risk factors for aggressive periodontitis

[2] The prevalence of LAP is less than 1% and that of GAP is 0.13%. In fact, 70.1% of adults65 years and older have periodontal disease. KEYWORDS aggressive periodontitis, diagnosis, epidemiology, genetics, inflammation and innate immunity, [15][16], Patients do not have any underlying systemic disease that would contribute to aggressive periodontitis. [37] Careful interpretation of the history is required but it may provide vital evidence in diagnosing AgP. [8], Capnocytophaga spp are implicated as prime periodontal pathogens, especially in localised aggressive periodontitis. This response is known to be present in the destructive phase, where there is presence of bone and attachment loss. Implants in function for a significant number years can develop peri-implantitis. Research has indicated that some people may be genetically susceptible to gum disease. Previous studies have focused on a single (among many possible) immunological risk factor and the association among the factors has not been assessed. Diseases such as rheumatoid … (lor additional information on smoking and periodontal disease, see < hapter 14. Instructions should also be given on how to clean adequately around fixed restorations and appliances, and how to clean removable prostheses. Genetic Factors. Certain medications that cause dry mouth or gum changes 11. Studies found that smokers have more affected teeth than non-smokers and high levels of attachment loss. Studies also have demonstrated that the antibody response to periodontal pathogens, particularly A. octinomycctcniconuUins. The objective of treatment is to create a conducive clinical condition for retaining as many teeth, for as long as possible.[40]. Using different methods, including immunocytochemistry and elec-tromicroscopy, several tissue-invading microorganisms have been identified as.actuiomyceleincatniliuts, (apito-cytophaga sputigena, Mycoplasma spp., and spirochetes. In Malayalam speaking Dravidian population, IL-4 + 33C/T loci appears to be an important risk factor for periodontal disease with a leaning towards aggressive periodontitis. However, segregational analyses and linkage analyses of families with a genetic predisposition for localized aggressive periodontitis suggest that a major gene plays a role in this disease, which is transmitted through ari autosomal dominant mode ot inheritance in U.S. populations11 (see Chapter 10). This page was last edited on 5 December 2020, at 10:50. Aggressive periodontitis runs in the patient's family. Box 4-1. However, age is only one of the risk factors of periodontal disease. It is also important for a dental practitioner to check for family history of periodontal disease for each patient. If a case of Agp is diagnosed, it is important to screen the patient's family members as well for AgP. Ilectron microscopic studies of localized aggressive periodontitis have revealed bacterial invasion of connective tissue9,11 that reaches the bone surface. Smoking, oral hygiene, and psychological factors seem to play a role in both chronic and aggressive periodontitis. diastema formation with disto-labial migration of the incisors. Hormonal changes (sometimes caused by pregnancy or menopause) 2. Smoking or chewing tobacco 7. According to the CDC, periodontal disease increased with age. [26] There is also a relatively fast progression of periodontal tissue loss. [23], Due to the increased responsiveness, the macrophages produce excessive levels of inflammatory mediator and cytokine, such as prostaglandin E2 (PGE2) and interleukin-1β (IL-1B). The inflammatory exudate in the gingival tissues and gingival crevicular fluid is mostly polymorph neutrophils but also includes B cells and plasma cells. This stage of treatment involves the reassessment of the individual's compliance (i.e. Prior to starting periodontal treatment, any overhanging or poorly contoured restorations should be modified or replaced. [14], According to the 1999 International Workshop for the Classification of Periodontal Diseases, aggressive periodontitis was defined according to 3 primary features, in contrast to chronic periodontitis. Results from several studies support the concept that all individuals are not equally susceptible to aggressive peri odontitis.1" Specifically, several authors have described a familial pattern of alveolar bone loss and have implicated genetic factors in aggressive periodontitis., :s u Currently, specific genes have not been identified that are responsible for these