Periodontitis PDF

NEAR EAST UNİVERSİTY FACULTY OF DEPARTMENT OF PERIODONTOLOGY PERİODONTİTİS Learning outcomes: 1-Will be able to describe chronic periodontitis, aggressive periodontitis, and necrotizing periodontitis according to the 1999...

NEAR EAST UNİVERSİTY FACULTY OF DEPARTMENT OF PERIODONTOLOGY PERİODONTİTİS Learning outcomes: 1-Will be able to describe chronic periodontitis, aggressive periodontitis, and necrotizing periodontitis according to the 1999 classification. 2-Will be able to list the causes and risk factors for chronic, aggressive, and necrotizing periodontitis. 3-Will be able to clinically differentiate and associate chronic, aggressive, and necrotizing periodontitis. Periodontitis is defined as a complex inflammatory disease that affects the tooth-supporting structures, including the periodontal ligament and alveolar bone. In this context, the word “complex” describes not only the fact that there are multiple clinical symptoms that account for the disease, but also because of the multiple factorsthat lead to and influence periodontal inflammation. Periodontitisoccurs most frequently in adults. Nonetheless, it may also be diagnosed in children and adolescents when associated with chronic plaque and calculus accumulation. Therefore, periodontitis should be understood as age-associated, but not age-dependent, complex chronic inÀammation of the periodontal tissues. As described below, systemic and/or environmental factors (e.g., diabetes mellitus, smoking) modify the host immune response to the dental biofilm so that the periodontal destruction becomes more progressive. Periodontitis is a highly prevalent progressing disease and is considered the sixth most common human disease which belongs to the group of chronic non- communicable diseases (CNCDs). It a ects approximately 10%, 5% up to 12% of the world population. In the past decade, it has been found that periodontitis exerts adverse e ects on systemic health, and in this context, important pathological interdependencies with, for example, diabetes mellitus have been identified. Also, it is known that systemic inflammatory markers, such as the C-reactive protein (CRP), are elevated in patients with periodontitis. In general, periodontitis is considered a slowly progressing disease, but in the presence of severe systemic conditions and/or environmental factors, such as smoking, this inflammatory disease progresses more rapidly. The former classification described two different major forms of periodontitis, aggressive and chronic periodontitis, with aggressive periodontitis being defined as a rapidly progressing entity in systemically healthy subjects with a familiar aggregation. The classical definition reffected periodontitis as “an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss.” In the past decades, the etiopathologic factors that lead to periodontal inflammation,and subsequently, in the destruction of periodontal tissues have been widely studied, and the interplay between the microbial environment and the individual host immune response gained attention in the scientific community. Periodontitis represents major clinical and etiologic characteristics of this complex disease: (1) microbial biofilm formation (dental plaque), (2) periodontal inflammation (gingival swelling, bleeding on probing), and (3) attachment as well as alveolar bone loss. Besides the local immune response to the dental biofilm periodontitis may also be associated with a number of systemic disorders and defined syndromes. In most cases, patients with systemic diseases, which lead to impaired host immunity, may also show periodontal destruction. On the other hand, periodontitis is a disease not only limited to the area of the oral cavity, but may be associated with severe systemic diseases such as cardiovascular disease, stroke, and diabetes mellitus. 1 As discussed in our 'Classification of Periodontal Diseases' course, the classification of periodontal diseases has been revised by the European Federation of Periodontology (EFP) and the American Academy of Periodontology (AAP) in 2017. A multidimensional staging and grading system has been established, which can be adapted over time as new evidence emerges for periodontitis. In order to avoid terminology confusion in current literature and research, this course will cover Chronic Periodontitis, Aggressive Periodontitis, and Necrotizing Periodontitis as described in the 1999 classification. CHRONİC PERİODONTİTİS According to the 1999 classification, periodontitis referred to as chronic periodontitis is a disease characterized by inflammation of the tissues supporting the teeth due to plaque accumulation, leading to attachment and bone loss. Environmental factors such as diabetes, smoking, and stress can influence the host's response to plaque accumulation, thereby affecting the speed and severity of the disease. While it is commonly observed in adults, chronic plaque and calculus accumulation can also manifest in children and adolescents. CLINICAL FEATURES Supragingival and subgingival plaque accumulation (often accompanied by calculus), gingival inflammation, pocket formation, alveolar bone and attachment loss, and occasionally suppuration are characteristic clinical features. If the patient's oral hygiene is poor, there will be an increase in bluish discoloration of the gingiva and the