Genetic and environmental risk factors for chronic periodontitis and aggressive periodontitis Periodontol 2000. Figure 25-3 Localized aggressive periodontitis. This would normally be carried out using a basic periodontal probe (WHO CPI). 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. Greater numbers of both Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans were found in active, destructive periodontal lesions in comparison to non-active sites. In addition to that, presence of angular or vertical bone loss (especially at 6's) and arrowhead or furcation lesions are also a strong suggestion of AgP. This could involve an open flap debridement with or without regenerative procedures, with the aim of gaining access and visibility to root and furcation areas so that a thorough instrumentation and debridement can be carried out. However, in general, the risk factors associated with periodontal disease may include: Inadequate nutrition, including vitamin C deficiency 9. 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 … The localized and generalized forms are not merely different in extent; they differ in etiology and pathogenesis. [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 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). The patient is said to have a high genetic susceptibility to aggressive periodontitis. They are implicated in the development of aggressive periodontitis by triggering inflammatory response in periodontal tissue. [38][39] Early detection of AgP allows intervention to be carried out before extensive periodontal destruction has taken place which further simplifies treatment. Periodontal treatment may help to stabilise the disease, but it does not change one's susceptibility to the disease. Those who have never smoked tobacco have the lowest risk of developing gum disease. Aggressive periodontitis is a multifactorial disease with many complex interactions including host factors, microbiology and genetics. Ayala Stabholz. Certain medications that cause dry mouth or gum changes 11. As well as Aggregatibacter actinomycetemcomitans being associated with this, the synergism of the disease also accounts for both Capnocytophaga spp and Porphyromonas gingivalis.[5]. [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. The generalized form mostly affects the permanent dentition (Figure 1). Common risk factors of severe gum disease in children and adolescents include:. In fact, 70.1% of adults65 years and older have periodontal disease. '0 T hese PMN and monocyte defects may be induced by the bacterial infection or may he genetic in origin. Substance abuse 5. 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. [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. [5] Both Capnocytophaga spp and Prevotella intermedia were the most frequently detected microorganisms in a study,[9] which also noted that Capnocytophaga spp was the most prominent bacteria in subgingival samples of aggressive periodontitis sufferers. Additionally, poorly functional inherited forms of monocyte FcyRII. One palindromic SNP (rs1537415) was harmonised between studies using the minor allele frequency reported for each population. Several investigators10,2*-'4 have shown that patients with aggressive periodontitis display functional defects of polymorphonuclear leukocytes (PMNs), monocytes, or both. Poor oral health habits 3. Local Risk Factors . Smoking, oral hygiene, and psychological factors seem to play a role in both chronic and aggressive periodontitis. Studies found that smokers have more affected teeth than non-smokers and high levels of attachment loss. [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). [2], Aggressive periodontitis is much less common than chronic periodontitis and generally affects younger patients than does the chronic form. This is suggested to be protective against wider spread periodontal breakdown. Genetics. Prof Dr. Eman Abd El-Sattar Tella 2. AgP classified into two categories named localized and generalized aggressive periodontitis. The main distinction between the localized and generalized form of AgP lies in the number of teeth affected. Substance abuse 7. Various studies have associated Aggregatibacter actinomycetemcomitans, formerly known as Actinobacillus actinomycetemcomitans, with 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. Background: The pathogenesis of early‐onset periodontitis (EOP) can be explained by various host risk factors. Hormonal changes, such as those related to pregnancy or menopause 6. 2010 Jun;53:138-53. doi: 10.1111/j.1600-0757.2010.00340.x. The localized form largely affects permanent incisors and first molars. Genetic Risk Factors for Periodontitis Bryan Michalowicz, D.D.S Division of Periodontology. Alleles were orientated so that the effect allele was the allele which increased risk of periodontitis. Periodontitis Diagnoses ... study of aggressive periodontitis . [4] Males seem to be at higher risk of GAP than females[2]. the receptor for human lgG2 antibodies, have been shown to be disproportionately present in patients with localized aggressive periodontitis. 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. [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. Given the 'right' concurrence of risk factors, a person with periodontitis can experience significant destruction of tooth-supporting bone, ultimately resulting in tooth loss. The amount of bacteria is often indicated by the level of dental plaque. This response is known to be present in the destructive phase, where there is presence of bone and attachment loss. 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. [2][3] Around 1 in every 1000 patients suffer more rapid loss of attachment. [20] Usually the loss of attachment is greater than 2mm per year. The purpose of this review was to summarize the genetic risk factors for AgP identified through a case-control genomewide association study (GWAS) and … Early diagnosis of aggressive periodontitis is important as it can cause rapid permanent destruction of the periodontal tissues. These amounts are greatly reduced following treatment.[11]. 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. Aggressive Periodontitis develops following a complex interaction of genetic factors, oral microbiology, and a variety of host factors such as body immune response, saliva, etc. ), 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. 