diseases. Genetic and environmental risk factors for chronic periodontitis and aggressive periodontitis Periodontol 2000. [27], The alveolar bone loss patterns are usually bilateral and similar on both sides and has been referred to as being a ‘mirror-image’ pattern. Although the findings with many HLA antigens have been inconsistent, I ILA-A9 and BIS antigens are consistently associated with aggressive periodontitis (see Chapter 10). Additionally, poorly functional inherited forms of monocyte FcyRII. Health conditions that decrease your immunity 9. [20] Usually the loss of attachment is greater than 2mm per year. Periodontal surgery: If it is a localised problem and if the case is non-response to non-surgical treatment despite the oral hygiene being consistently excellent. The main distinction between the localized and generalized form of AgP lies in the number of teeth affected. Monocytes respond to bacterial and inflammatory stimuli with very high levels of local release inflammatory mediators and induce hyper-inflammatory reaction with activation of tissue degrading matrix-metalloproteinases. [26], Secondary features of LAP may also be present including;[26], Radiographically, the periodontal lesion often presents with alveolar bone loss in a horizontal pattern at the interproximal surface of the permanent first molars [26][27][28] and usually horizontal bone pattern of bone loss at the interproximal surface of the incisors as the bone is thinner than at the interproximal surface of the molars. These is also evidence they produce increased amounts IL-1α and IL-1β which cause osteoclastic bone resorption. In addition, A. actinomya'taneon tit at is often can be detected in periodontalty healthy subjects, suggesting that this microorganism may be part of the normal flora in many individuals. The patient is said to have a high genetic susceptibility to aggressive periodontitis. Genetic and environmental risk factors for chronic periodontitis and aggressive periodontitis. [27], The amount of plaque present is inconsistent with the amount and severity of tissue destruction [26][27] but with a high plaque pathogenicity due to the presence of increased levels of bacteria like Aggregatibacter actinomycetemcomitans (A.a) and Porphyromonas Gingivalis (P.g). These features are common for both localized and generalized form of disease. Host defences involve multiple factors; saliva, epithelium, inflammatory response, immune response and chemical mediators. These amounts are greatly reduced following treatment.[11]. Genetics. Aggressive periodontitis (AgP) is a disease characterized by rapid loss of periodontal tissues affecting systemically healthy individuals under age of 30 years. ), Treating gum disease with homemade remedies, Periodontal Flap Surgery Continous Sling Suture, Bone Destruction Patterns In Periodontal Disease, Undercontoured Teeth - Periodontal Disease, Internal Bevel Incision - Periodontal Disease. However, for the disease process to initiate the person must be exposed to the presence of periodontal pathogens and potentially also various environmental factors. Patients with generalized aggressive periodontitis who smoke have more affected teeth and more loss ol clinical attachment than nonsmoking patients with generalized aggressive periodontitis.1" However, smoking may not have the same impact on attachment levels in younger patients with localized aggressive periodontitis. Aggressive periodontitis is classified into localized and generalized forms. They are implicated in the development of aggressive periodontitis by triggering inflammatory response in periodontal tissue. Genetics 3. Even though the prevalence of aggressive periodontitis is much lower than chronic periodontitis, the management of aggressive periodontitis is more challenging compared to that of chronic periodontitis because of its strong genetic predisposition as an unmodifiable risk factor. [5], Porphyromonas gingivalis is a Gram-negative anaerobe associated with the pathogenicity of periodontal disease,[8] and aggressive periodontitis is no exception. Gingivitis 2. '0 T hese PMN and monocyte defects may be induced by the bacterial infection or may he genetic in origin. Ayala Stabholz. Dental practitioners should also be aware of false pocketing around erupting/newly erupted teeth in the mixed dentition phase and also in the presence of gingival inflammation. Of the microflora characterised in aggressive periodontitis, approximately 65-75% of bacteria are Gram-negative bacilli, with few spirochaetes or motile