appearance of swelling. Spontaneous or bleeding during probing may be observed. In long-standing chronic cases, the gingiva may exhibit thickening and a fibrotic appearance. Gingival pockets can vary in depth. Horizontal and/or vertical bone loss is present. The extent of destruction of periodontal tissues is proportional to oral hygiene and plaque levels, local, predisposing factors, and systemic risk factors such as smoking and stress. Subgingival biofilm (plaque) contains various bacterial species, and the composition of the biofilm can vary from person to person and region to region. Permanent subgingival calculus is found in diseased areas. While microbial plaque initiates the disease, the pathogenesis and progression are determined by host factors. The rate of progression, although generally slow, can have periods of rapid destruction in some cases. Untreated diseased areas tend to continue experiencing periodontal destruction. Characteristic clinical findings in patients with untreated chronic periodontitis include the following: Supragingival and subgingival plaque and calculus Gingival swelling, redness, and loss of gingival stippling Altered gingival margins (e.g., rolled, flattened, cratered papillae, recessions) Pocket formation Bleeding on probing Attachment loss (angular or horizontally) Bone loss Root furcation involvement (exposure) Increased tooth mobility Change in tooth position Tooth loss Site Specificity of Chronic Periodontitis Not all sites in the mouth are equally prone to chronic periodontitis, and it exhibits site specificity. The progression of the disease occurs in certain sites but not uniformly. Interproximal sites, in general, are more prone to periodontal destruction, compared to buccal/facial sites. Disease Distribution Chronic periodontitis is considered a site-specific disease. Local inflammation, pocket formation, attachment loss, and bone loss are the consequences of direct exposure to the subgingival plaque 2 (biofilm). As a result of this local effect, pocket formation and attachment as well as bone loss may occur on one surface of a tooth, whereas other surfaces maintain normal attachment levels. As a result of the site-specific nature, the number of teeth with clinical attachment loss classifies chronic periodontitis into the following types: Localized chronic periodontitis: less than 30% of the sites show attachment and bone loss Generalized chronic periodontitis: 30% or more of the sites show attachment and bone loss Disease Severity The severity of periodontal destruction that occurs as a result of chronic periodontitis is generally considered a function of time in combination with systemic disorders that impair or enhance host immune responses. With increasing age, attachment loss and bone loss become more prevalent and more severe as a result of an accumulation of destruction. Disease severity may be described as mild, moderate, or severe: Mild chronic periodontitis: when no more than 1 mm to 2 mm of clinical attachment loss has occurred Moderate chronic periodontitis: when 3 mm to 4 mm of clinical attachment loss has occurred Severe periodontitis: when 5 mm or more of clinical attach- ment loss has occurred Symptoms Chronic periodontitis is commonly a slowly progressive disease that does not cause the affected individual to feel pain. Therefore, most patients are unaware that they have developed a chronic disease that is also associated with other systemic diseases (e.g.,cardiovascular disease). For the majority of the patients, gingival bleeding during oral hygiene procedures or eating may be the first self-reported sign of disease occurrence. As a result of gingival recession, patients may notice black triangles between the teeth or tooth sensibility in response to temperature changes. Progression Patients appear to have the same susceptibility to plaque induced chronic periodontitis throughout their lives. The rate of disease progression is usually slow, but it may be modified by systemic, environmental, and behavioral factors. The onset of chronic periodontitis can occur at any time, and the first signs may be detected during adolescence in the presence of chronic plaque and calculus accumulation. Because of its slow rate of progression, however, chronic periodontitis usually becomes clinically significant when a patient reaches his or her mid-30s or later. Chronic periodontitis does not progress at an equal rate in all affected sites throughout the mouth. Some involved areas may remain static for long periods,whereas others may progress more rapidly. More rapidly progressive lesions occur most frequently in interproximal areas, and they may also be associated with areas of greater plaque accumulation and inaccessibility to plaque control measures (e.g., furcation areas, overhanging margins of restorations, sites of malposed teeth, areas of food impaction). Prevalence Chronic periodontitis increases in prevalence and severity with age, and it generally affects both genders equally. Periodontitis is an age-associated (not an age-related) disease. Nonetheless, the prevalence of periodontitis increases with age so that 40% of patients who are 50 years old or older and almost 50% of patients who are 65 years old or older show moderate periodontal destruction. The prevalence of severe forms of periodontitis also increases with age. Up to 30% of