Periodontal diseases are inflammatory conditions affecting the tissues that surround and support the tooth. Two common conditions of the periodontium, gingivitis and periodontitis, are inflammatory disorders of microbial etiology. Gingivitis is the inflammation of the gingival epithelium that does not impact the tooth-supporting connective tissue. Gingivitis is reversible inflammation, as physical removal of the polymicrobial plaque biofilm by proper oral hygiene can return inflammation to healthy levels, and damage to the gingival epithelium heals. Failure to control the outgrowth of the oral biofilm results in inflammation of the tooth-supporting structures and subsequent attachment loss and alveolar bone resorption, termed periodontitis. The immunopathology of periodontitis is irreversible damage that is the leading cause of tooth loss worldwide. In this chapter, we examine the polymicrobial biofilm that is the etiologic agent of gingivitis and periodontitis and its role in disease initiation and progress. Periodontitis is a complex bacterial infection as disease initiation and progression is not mediated by a single pathogen that causes disease, but rather the synergistic interactions of a dynamic polymicrobial community. The pathogenesis is immune-driven as the plaque biofilm induces unproductive, frustrated inflammation that damages host tissues. The changing ecology of the gingiva due to inflammation promotes the growth of a more bacterially diverse community that sustains its optimal ecology by the continued induction of inflammation. First, we discuss the clinical signs and symptoms of periodontal disease, highlight specific risk factors for developing periodontitis, and the overall impact of chronic periodontal inflammation on human health. Then, we will discuss the microbial composition of the biofilm and both spatial and temporal changes in the biofilm development relevant to disease progression. We will examine how the complex polymicrobial community is sustained through both synergistic and antagonistic interactions that facilitate the fitness of the entire community while influencing the biofilm architecture as physiologically compatible species co-localize into well-organized micro-communities. Finally, we will examine the role the plaque biofilm plays in interacting with the gingival epithelial barrier to colonize host tissues and promote the inflammation that both sustains the plaque biofilm while also causing the hallmark immunopathology.

Microbial Biofilms and Pathobiology of Gingivitis and Periodontitis

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发表日期：

2025年

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Daniel P. Miller

摘要

Periodontal diseases are inflammatory conditions affecting the tissues that surround and support the tooth. Two common conditions of the periodontium, gingivitis and periodontitis, are inflammatory disorders of microbial etiology. Gingivitis is the inflammation of the gingival epithelium that does not impact the tooth-supporting connective tissue. Gingivitis is reversible inflammation, as physical removal of the polymicrobial plaque biofilm by proper oral hygiene can return inflammation to healthy levels, and damage to the gingival epithelium heals. Failure to control the outgrowth of the oral biofilm results in inflammation of the tooth-supporting structures and subsequent attachment loss and alveolar bone resorption, termed periodontitis. The immunopathology of periodontitis is irreversible damage that is the leading cause of tooth loss worldwide. In this chapter, we examine the polymicrobial biofilm that is the etiologic agent of gingivitis and periodontitis and its role in disease initiation and progress. Periodontitis is a complex bacterial infection as disease initiation and progression is not mediated by a single pathogen that causes disease, but rather the synergistic interactions of a dynamic polymicrobial community. The pathogenesis is immune-driven as the plaque biofilm induces unproductive, frustrated inflammation that damages host tissues. The changing ecology of the gingiva due to inflammation promotes the growth of a more bacterially diverse community that sustains its optimal ecology by the continued induction of inflammation. First, we discuss the clinical signs and symptoms of periodontal disease, highlight specific risk factors for developing periodontitis, and the overall impact of chronic periodontal inflammation on human health. Then, we will discuss the microbial composition of the biofilm and both spatial and temporal changes in the biofilm development relevant to disease progression. We will examine how the complex polymicrobial community is sustained through both synergistic and antagonistic interactions that facilitate the fitness of the entire community while influencing the biofilm architecture as physiologically compatible species co-localize into well-organized micro-communities. Finally, we will examine the role the plaque biofilm plays in interacting with the gingival epithelial barrier to colonize host tissues and promote the inflammation that both sustains the plaque biofilm while also causing the hallmark immunopathology.