rods present. Inadequate nutrition, including vitamin C deficiency 9. For example. Some immune detects have been implicated in the pathogenesis of aggressive periodontitis. The neutrophils may show an intrinsic functional defect and respond abnormally when challenged by certain pathogens. Several investigators10,2*-'4 have shown that patients with aggressive periodontitis display functional defects of polymorphonuclear leukocytes (PMNs), monocytes, or both. Although several specific microorganisms frequently are detected in patients with localized aggressive periodontitis {A. actinomycetemconntans, (Atpnocytophaga sp., Tikcncllu corrodens, Prevotella intermedia, and Campylobacter rectus), A. actinomycetemcomitans has been implicated as the pri mary pathogen associated with this disease. Risk factors for aggressive form of periodontitis Microbiologic factors Immunologic factors Genetic factors Environmental factors 25. Necrotizing periodontal disease: Death of periodontal tissue caused by a lack of blood supply can pave the way for a severe infection, and this usually affects people with a suppressed immune system. Genetic Risk Factors for Periodontitis Bryan Michalowicz, D.D.S Division of Periodontology. The localized and generalized forms are not merely different in extent; they differ in etiology and pathogenesis. Other risk factors include: 1. [24], In some patients, the disease may burnout without any cause-related therapy. Given the 'right' concurrence of risk factors, a person with periodontitis can experience significant destruction of tooth-supporting bone, ultimately resulting in tooth loss. [21] In this case, the manifestation of aggressive periodontitis is believed to be the result of genetic mutation, combined with environmental factors.[21]. Effect sizes were taken as the natural-log of the odds ratio (OR) per periodontitis risk-increasing allele. [3] Estimates of the disease prevalence are 1-5% in the African population and in groups of African descent, 2.6% in African-Americans, 0.5-1.0% in Hispanics in North America, 0.3-2.0% in South America, and 0.2-1.0% in Asia. Hormonal changes, such as those related to pregnancy or menopause 6. These gram-negative microbes are considered the chief aetiological agent of aggressive periodontitis. Of the microflora characterised in aggressive periodontitis, approximately 65-75% of bacteria are Gram-negative bacilli, with few spirochaetes or motile rods present. As summarized by Tonetti and Mombelli,4'' this link is based on the following evidence: (1) A. actinomycetcmcomitans is found in high frequency (approximately 90%) in lesions characteristic of localized aggressive periodontitis, (2) sites with evidence of disease progression often show elevated levels of .4. actinomycetemcomitans, M) many patients with the clinical manifestations of localized aggressive periodontitis have significantly elevated serum antibody titers to A. actinomycetemcomitans, (4) (linical studies show a correlation between reduction in the subgingival load of A. uctinomycetemcomitans during treatment and a successful clinical response, and (5) A. uitinonlyceteincotni* tans produces a number of virulence factors that may contribute to the disease process (see also ( hapter 6). [38][39] Early detection of AgP allows intervention to be carried out before extensive periodontal destruction has taken place which further simplifies treatment. Aggressive periodontitis generally affects svstemicallyhealthy individuals less than 30 years old althoughpatients may be older.Aggressive periodontitis may be distinguished fromchronic periodontitis by the age of onset, the rapid rateof disease progression, the nature and composition ofthe subgingival microflora, alterations … As summarized by lonetti and MomheUi,1' "It seems that specific genes may be different in various populations and/or ethnic groups and therefore true heterogeneity in disease susceptibility may be present. However, it is unlikely that all patients affected with aggressive periodontitis have the same genetic defect. Studies of families, twins and sibling pairs have provided strong evidence for a genetic basis for aggressive periodontitis. [49] It is thus necessary to attend frequent review appointments at the dentist to ensure there is no relapse of the disease, and that the periodontal health is maintained after active periodontal therapy. Knowledge of the risk indicators of aggressive periodontitis (AgP) will help clinicians to better diagnose the disease, put a treatment plan that involves