"Periodontitis, a complex inflammatory disease leading to the destruction of tooth-supporting structures, has a multifactorial etiology involving the interplay between microbial dysbiosis and host immune response (Pihlstrom, Michalowicz, & Johnson, 2005). It is crucial to understand the host immune factors that contribute to periodontitis pathogenesis for effective diagnosis and treatment development.

Periodontitis is a chronic multifactorial inflammatory disease characterized by the progressive destruction of periodontal tissues, including the gingiva, periodontal ligament, and alveolar bone (Pihlstrom, Michalowicz, & Johnson, 2005). It is one of the leading causes of tooth loss among adults, affecting approximately 42% of US adults aged 30 years and older (Eke et al., 2015). Besides its impact on oral health, periodontitis has also been linked to systemic diseases, such as diabetes, cardiovascular disease, and adverse pregnancy outcomes (Loos & Van Dyke, 2020).

Diagnosis of periodontitis is crucial for effective prevention, early intervention, and disease control. Accurate and timely identification of periodontitis allows for appropriate treatment planning and assessment of treatment success or failure. Currently, the diagnosis of periodontitis is based on clinical and radiographic evaluations, combined with patient-reported symptoms and medical and dental history (Caton et al., 2018). However, these conventional diagnostic methods have been criticized for their subjective nature, lack of sensitivity, and specificity, as well as their inability to predict disease progression and assess the therapeutic response in real time (Meyle & Chapple, 2015).

Periodontitis is defined as the chronic, multifactorial inflammatory disease of periodontal tissues that results in progressive destruction of the supporting structures of teeth (Pihlstrom, Michalowicz, & Johnson, 2005). It is the primary cause of tooth loss in adults, affecting approximately 42% of US adults aged 30 years and older (Eke et al., 2015). Moreover, periodontitis has been linked to other systemic diseases like diabetes, cardiovascular disease, and adverse pregnancy outcomes (Loos & Van Dyke, 2020). Given these relationships, early diagnosis of periodontitis is essential for effective prevention, intervention, and disease control.

Periodontitis diagnosis typically begins with a clinical examination that includes a periodontal probing to assess gingival inflammation, attachment level, suppuration, tooth mobility, and furcation involvement (Kinane, Stathopoulou, & Papapanou, 2017). Clinical attachment loss (CAL) and probing depth (PD) measurements are major indicators of periodontitis severity (Caton et al., 2018). The limitation of using these measurements lies in their subjectivity and sensitivity to inter-examiner variations (Meyle & Chapple, 2015).

Radiographic assessment is primarily used for detecting alveolar bone loss associated with periodontitis. Intraoral radiography, including periapical and bitewing radiographs, often holds their standard use in dentistry (Meyle & Chapple, 2015). However, this method provides limitations in reflecting the actual extent of bone loss, and detecting early changes in the disease, also posing exposures to radiation (Meyle & Chapple, 2015).

PRA is performed using indices such as the Periodontal Risk Assessment (Lang & Tonetti, 2003) or CDA Periodontal Screening Index (PSI) (Rams, 2015) to assess future risks of periodontal disease progression or tooth loss based on individual risk factors. However, these indices have limitations in their specificity and applicability, especially when determining the efficacy of individualized treatment plans.

The analysis of biomarkers, including inflammatory mediators, host-derived enzymes, and microbial products in saliva or gingival crevicular fluid (GCF), has shown potential for identifying active periodontal breakdown, monitoring disease progression, and evaluating treatment outcomes (Bartold, Van Dyke, & Reynolds, 2019).

Advancements in next-generation sequencing enable practitioners to explore complex oral microbiota and identify pathogens in periodontitis development (Camanocha & Dewhirst, 2014). Furthermore, multiplex Polymerase Chain Reaction (PCR) methods facilitate simultaneous detection of targeted periodontopathogens, informing tailored periodontitis therapy (Daalderop, Wieland, Tomsin, 'Rebel, & Van den Bosch, 2017).

With higher resolution, accuracy, and three-dimensional (3D) representation, technologies such as cone-beam computed tomography (CBCT), magnetic resonance imaging (MRI), and fluorescence imaging facilitate more precise detection of periodontitis-related bone loss and inflammation (Walter, Kaner, & Berndt, 2018).

Periodontitis is a multifactorial inflammatory disease involving the periodontal tissues and affecting a significant proportion of the global population (Pihlstrom, Michalowicz, & Johnson, 2005). It is characterized by the progressive destruction of supporting structures around teeth, including the periodontal ligament and alveolar bone, leading to tooth loss if left untreated (Bartold & Van Dyke, 2019). Traditionally, periodontitis has been associated with the presence of specific bacterial species; however, this view has evolved over time to encompass the complex interplay between microbial, host, and environmental factors that contribute to disease onset and progression (Hajishengallis & Lamont, 2012).

