PERIODONTAL DISEASE: MECHANISMS OF PATHOGENESIS – A LITERATURE REVIEW

Аннотация

Periodontal disease is a chronic inflammatory condition affecting the supporting structures of the teeth, including the gingiva, periodontal ligament, cementum, and alveolar bone. It is primarily caused by the accumulation of microbial biofilms on tooth surfaces, leading to host immune responses that can result in progressive tissue destruction. This literature review aims to summarize current knowledge on the etiology and pathogenesis of periodontal disease, highlighting the role of microbial factors, host immune response, genetic predisposition, and environmental influences such as smoking and stress. Understanding the multifactorial nature of periodontal disease is essential for developing targeted preventiveand therapeuticstrategies. Keywords: periodontal disease, pathogenesis, inflammation, oral microbiota, host immune response, risk factors, biofilm, gingival inflammation Introduction. Periodontal disease, encompassing a spectrum of inflammatory conditions affecting the supporting structures of the teeth, stands as a significant global public health concern. Characterized by the progressive destruction of the periodontal ligament and alveolar bone, it often culminates in tooth loss if left untreated. The etiology of periodontal disease is multifactorial, involving complex interactions between pathogenic microorganisms in dental biofilmsand thehost's immuneresponse [1,5].​ Epidemiological data underscore the extensive prevalence of periodontal disease worldwide. According to the Global Burden of Disease Study 2021, over 1 billion individuals were affected by severe periodontitis, with an age-standardized prevalence of 12.5% . Notably, South Asia exhibited the highest prevalence rate at 17.6%. Projections indicate a substantial increase in the burden of severe periodontitis, with estimates suggesting that by 2050, more than 1.5billion peoplewill beaffected, marking a 44.3%risefrom 2021[11].​ The pathogenesis of periodontal disease is intricately linked to the host's immune- inflammatory response to microbial colonization. Initial bacterial accumulation triggers an innate immune response, characterized by the recruitment of neutrophils and the release of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α). These mediators not only orchestrate the inflammatory response but also stimulate the production of matrix metalloproteinases (MMPs), enzymes responsible for the degradation of extracellular matrix components, leading to connective tissue breakdown [12].​ Furthermore, the receptor activator of nuclear factor kappa-Β ligand (RANKL)/osteoprotegerin (OPG) axis plays a pivotal role in alveolar bone resorption associated with periodontitis [4,12]. An imbalance favoring RANKL promotes osteoclast differentiation and activation, resulting in bone loss. Additionally, emerging evidence 98,7:ROTCAFTCAPMI .SECNEICSLACIDEM,5202,yaM,5emuloV gro.srehsilbupcimedaca.www highlights the contribution of dysbiosis—a disruption in the composition of the oral microbiota—to thechronicity and progression ofperiodontal disease[14].​ Given the complex interplay of microbial, immunological, and environmental factors in periodontal disease pathogenesis, a comprehensive understanding of these mechanisms is essential for the development of effective preventive and therapeutic strategies. This literature review aims to elucidate the current knowledge on the etiopathogenic mechanisms underlying periodontal disease, with a focus on microbial interactions, host immune responses, and themolecular pathways involved in tissuedestruction[2, 8]. Periodontal disease, a chronic inflammatory condition affecting the supporting structures of the teeth, has been extensively studied due to its high prevalence and association with systemic health issues. Globally, periodontal diseases affect up to 90% of the population, making them the most common oral diseases [10,14]. In 2021, over 1 billion individuals were affected by severe periodontitis, with an age-standardized prevalence of 12.5% [9,11]. The pathogenesis of periodontal disease involves a complex interplay between microbial biofilms and the host's immune response. The commensal oral bacteria initiate the disease through dysbiosis, leading to an inflammatory response characterized by the release of pro- inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α). These mediators stimulate the production of matrix metalloproteinases (MMPs), enzymes responsible for the degradation of extracellular matrix components, resulting in connective tissuebreakdown [14]​ . Moreover, the receptor activator of nuclear factor kappa-Β ligand (RANKL)/osteoprotegerin (OPG) axis plays a pivotal role in alveolar bone resorption associated with periodontitis. An imbalance favoring RANKL promotes osteoclast differentiation and activation, leading to boneloss. ​ Several risk factors contribute to the development and progression of period