modification of modifiable risk indicators, understand non-modifiable risk indicators, and may potentially serve as an aid in developing preventive programs. [34][35] The presence of bleeding on probing (BOP) should be noted which is an indicator of active disease. Phagocytes are essential in resolving inflammation. AgP classified into two categories named localized and generalized aggressive periodontitis. Local risk factors can increase the risk of periodontal disease development and progression principally by acting as plaque retention factors. It has also been found that a low T-helper to T-suppressor ratio is found in aggressive periodontitis which may alter local immune regulation. Localized aggressive periodontitis in 15-year-old black, female patient who had a twin with similar disease. Genetic Risk Factors for Periodontitis Bryan Michalowicz, D.D.S Division of Periodontology 1 Pathogenic Bacteria Susceptible Host Modifying Environmental Factors Periodontitis is a COMMOM, COMPLEX, MULTIFACTORIAL disease. Progression of attachment loss and bone loss may be self-arresting. In addition to this mild appearance there may be deep pockets upon probing. [40], Dentistry involving supporting structures of teeth (, Clinical & Radiographic Features of Localised and Generalized Aggressive Periodontitis, 1999 International Workshop for the Classification of Periodontal Diseases, Aggregatibacter (or Actinobacillus) actinomycetemcomitans, Light Amplification by Stimulated Emission of Radiation (LASER) Therapy, "Guidelines for periodontal screening and management of children and adolescents under 18 years of age", "The Good Practitioner's Guide to Periodontology", "Essential microbiology for dentistry (3rd edition)", "Microbiological characteristics of subgingival microbiota in adult periodontitis, localized juvenile periodontitis and rapidly progressive periodontitis subjects", "Use and interpretation of microbiological assays in periodontal diseases", "UTCAT2409, Found CAT view, CRITICALLY APPRAISED TOPICs", "Genes and gene polymorphisms associated with periodontal disease", "SMOKING and its Effects on Early-Onset Periodontitis", "Managing Aggressive Periodontitis - Decisions in Dentistry", "Periodontitis and diabetes: a two-way relationship", "Periodontitis, aggressive - Oxford Reference", "Impaired phagocytosis in localized aggressive periodontitis: rescue by Resolvin E1", "Hyper-responsive Phenotype in Localized Aggressive Periodontitis", "Case Report of an Early-onset Periodontitis Patient Showing Self-Arrest of Alveolar Bone Loss after Puberty", "Generalized Aggressive Periodontitis and Its Treatment Options: Case Reports and Review of the Literature", "Detection and diagnosis of periodontal conditions amenable to prevention", "Guidelines for Periodontal Screening and Management of Children and Adolescents Under 18 Years of Age", "Trends in Susceptibility to Aggressive Periodontal Disease", "Prevention and Treatment of Periodontal Diseases in Primary Care, Dental Clinical Guidance", "Periodontal Treatment: The Delivery and Role of Locally Applied Therapeutics", Periodontitis as a manifestation of systemic disease, https://en.wikipedia.org/w/index.php?title=Aggressive_periodontitis&oldid=992457140, Creative Commons Attribution-ShareAlike License, Generalized aggressive periodontitis (GAP). & the patient has high titre of serum antibodies against Aa. What are the Risk Factors for Localized Aggressive Periodontitis? This is because AgP may have an autosomal dominant inheritance pattern which suggests that up to 50% of siblings could be affected if one parent has the disease. I he human leukocyte antigens (IILA), which regulate immune responses, have been evaluated as candidate markers for aggressive periodontitis. Familial aggregation of aggressive periodontitis is often discovered by taking a thorough medical history of the patient. The key diagnostic feature of AgP is vertical bone loss around teeth including the first molars and incisors. Older age 5. Pathogenic Bacteria Susceptible Host Modifying Environmental Factors Periodontitis is a COMMOM, COMPLEX, MULTIFACTORIAL disease. The other response is known as a period of quiescence, where gingival tissue may appear with no inflammation, pink appearance with some possible stippling. Certain medications 8. Nevertheless, the considerable amount of bone loss relative to the young age of the individual in AgP necessitates an often more aggressive treatment approach, to halt further periodontal destruction and regain as much periodontal attachment as possible. Van Dyke et al* reported a familial clustering of the neutrophil abnormalities seen in localized aggressive periodontitis, this clustering suggests that the defect(s) may be inherited.' The purpose of this review was to summarize the genetic risk factors for AgP identified through a case-control genomewide association study (GWAS) and … Prof Dr. Eman Abd El-Sattar Tella 2. Figure 25-3 Localized aggressive periodontitis. 