The etiology of periodontitis is complex and multifactorial, involving interrelated factors such as oral bacteria, host immune response, and genetic and environmental influences (Hajishengallis, 2014). Oral biofilms, comprising a diverse bacterial community, develop in the subgingival environment, where certain bacterial species are implicated in the pathogenesis of periodontitis (Socransky et al., 1998). Among these, Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola, part of the so-called “red complex,” have been consistently associated with periodontal disease (Holt & Ebersole, 2005).

Importantly, host immune responses play a critical role in the pathogenesis of periodontitis, with the presence of bacterial pathogens alone not sufficient to induce disease (Hajishengallis, 2014). In response to bacterial insult, the host elicits an inflammatory reaction aimed at eliminating the microbial source. However, dysregulated and excessive host response, mediated by pro-inflammatory cytokines, can result in tissue breakdown and alveolar bone resorption, manifesting as clinical signs of periodontitis (Garlet, 2010).

Furthermore, the susceptibility to periodontitis is influenced by genetic factors and various environmental risk factors, such as smoking, diabetes mellitus, and obesity (Kinane & Stathopoulou, 2017). For instance, genetic polymorphisms in the interleukin-1 (IL-1) gene have been associated with increased risk of severe periodontitis (Kornman et al., 1997).

Periodontitis manifests as the progressive destruction of the tooth-supporting structures, including loss of attachment, pocket formation, and alveolar bone loss (Bartold & Van Dyke, 2019). The recent classification scheme, based on the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions, has replaced the traditional categories with a staging and grading system that allows better risk assessment and tailored treatment planning (Caton et al., 2018).

The primary goal of periodontitis treatment is to control the microbial etiology and halt the progression of the disease (Bartold & Van Dyke, 2019). Therapy modalities include non-surgical approaches, such as scaling and root planing (SRP), which entails mechanical removal and disruption of subgingival biofilms (Cobb, 2002). In cases of advanced periodontitis, surgical techniques may be employed to access deeper periodontal pockets and restore lost periodontal structures (Pihlstrom et al., 2005).

Preventative strategies for periodontitis mainly focus on oral hygiene practices to minimize plaque accumulation and control gingival inflammation, including daily oral care and regular dental check-ups (Bartold & Van Dyke, 2019).

Periodontitis is a chronic inflammatory disease of the periodontium, characterized by the destruction of the supporting structures of the teeth, including the periodontal ligament, alveolar bone, and connective tissue attachment (1). It results from a complex interplay between a dysregulated host immune-inflammatory response and specific subsets of bacteria within the dental plaque biofilm, such as Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola (2).

The initiation of periodontitis begins with the accumulation of dental plaque, which triggers inflammation in the gingival tissue, leading to gingivitis. If left untreated, the inflammatory response can progress to periodontitis, involving the irreversible loss of periodontal tissues and ultimately resulting in tooth loss (3). The host immune response plays a crucial role in the pathogenesis, as the immune system attempts to defend against invading pathogens by secreting cytokines, chemokines, and antimicrobial peptides, including defensins (4).
References:

1. Hajishengallis G. Periodontitis: from microbial immune subversion to systemic inflammation. Nat Rev Immunol. 2015;15(1):30-44.

2. Socransky SS, Haffajee AD. The bacterial etiology of destructive periodontal disease: current concepts. J Periodontol. 1992;63(4 Suppl):322-331.

3. Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontol 2000. 1997;14:9-11.

4. Gemmell E, Seymour GJ, Payne W. Cytokines and inflammation in periodontitis: a current understanding and implications for a future therapeutic paradigm. Periodontol 2000. 2021;87(1):127-137.

Periodontitis is a multifactorial chronic inflammatory disease characterized by the destruction of the tooth-supporting structures, leading ultimately to tooth loss (Pihlstrom et al., 2005). It affects a large percentage of the global population and is considered a significant oral health problem with severe implications for an individual’s overall health (Nazir, 2017).

The primary etiological agents driving periodontitis are bacteria that colonize the tooth surface and subgingival environment, forming dental biofilms, more commonly known as dental plaque (Hajishengallis, 2014). These bacteria initiate an inflammatory response, which can lead to the stimulation of osteoclastogenesis and alveolar bone resorption triggered by host inflammatory mediators (Darveau, 2010).