patients develop severe periodontitis by the time they are 40 years old or older. Generally, 50% of the human population experiences at least one form of periodontal disease 3 Risk Factors for Disease Risk factors can be part of the causal chain of a disease and/or make the host more susceptible to disease development. The risk factors for chronic periodontitis are primarily classified into the following main groups: 1-Prior history of periodontitis 2-Microbiological aspects 3-Systemic factors 4- Local factors 5-Immunological factors 6-Genetic factors 7-Environmental and behavioral factors 1-Prior history of periodontitis A history of previous periodontitis is not a true risk factor for new attachment and bone loss. However, it is crucial to continuously monitor patients, even if they have successfully received treatment, as inadequate plaque control after treatment can lead to disease recurrence. In untreated cases, the disease may progress, and tissue destruction continues. In treated cases, the likelihood of disease recurrence is summarized in terms of the disease's progression and ongoing tissue destruction in the absence of sufficient plaque control. Regular follow-ups are essential to ensure the long-term success of periodontal treatment. 2-Microbiological Aspects Plaque accumulation on tooth and gingival surfaces at the dento gingival junction is considered the primary initiating agent in the etiology of gingivitis and chronic periodontitis. Attachment and bone loss are associated with an increase in the proportion of gram-negative organisms in the subgingival biofilm, with specific increases in organisms that are known to be exceptionally pathogenic and virulent. Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola—otherwise known as the “red complex”—are frequently associated with ongoing attachment and bone loss in patients with chronic periodontitis. The development and progression of chronic periodontitis may not depend on the presence of one specific bacterium or bacterial complex alone. It is assumed that chronic periodontitis is the result of a multispecies infection with a number of different bacteria that influence the pro-inflammatory immune response of the host. 3-Local Factors Plaque accumulation and biofilm development are the primary causes of periodontal inflammation and destruction. Therefore,factors that facilitate plaque accumulation or that prevent plaque removal by oral hygiene procedures can be detrimental to the patient. Plaque-retentive factors are important for the development and progression of chronic periodontitis, because they retain microorganisms in proximity to the periodontal tissues, thereby providing an ecologic niche for biofilm maturation. Calculus is considered the most important plaque-retentive factor as a result of its ability to retain and harbor plaque bacteria on its rough surface as well as inside. As a consequence, calculus removal is essential for the maintenance of a healthy periodontium. In addition, tooth morphology may influence plaque retention. Roots may show grooves or concavities, and, in some instances, enamel projections on the surface or the furcation entrances. These morphologic variations may facilitate plaque retention, subgingival calculus formation, and disease progression.In addition, subgingival and overhanging margins of restorations, carious lesions that extend subgingivally, and furcations exposed by loss of bone promote plaque retention. 4  Common Retentive Local Factors That Contribute to Chronic Periodontitis Dental calculus Crown margins Restoration overhangs Furcation involvement Deep probing depths Anatomic grooves on the roots Subgingival caries or resorptive lesions 4-Systemic Factors Periodontitis is reported to be associated with other systemic disorders such as Haim-Munk, Papillon-Lefèvre, Ehlers-Danlos, Kindlers, and Cohen syndromes. Diseases that disrupt the host's immune response, such as acquired immune deficiency syndrome (AIDS), can also lead to periodontal breakdown. Osteoporosis, irregular nutrition, stress, dermatological, hematological, and neoplastic issues can impact inflammatory periodontal responses. Additionally, uncontrolled diabetes mellitus is a risk factor for periodontal diseases. There is a bidirectional relationship between Diabetes Mellitus and periodontitis. Diabetic patients are at a higher risk for the development of periodontitis, as periodontal infection and inflammation can negatively impact the diabetic patient's glycemic control. It has been observed that average pocket depth and clinical attachment loss are increased in diabetics. Patients with poor glycemic control (HbA1c > 9) have been shown to develop more severe periodontitis compared to those with good glycemic control (HbA1C < 9). No significant differences were found between individuals with good glycemic control who had diabetes and those without diabetes. In the presence of diabetes mellitus, increased release of Advanced Glycation End Products (AGEs), free oxygen, and pro-inflammatory mediators (e.g., cytokines) occurs. AGEs also enhance chemotaxis and adhesion of inflammatory cells to periodontal tissues, and there is increased apoptosis of fibroblasts and osteoblasts. Moreover, diabetic patients exhibit a higher body mass index, leading to increased concentrations of adipokines that directly affect the