2 Periodontitis Diagnoses • Aggressive Periodontitis (Grade II or III, Stage C under new scheme) – Localized – Generalized Maélson Klever da Silva, Antonio Carlos Gonçalves de Carvalho, Even Herlany Pereira Alves, Felipe Rodolfo Pereira da Silva, Larissa dos Santos Pessoa, Daniel Fernando Pereira Vasconcelos, " Genetic Factors and the Risk of Periodontitis Development: Findings from a Systematic Review Composed of 13 Studies of Meta-Analysis with 71,531 Participants ", International Journal of Dentistry,. It should be noted that most of the segregational studies were conducted in African-American populations and therefore other modes of inheritance may exist in different populations. Genetic and environmental risk factors for chronic periodontitis and aggressive periodontitis. The severity of periodontal tissue destruction is out of proportion to amount of bacteria present . Early diagnosis and rapid treatment to prevent permanent damage to oral cavity tissues and bones is necessary. [13] A person's genetic predisposition to the condition is determined by a single gene of major effect, inherited as an autosomal dominant trait. Use of Locally Delivered Antimicrobials (LDA) as an adjunct to non-surgical periodontal treatment: For use in deep pockets which fail to respond to repeated non-surgical treatment in patients with adequate oral hygiene. These defects can impair cither the chemotactic attraction of PMN to the site of infection or their ability to phagocytose and kill microorganisms. Early diagnosis of aggressive periodontitis is important as it can cause rapid permanent destruction of the periodontal tissues. Another study found elevated levels of P. gingiva lis, P. intermedia, huso hue ten inn nucleatum, C. rectus, and Treponema denticola in patients with either teft'v.v/iv Periodontitis ■ c 11 API IK 28 4 l.i localized or generalized aggressive disease, hut no significant association was found between the presence of aggressive disease and A. ucliiiomya'tcmcoinitaiis. Smoking or chewing tobacco 4. This is due to the suppression of serum IgG2 and antibody against Aggregatibacter actinomycetemcomitans found in smokers. These factors include: immunological host factors, ethnicity, [2], Therefore, the prevalence of LAP varies considerably between continents, and differences in race or ethnicity seem to be a major contributing factor. Hormonal imbalance in women due to pregnancy, puberty and menopause [12] . Researchers are going on employing the potential several novel technologies in regenerating the lost periodontium including tissue engineering and genetic engineering. [28][27], In advanced cases the alveolar bone loss may be depicted as a horizontal bone loss pattern radiographically.[27][28]. GAP brings about attachment loss involving more than 30% of sites on teeth; Tissue may have severe acute inflammation and often presents with an angry red appearance and ulceration. Substance abuse 5. In GAP, the clinical appearance of the disease resembles chronic periodontitis. Alleles were orientated so that the effect allele was the allele which increased risk of periodontitis. [2] Approximately 0.1% of white Caucasians[3] (with 0.1% in northern and in central Europe, 0.5% in southern Europe, and 0.1-0.2% in North America[2]) and 2.6% of black Africans may suffer from LAP. [34] On probing, patients with AgP should have evidence of significant periodontal pocket depths and loss of attachment (LOA). [17] For instance, diabetes is proved to be associated with periodontitis- it is a major risk factor when glycaemic control is poor.