Additionally, several risk factors, both genetic and environmental, are implicated in the development and progression of periodontitis. Environmental factors, such as smoking, nutrition, stress, and diabetes, significantly contribute to disease development (Tonetti et al., 2013). Genetic factors are also pivotal in determining an individual’s susceptibility to periodontitis, with genetic polymorphisms associated with the regulation of the immune response and host inflammation identified as significant contributors (Nibali et al., 2010).

The pathophysiology of periodontitis involves a complex interplay between the dental biofilm, host immune response, and genetic predisposition (Lamont & Hajishengallis, 2015). Initial microbial colonization leads to a host immune response characterized by the infiltration of various immune cells, such as neutrophils, macrophages, and lymphocytes, and the release of pro-inflammatory cytokines, which can exacerbate the inflammatory response (Hajishengallis & Lamont, 2012). Chronic inflammation induces tissue destruction and alveolar bone resorption mediated primarily by tumor necrosis factor-alpha (TNF-α), interleukins (IL-1, IL-6, and IL-8), and matrix metalloproteinases (MMPs) (Bartold & Narayanan, 2006).

The role of the immune system in periodontitis has expanded beyond the initial view of just protecting the host against periodontal pathogens. It is becoming increasingly evident that dysbiosis in the host immune response contributes significantly to the overall disease pathogenesis (Graves et al., 2016). A simplified model of this scenario is as follows: an imbalance in the local environment, driven by periodontopathogens, disrupts the equilibrium between the host’s pro-inflammatory and anti-inflammatory responses, leading to an exacerbation of the inflammatory process and subsequent tissue destruction (Hajishengallis & Lamont, 2014).

The diagnosis of periodontitis is primarily based on clinical examination, including periodontal pocket probing, the assessment of clinical attachment loss, and radiographic analysis of alveolar bone levels (Armitage & Cullinan, 2010). Periodontitis is characterized by clinical signs and symptoms such as bleeding on probing, gingival recession, halitosis, suppuration, tooth mobility, and migration (Rosenberg et al., 2018).

Periodontitis is categorized into various stages and grades based on severity, complexity, and the rate of disease progression (Tonetti et al., 2018). The staging of periodontitis is determined by the extent of clinical attachment loss, pocket depth, and radiographic bone loss, while the grading system reflects the rate of disease progression, taking into account factors such as risk factors and response to therapy (Caton et al., 2018).

The management of periodontitis involves a combination of non-surgical and surgical approaches, focusing on controlling the local factors contributing to disease progression and managing systemic risk factors (Sanz et al., 2020). The primary goal of periodontal therapy is to disrupt the bacterial load in the subgingival environment to halt disease progression and foster tissue regeneration (Cobb, 2002).

Non-surgical therapy includes oral hygiene instructions, scaling, root planing, and adjunctive use of antimicrobials (Singhrao & Olsen, 2020). Systemic antibiotics, such as amoxicillin and metronidazole, are prescribed in conjunction with non-surgical therapy in specific cases to enhance the elimination of periodontopathogens (Jepsen et al., 2016).

Surgical approaches, including flap surgery, guided tissue regeneration, and osseous surgery, are indicated in cases where non-surgical therapy fails to achieve desired results, or when periodontal pockets are too deep for adequate debridement (Cortellini & Tonetti, 2015).

Advances in regenerative periodontal therapies have been a significant area of interest, with the primary objective of regenerating lost periodontal tissues (Chen et al., 2016). Techniques such as enamel matrix derivative application, the use of platelet-rich plasma, growth factors, and bone morphogenetic proteins have shown promising results in promoting periodontal regeneration (Alayan & Vaquette, 2018). 

Other therapeutic strategies have emerged in recent years, such as photodynamic therapy, which employs photosensitizing dyes activated by specific wavelengths of light to eliminate periodontopathogens (Buchmann et al., 2016). Additionally, the use of probiotics, prebiotics, and synbiotics has gained considerable interest as an adjunctive treatment for periodontitis, aiming to modulate the oral microbiota and restore the ecological balance (Vicario et al., 2018).\

The bidirectional association between periodontitis and systemic health has long been a subject of interest, with several studies linking periodontitis to systemic conditions like diabetes, cardiovascular disease, adverse pregnancy outcomes, and respiratory diseases (Nazir, 2017). The underlying mechanisms for these associations range from the systemic dissemination of periodontal pathogens and their products to the influence of periodontitis-associated inflammatory mediators on systemic inflammation (Borgnakke, 2020)." Please rewrite the above text again taking out any duplicate and including every reference. Try to give a structure as follow : 1. definition of periodontitis,  2. etiology, 3. classification, 4. possible use of  other methods for detection of periodontitis.