inflammatory response. Hyperglycemia alone induces the release of pro-inflammatory mediators, contributing to increased glucose concentration in the bloodstream. Periodontal treatment contributes to glycemic control in diabetic patients. Systemic periodontal treatment has been shown to reduce HbA1C by 0.4%. Each treatment procedure that reduces HbA1C levels contributes to reducing complications such as myocardial infarction and microvascular complications that diabetes can lead to in the long term. 5- Immunologic Factors Chronic periodontitis is a disease that is induced by bacteria organized in the dental biofilm. However, the onset, progression, and severity of the disease depend on the individual host’s immune response. Patients may show alterations in their peripherial monocytes, which are related to the reduced reactivity of lymphocytes or an enhanced B-cell response. B-cells, macrophages, periodontal ligament cells, gingival fibroblasts, and epithelial cells synthesize pro-inflammatory mediators (e.g., interleukin-1β, interleukin-6, interleukin-8, prostaglandin E2, tumor necrosis factor- α) that modify innate and adaptive immune responses at periodontal site. 6-Genetic Factors Periodontitis is considered to be a multifactorial disease that is influenced by local, systemic, and immunologic factors, as described previously. Each factor is in turn directly related to individual genetic conditions. Genetic variations such as single nucleotide polymorphisms (SNPs) and genetic copy number variations may directly influence innate and adaptive immune responses as well as the structure of periodontal tissues. Periodontal destruction has been found among family members and across different generations within a family, thereby suggesting a genetic basis for the susceptibility to periodontal disease. In a number of studies, the prevalence of aggressive and 5 chronic periodontitis has been investigated in families with a history of one or more family members with periodontitis. 7-Environmental and Behavioral Factors In addition to microbial, immunologic, and genetic factors, the development and progression of chronic periodontitis is further influenced by environmental and behavioral factors, such as smoking and psychological stress. Smoking is a major risk factor for the development and progression of generalized chronic periodontitis. Periodontitis is influenced by smoking in a dose dependent manner. The intake of more than 10 cigarettes per day tremendously increases the risk of disease progression as compared with non-smokers and former smokers. As compared with non-smokers, the following features are found in smokers: Increased periodontal pocket depth of more than 3 mm Increased attachment loss More recessions Increased loss of alveolar bone Increased tooth loss Fewer signs of gingivitis (e.g., less bleeding with probing) Greater incidence of furcation involvement As a result of the consumption of tobacco, reactive oxygen (i.e., radicals) is released that chemically irritates periodontal tissues via DNA damage, the lipid peroxidation of cell membranes, the damage of endothelial cells, and the induction of smooth muscle cell growth. Stress and Periodontal Disease: Potential Mechanisms 1. Immunosuppression via cortisol secretion 2. Poor oral hygiene compliance in patients with chronic stress 3. Patients with stress are less likely to seek professional care 4. Patients with stress may smoke more frequently Treatment of Chronic Periodontitis Chronic periodontitis can be treated effectively by a systematic periodontal therapy that includes optimal long-term plaque control, debridement of soft and hard deposits, or surgical pocket reduction (case-dependently either resective osseous surgery or regenerative surgery. Depending on the individual periodontal risk, each patient should be remotivated, reinstructed, and retreated (if necessary) during a systematic supportive periodontal therapy regimen (revisits every 3, 6, or 12 months). AGGRESSİVE PERİODONTİTİS Aggressive Periodontitis (AgP), as named in the 1999 classification, is generally an inflammatory disease associated with many complex factors, characterized by advanced bone loss and tooth loss that typically begins at an early age. The progression and severity of the disease are shaped by various factors such as microbiological, immunological, genetic, environmental, and racial factors, as well as interactions with unmodifiable risk factors like age, gender, and race. The etiology is not fully understood. The part previously referred to as Aggressive Periodontitis (AgP) in the 1999 classification is represented in the table in the new classification. The disease progresses rapidly, and in the grading, the presence of more than 2 mm of attachment loss within a period of over 5 years is established as a criterion, observable only through the follow-up of the patient. However, when the patient is young (e.g., in their 20s) and there is severe bone and attachment loss, it can be presumed that the patient has a rapidly progressing type. 6 Periodontitis stage Stage I (Mild Disease) Stage II (Modarate Stage III (Severe Stage IV (Very Severe Disease) Disease) Disease) Severity Interdental CAL 1-2 mm 3-4 mm ≥ 5 mm ≥ 5 mm Radiographic Coronal third of the root Coronal triple (%15-33) extending to the middle or extending to the middle or bone loss (RL) (