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]. It is essential that all patients undergo a routine periodontal examination to screen for any form of periodontal disease during a dental checkup. [19] The loss can be determined by using a calibrated periodontal probe and taking radiographs of the dentition. [34] On probing, patients with AgP should have evidence of significant periodontal pocket depths and loss of attachment (LOA). 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). increased mobility of the affected teeth, sensitivity due to exposed root, periodontal abscess with lymph node enlargement. Obesity 8. Poor oral health habits 6. [24], In some patients, the disease may burnout without any cause-related therapy. Host defences involve multiple factors; saliva, epithelium, inflammatory response, immune response and chemical mediators. 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. What are the Risk Factors for Localized 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). 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. Pathogenic Bacteria Susceptible Host Modifying Environmental Factors Periodontitis is a COMMOM, COMPLEX, MULTIFACTORIAL disease. There may be spontaneous bleeding or suppuration. Many studies have shown that genetic factors contribute to the pathogenesis of this disease. Natural Autoimmune Diseases Cure and Treatment. Genetic and environmental risk factors for chronic periodontitis and aggressive periodontitis. [28][29] The periodontal tissue also exhibits minimal signs of inflammation clinically[30] and show a robust response with serum antibodies to pathogens. Localized aggressive periodontitis in 15-year-old black, female patient who had a twin with similar disease. Periodontitis, an inflammatory reaction triggered by bacteria in dental plaque, is the most severe form of gum disease and the leading cause of tooth loss in adults. [21] In this case, the manifestation of aggressive periodontitis is believed to be the result of genetic mutation, combined with environmental factors.[21]. These is also evidence they produce increased amounts IL-1α and IL-1β which cause osteoclastic bone resorption. The impairment of their phagocytic activity results in persistent inflammation in periodontal tissues. [2] The prevalence of LAP is less than 1% and that of GAP is 0.13%. Aggressive periodontitis is classified into localized and generalized forms. Phagocytes are essential in resolving inflammation. Generally, no underlying associated conditions are known to be present. [5] Aggressive periodontitis is often characterised by a rapid loss of periodontal attachment associated with highly pathogenic bacteria and an impaired immune response. In GAP, generalized bone destruction is present that ranges from mild crestal bone resorption to severe alveolar bone destruction, depending on the severity of the disease. Implants in function for a significant number years can develop peri-implantitis. [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). [37] Careful interpretation of the history is required but it may provide vital evidence in diagnosing AgP. 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. Instructions should also be given on how to clean adequately around fixed restorations and appliances, and how to clean removable prostheses. The key to successful management at present lies in early diagno… If a case of Agp is diagnosed, it is important to screen the patient's family members as well for AgP. These factors include: immunological host factors, ethnicity, [15] Their hyperactivity is associated with periodontal tissue destruction and bone loss. (2000) have categorised the virulence factors of Aggregatibacter actinomycetemcomitans as follows. Aggressive periodontitis (AgP) is a disease characterized by rapid loss of periodontal tissues affecting systemically healthy individuals under age of 30 years. These defects can impair cither the chemotactic attraction of PMN to the site of infection or their ability to phagocytose and kill microorganisms. 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. [2], Therefore, the prevalence of LAP varies considerably between continents, and differences in race or ethnicity seem to be a major contributing factor. [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. These features are common for both localized and generalized form of disease. Previous studies have focused on a single (among many possible) immunological risk factor and the association among the factors has not been assessed. However, age is only one of the risk factors of periodontal disease. 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). The difference is that individuals affected by GAP are much younger and the progression of disease appears more rapid. 2 Periodontitis Diagnoses • Aggressive Periodontitis (Grade II or III, Stage C under new scheme) – Localized – Generalized An early study dating back to 1983 explains its prevalence and documents its role in localised aggressive periodontitis. The key diagnostic feature of AgP is vertical bone loss around teeth including the first molars and incisors. Autoimmunity has been considered to have a role in generalized aggressive periodontitis according to Anusak-sathien and Dolby,1 who found host antibodies to collagen, DMA, and immunoglobulin G (lgG). [26] There is also a relatively fast progression of periodontal tissue loss. 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. However, for the disease process to initiate the person must be exposed to the presence of periodontal pathogens and potentially also various environmental factors. Other risk factors include: 1. Several factors are identified as increasing the risk of developing periodontal disease [9,10]. [33] After that, gingival probing depths would be checked. 21. 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 gram-negative microbes are considered the chief aetiological agent of aggressive periodontitis. This stage involves discussion of the disease with the patient. Studies have shown that tobacco use may be one of the most significant risk factors in the development and progression of periodontal disease. Inadequate nutrition 4. Results from several studies support the concept that all individuals are not … 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. 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. [5], Porphyromonas gingivalis is a Gram-negative anaerobe associated with the pathogenicity of periodontal disease,[8] and aggressive periodontitis is no exception. Health conditions that decrease your immunity 9. The risk factors for developing these diseases are prior history of periodontitis, poor oral hygiene, smoking, diabetes, implant cement beyond the margin of the crown, occlusal overload and genetic factors. The objective of treatment is to create a conducive clinical condition for retaining as many teeth, for as long as possible.