Maintaining a protective state for human periodontal tissue

Abstract

In the 20th century, dentists largely classified periodontal diseases according to patient age at onset, rate of progression, and pathology. Accordingly, the main concepts of periodontitis were "adult," "early-onset," and "refractory"; however, these names did not correspond to the specific bacterial species identified, in such cases, using bacteriological approaches. Therefore, in 1999, the American Academy of Periodontology reorganized this tripartite classification into 2 broad groups: severe, rapid destruction of periodontal tissue not attributable to systemic diseases; and periodontitis as a manifestation of systemic diseases. 1 The former group is considered to be "aggressive periodontitis" (class III in the American Academy of Periodontology Periodontal Disease Classification System), while the latter can be grouped under periodontitis associated with hematological or genetic disorders (classes IVa and IVb in the American Academy of Periodontology Periodontal Disease Classification System), often presenting with comorbid immune (neutrophil) dysfunction. 1,2 However, researchers could not identify specific bacteria or pathologies unique to any of these classes. Subsequently, the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions led to a series of changes in periodontal disease taxonomy, transforming classification into a stage-and grade-based system. 3 | Periodontitis as a multifactorial diseaseClinical manifestations of incipient periodontitis vary considerably across individuals, depending on where the tissue damage originates and how it progresses; thus, it is impossible to explain the symptomatology in terms of bacterial infection alone. We now know that destruction of the periodontal tissue does not progress continuously and linearly, but is rather a result of repeated switches between dormant and active stages of resident bacteria. 4,5 Simplistically describing periodontitis as an infection with certain bacteria cannot completely explain the diverse patterns observed. The fact that periodontitis is a multifactorial disease lies at the heart of this complexity. The tissue damage is thought to be driven by a variety of factors, 6,7 which have started to be illuminated in recent years, and these risk factors have now been conceptually organized into 3 main groups: bacterial, host, and environmental. A host factor can include an underlying metabolic disease that affects the whole body, while smoking is an archetypal environmental factor. Changes in the biological properties of host cells can have an enormous influence on defense mechanisms in the periodontal tissue. In vitro analyses can be used to chronicle the detailed changes in immunocytes and resident cell populations; however, physiological samples are more useful for investigating systemic shifts in host defense mechanisms. Data from analyses of the gingival crevicular fluid have provided intriguing insights into how the protective state evolves and changes as humans grow and age. For example, by comp...

Polarized Macrophages in Periodontitis: Characteristics, Function, and Molecular Signaling

“…The expression of CSF-1 is increased in the gingival tissues of patients with periodontitis ( 27 ). Macrophages and neutrophils can be recruited to junctional epithelium and other periodontal tissues by keratinocyte-derived chemokines, macrophage inflammatory protein-2, and other chemotactic and adhesion factors, and this process is not affected by bacterial flora ( 28 ).…”

Embracing multi‐causation of periodontitis: Why aren’t we there yet?

“…The concept of periodontitis etiology as a combination of the microbiota, the host, and the environment is broadly accepted (Jepsen et al, 2017; Joseph & Curtis., 2021; Yamamoto & Aizawa, 2021). Consequently, periodontal treatment includes initiatives to clarify host predispositions and handle behavioral/environmental risk factors, such as smoking.…”

“…The concept of periodontitis etiology as a combination of the microbiota, the host, and the environment is broadly accepted (Jepsen et al, 2017;Joseph & Curtis., 2021;Yamamoto & Aizawa, 2021).…”

Eriodictyol Suppresses Porphyromonas gingivalis-Induced Reactive Oxygen Species Production by Gingival Keratinocytes and the Inflammatory Response of Macrophages

“…In a healthy periodontium, the immune response of mucosal and infiltrating immune cells triggered by periodontal pathogens in the dental biofilm is moderate and protective [ 7 , 8 ]. More specifically, macrophages and monocytes play a key role in host defenses against periodontal infections and contribute to the initiation of an adaptive immune response to periodontal pathogens such as P. gingivalis [ 9 , 10 ].…”

“…However, if periodontal pathogens proliferate and increase in number, a state of dysbiosis develops in the subgingival sites, inducing an exaggerated inflammatory response, which leads to the secretion of cytokines and matrix metalloproteinases (MMPs) that sustain the chronic inflammatory reaction and modulate connective tissue and alveolar bone destruction [ 11 ]. The NF-κB signaling pathway, which consists of the NF-κB p50/p65 heterodimer and is inhibited by the suppressive protein inhibitor kappa B (IκB), plays a central role inflammatory mediator secretion [ 2 , 7 , 8 ]. Moreover, reactive oxygen species (ROS) production by resident and inflammatory cells of the periodontium is drastically increased during periodontitis and antioxidant host defense system cannot balance this process resulting in an oxidative stress condition and tissue damage [ 12 ].…”