[18]. The role of specific genes remains to be elucidated." [19] The loss can be determined by using a calibrated periodontal probe and taking radiographs of the dentition. Further RSD at sites which require treatment. is under genetic control and that the ability to mount high titers of specific, protective antibody (primarily lg(»2) against A. iicttnoinycctcmconunuis may be race dependent.1, In summary, data support the idea that a gene ot major effect exists for aggressive periodontitis. Data also support a genetic basis for some of the immunologic detects seen in patients with aggressive periodontitis. Periodontal treatment may help to stabilise the disease, but it does not change one's susceptibility to the disease. They produce mainly IgG, with some IgA. [49] The association between IL-17F at 7383A/G and 7488A/G loci with either chronic or an aggressive periodontitis could not be ascertained. As well as Aggregatibacter actinomycetemcomitans being associated with this, the synergism of the disease also accounts for both Capnocytophaga spp and Porphyromonas gingivalis.[5]. Evidence suggests that some immunologic defects associated with aggressive periodontitis may be inherited. Conditions that cause decreased immunity, such as leukemia, HIV/AIDS and cancer treatment 12. Inadequate nutrition 4. These intra-oral appliances should also be well-designed and fitting. One palindromic SNP (rs1537415) was harmonised between studies using the minor allele frequency reported for each population. As the overall treatment concepts and goals for AgP are not significantly different from that of chronic periodontitis, the different treatment phases (cause related therapy; re-examination for response to therapy; definitive therapy; and maintenance) are similar for both types of periodontitis. Various studies have associated Aggregatibacter actinomycetemcomitans, formerly known as Actinobacillus actinomycetemcomitans, with aggressive … At the start of the clinical examination of the gingival and periodontal tissues, the dental practitioner would look at the appearance of the gingiva first. Microbiologic factors Presence of Aggregatibacter actinomycetemcomitans (Aa) is a key agent in LAP as it is present in high nos. Antibiotics: There is evidence that the additional use of systemic antibiotics in conjunction with non-surgical periodontal treatment results in a more favourable clinical response, as compared to just periodontal treatment alone, as it helps to suppress pathogenic bacteria and create a health-associated biofilm. [7] Fives Taylor et al. Current studies have also demonstrated a hyperresponsiveness of monocyte from localized aggressive periodontitis patients with respect to their production of PGK2 in response to lipopolysaccbaride d.I\S).4< This hyperresponsive pheno-type could lead to increased connective tissue or bone loss due to excessive production of these cataholic factors. [11] The plasma cells produce specific antibodies in response to the periodontal pathogens, which diffuse into the gingival crevicular fluid. Esra Guzeldemir, Meral Gunhan, Onur Ozcelik, Hakki Tastan, Interleukin-1 and tumor necrosis factor-α gene polymorphisms in Turkish patients with localized aggressive periodontitis, Journal of Oral Science, 10.2334/josnusd.50.151, 50, 2, (151-159), (2008). Possible immune mechanisms include an increase in the expression of type II major histocompatibility complex (MHO molecules, HLA Dl<4\ altered helper or suppressor T-cell function, polyclonal activation of B cells by microbial plaque, and genetic predisposition, (lor additional information on the immunology of aggressive periodontitis, see Tart Three.). However, in general, the risk factors associated with periodontal disease may include: It should be noted that not «HI reports support the association of A. actinomycetemcomitans and localized aggressive periodontitis. Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis as defined by the 1999 classification system:[1], LAP is localised to first molar or incisor interproximal attachment loss, whereas GAP is the interproximal attachment loss affecting at least three permanent teeth other than incisors and first molar. ), The amount and duration of smoking are important variables that can influence the extent of destruction seen in young adults.'" The risk factors are environmental, behavioral, or biological factors that have been confirmed in longitudinal studies to have a punitive impact on the disease process [3-8]. be made in identifying a robust group of genetic, host, and microbial risk-markers associated with periodontal disease that can improve diagnostic capability in disease associated with juveniles, adolescents, and post-adolescent individuals. Obesity 8. Those who have never smoked tobacco have the lowest risk of developing gum disease. [2][3] Around 1 in every 1000 patients suffer more rapid loss of attachment. (For additional information on genetic factors, see Chapter 10. Local Risk Factors for Periodontal Diseases.

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