[40]. 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. They produce mainly IgG, with some IgA. Aggressive Periodontitis 1. (Predisposing Factors) Localized Aggressive Periodontitis is typically seen in children with normal immunity. [7], Samaranayake notes the evidence for the specific involvement of Aggregatibacter actinomycetemcomitans includes: an increased incidence of it found in subgingival plaque obtained from lesional sites, high level of its antibody which tends to fall following successful treatment, its possession of a wide range of potentially pathogenic products and its elimination with concordant disease regression, following treatment with successful periodontal therapy and adjunctive tetracycline. This is carried out 10–12 weeks following RSD. Smoking is a generalized risk factor for generalized forms of aggressive 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. However, patients with generalized aggressive periodontitis have decreased ability to mount high titres of IgG to Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. Evidence suggests that some immunologic defects associated with aggressive periodontitis may be inherited. Further RSD at sites which require treatment. Currently, the available LDA include tetracycline, minocycline, chlorhexidine gluconate and doxycycline, with the mode of delivery being in the form of fibers, chips, polymers and trays. [7] Fives Taylor et al. Smoking or chewing tobacco 4. Factors that can increase your risk of periodontitis include: 1. 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. Box 4-1. 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,. To identify the genetic risk factors for aggressive periodontitis (AgP), it is important to understand the progression and pathogenesis of AgP. Periodontal disease by definition involves the destruction of alveolar bone and therefore presents a risk factor for the development of osteoradionecrosis if the disease is left untreated in the irradiated field. Aggressive periodontitis is often characterised by a rapid loss of periodontal attachment associated with highly pathogenic bacteria and an impaired immune response. 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. Genetic Factors. If the disease is stabilised, the treatment progresses on to the maintenance stage. [13] A person's genetic predisposition to the condition is determined by a single gene of major effect, inherited as an autosomal dominant trait. [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. Tobacco use is a co–risk factor for oral, head and neck squamous cell carcinoma and for periodontitis. Further studies are needed to characterize the origin of these cellular alterations. 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.). Genetic and environmental risk factors for chronic periodontitis and aggressive periodontitis. Removal of plaque retentive factors: Local plaque retentive factors such as mal-positioned teeth, overhanging restorations, crown and bridgework, partial dentures and fixed/removable orthodontic appliances can increase the risk of periodontal disease and prevent successful treatment and resolution of associated pockets. Some immune detects have been implicated in the pathogenesis of aggressive periodontitis. [34] In healthy periodontal tissues, the distance from the amelocemental junction (ACJ) to the alveolar bone crest is typically in the order of 1mm in young people. Various studies have associated Aggregatibacter actinomycetemcomitans, formerly known as Actinobacillus actinomycetemcomitans, with aggressive … (lor additional information on smoking and periodontal disease, see < hapter 14. Of the microflora characterised in aggressive periodontitis, approximately 65-75% of bacteria are Gram-negative bacilli, with few spirochaetes or motile rods present. Loss of attachment refers to the destruction of periodontium whereas the bone refers to the alveolar bone supporting the teeth. Studies also have demonstrated that the antibody response to periodontal pathogens, particularly A. octinomycctcniconuUins. These factors should be investigated during a thorough dental examination of the patient (Box 4-1). This is due to the suppression of serum IgG2 and antibody against Aggregatibacter actinomycetemcomitans found in smokers. Studies of families, twins and sibling pairs have provided strong evidence for a genetic basis for aggressive periodontitis. Older age 5. Smoking or chewing tobacco 7. However, it is unlikely that all patients affected with aggressive periodontitis have the same genetic defect. 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. 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. Following the initial assessment and diagnosis of AgP, a treatment plan is usually developed for each individual undergoing therapy. [8], Capnocytophaga spp are implicated as prime periodontal pathogens, especially in localised aggressive periodontitis. A healthy periodontium in a Caucasian would appear stippled and pink with a knife edge margin where it abuts the tooth (pigmentation may differ in other races). level of oral hygiene) and the tissue response to the treatment. Risk factors identified for periodontal diseases are similar to the ones for chronic periodontitis and aggressive periodontitis (28) . & the patient has high titre of serum antibodies against Aa. These intra-oral appliances should also be well-designed and fitting. Researchers are going on employing the potential several novel technologies in regenerating the lost periodontium including tissue engineering and genetic engineering. [2] On the other hand, in Asia, the prevalence rate of 1.2% for LAP and 0.6% for GAP in Baghdad and Iran population, and 0.47% in Japanese population. 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.' There is a poor serum response against infecting agents, Destruction is present that is not in balance with the amount of local irritants present, Generalized inter-proximal attachment loss on 3 or more permanent teeth, excluding the first molars or incisors. Regenerative surgical therapy currently available include the use of bone replacement grafts, barrier membranes or guided tissue regeneration (GTR), biologic modifiers like growth and differentiation factors (GDF), and extracellular matrix proteins like enamel matrix proteins (EMD). Genetics 10. 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