. Some survey results show that the prevalence of periodontal disease among those in the middle-aged group (45-64 years old) is higher than that among the elderly group (over 65 years old). This is because the oral condition of the elderly group is prone to bias in statistics due to tooth loss and other reasons. The occurrence and development of periodontal disease in the elderly is related to a variety of factors: aging triggers physiological degeneration of periodontal tissue and decline in immune function; weakened mobility and weak oral health awareness lead to insufficient daily oral cleaning; certain systemic diseases can aggravate periodontal tissue inflammation, such as diabetes, osteoporosis, and cognitive impairment; and the cumulative impact of factors such as smoking, high-calorie diet, and nutrient deficiencies on periodontal tissue. At present, China has entered the stage of aging, which means that there is an increase in the burden of oral disease, and this puts higher requirements for the allocation of social medical resources in the future. Therefore, the prevention and treatment of periodontal disease in the elderly population is particularly important. This article, which takes the elderly over 65 years old as the research group, collects and summarizes the prevalence of periodontal disease in this group at home and abroad, and explores the influencing factors of periodontal disease in the elderly. In order to provide a basis for the early prevention of periodontal disease in the elderly, a focus must be placed on disease control and prevention as well as treatment of specific susceptible groups.

Ulcerative Colitis (UC) has been reported to be related to Porphyromonas gingivalis (P. gingivalis). Porphyromonas gingivalis peptidylarginine deiminase (PPAD), a virulence factor released by P. gingivalis, is known to induce inflammatory responses. To explore the pathological relationships between PPAD and UC, we used homologous recombination technology to construct a P. gingivalis strain in which the PPAD gene was deleted (Δppad) and a Δppad strain in which the PPAD gene was restored (comΔppad). C57BL/6 mice were orally gavaged with saline, P. gingivalis, Δppad, or comΔppad twice a week for the entire 40 days (days 0-40), and then, UC was induced by dextran sodium sulfate (DSS) solution for 10 days (days 31-40). P. gingivalis and comΔppad exacerbated DDS-induced colitis, which was determined by assessing the parameters of colon length, disease activity index, and histological activity index, but Δppad failed to exacerbate DDS-induced colitis. Flow cytometry and ELISA revealed that compared with Δppad, P. gingivalis, and comΔppad increased T helper 17 (Th17) cell numbers and interleukin (IL)-17 production but decreased regulatory T cells (Tregs) numbers and IL-10 production in the spleens of mice with UC. We also cocultured P. gingivalis, Δppad, or comΔppad with T lymphocytes in vitro and found that P. gingivalis and comΔppad significantly increased Th17 cell numbers and decreased Treg cell numbers. Immunofluorescence staining of colon tissue paraffin sections also confirmed these results. The results suggested that P. gingivalis exacerbated the severity of UC in part via PPAD.
Animals ; Colitis, Ulcerative/microbiology* ; Mice ; Mice, Inbred C57BL ; Porphyromonas gingivalis/pathogenicity* ; Protein-Arginine Deiminases ; Virulence Factors