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Periodontal disease, specifically periodontitis, is a leading cause of tooth loss that affects a significant portion of the global adult population. This condition is characterized by an inflammatory response to bacterial infection of the tissue surrounding teeth, leading to gum recession and bone loss. Given the increasing prevalence of periodontitis with age and the growing aging population globally, understanding its causes and progression is crucial. Researchers from Tokyo Medical and Dental University (TMDU) recently published a study in Nature Communications on March 28, 2024, outlining a new approach to studying periodontitis using an improved animal model.

Studying periodontitis directly in humans is challenging, prompting researchers to use animal models for preclinical research. The “mouse ligature-induced periodontitis model” has been widely utilized since 2012 to study the cellular mechanisms of this condition. However, this model has limitations as it primarily focuses on gingival samples, neglecting other important tissue components like the periodontal ligament, alveolar bone, and cementum. In response to this limitation, the research team at TMDU developed a modified ligature-induced periodontitis model that allows for the simultaneous analysis of all tissue components, thereby providing a more comprehensive understanding of the disease.

By using a triple ligature approach instead of a single ligature on the upper left molar of male mice, the researchers were able to increase the yield of different types of periodontal tissue while expanding the range of bone loss without causing severe destruction. This approach enabled them to evaluate gene expression related to inflammation and osteoclast differentiation over time, leading to the discovery of the Il1rl1 gene and its role in the IL-33/ST2 pathway in inflammatory and immunoregulation processes. Further investigation using genetically modified mice lacking the Il1rl1 or Il33 genes revealed the protective role of the IL-33/ST2 pathway in preventing inflammatory bone destruction.

The researchers identified a unique population of cells expressing the mST2 protein in its receptor form, which they named “periodontal tissue-resident macrophages.” These cells exhibited a combination of markers for both pro-inflammatory and anti-inflammatory macrophages and were present in the peri-root tissue before inflammation occurred. This discovery sheds light on a novel pathway regulating inflammation and bone destruction in periodontal disease and presents opportunities for the development of new treatment strategies and prevention methods. Overall, the study highlights the potential of the modified animal model to provide detailed insights into the molecular mechanisms underlying periodontitis and its tissue-specific effects.

In conclusion, periodontal disease, particularly periodontitis, is a prevalent condition that affects a significant portion of the global adult population and is associated with tooth loss. Research on the underlying causes and progression of periodontitis is essential, especially as populations worldwide are living longer. By utilizing an improved animal model that allows for the simultaneous analysis of all tissue components, researchers at TMDU were able to investigate the molecular mechanisms of periodontitis in greater detail. Their findings shed light on the role of the IL-33/ST2 pathway and novel macrophages in regulating inflammation and bone destruction in periodontal disease, paving the way for new therapeutic approaches.

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