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21ЗАБОЛЕВАНИЯ ПАРОДОНТА И СОВРЕМЕННЫЕ МЕТОДЫ ИХ ЛЕЧЕНИЯ
Абдурахмонова Мухаёхон Абдурахимовна
Андижанский государственный медицинский институт
Заболевание пародонта или десен — это инфекция десны, кости и окружающих тканей зубов, вызванная бактериями, находящимися в зубном налете. Болезнь десен прогрессирует, циклична и часто безболезненна, поэтому вы можете даже не подозревать, что она у вас есть или что она снова активна. В настоящее время проводится ряд исследований по лечению этого заболевания. В этой статье мы обсудим современные методы лечения заболевания.
Ключевые слова: Пародонт, ткань, десна, инфекция, бактериальная, прогрессирующая, циклическая.
PARADONTAL KASALLIKLARI VA ULARNI ZAMONAVIY DAVOLASH
USULLARI
Paradont yoki tishni o'rab turgan to'qimalarning kasalligi - bu milk, suyak va tishlarning atrofidagi to'qimalarning infeksiyasi bo'lib, asosan bakteriyalar sababli kelib chiqadi. Tish go'shti kasalligi progressiv va siklik bo'lib, ko'pincha og'riqsizdir va shuning uchun uning faol ekanligini sezilmasligi mumkin. Hozirgi vaqtda ushbu kasallikni davolash bo'yicha bir qancha izlanishlar olib borilmoqda. Ushbu maqolada bu kasallikni zamonaviy davolash usullarini ko'rib chiqamiz.
Kalit so'zlar: Paradont, to'qima, milk, infeksiya, bakteriya, progressiv, siklik.
PERIODONTAL DISEASES AND MODERN METHODS OF THEIR TREATMENT
Periodontal or gum disease is an infection of the gum, bone and surrounding tissues of the teeth caused by the bacteria found in plaque. Gum disease is progressive and cyclical, and often painless-so you may not even be aware you have it or that it is active again. A number of studies are currently underway to treat this disease. In this article we will discuss modern treatments for the disease.
Keywords: Periodontal, tissue, gums, infection, bacterial, progressive, cyclic.
Introduction: Periodontitis, also called gum disease, is a serious gum infection that damages the soft tissue and, without treatment, can destroy the bone that supports your teeth. Periodontitis can cause teeth to loosen or lead to tooth loss. Periodontitis is common but largely preventable. It's usually the result of poor oral hygiene. Brushing at least twice a day, flossing daily and getting regular dental checkups can greatly improve your chances of successful treatment for periodontitis and can also reduce your chance of developing it. It is the leading cause of tooth loss in adults, and can cause halitosis (bad breath), bleeding gums, mobile teeth, and a displeasing smile for some. Gum disease is progressive and cyclical, and often painless-so you may not even be aware you have it or that it is active again. There is no cure for gum disease, however with treatment the disease can be halted and arrested. Gum diseases shares many risk factors and is associated with various diseases such as diabetes, adverse pregnancy outcomes, rheumatoid arthritis and certain cancers.
Periodontal disease is primarily associated with bacterial infection such as dental plaque. Dental plaque, an oral biofilm harboring a complex microbial community, can cause
various inflammatory reactions in periodontal tissue. In many cases, the local bacterial invasion and host-mediated immune responses lead to severe alveolar bone destruction. To date, plaque control, non-surgical, and surgical interventions have been the conventional periodontal treatment modalities. Although adjuvant therapies including antibiotics or supplements have accompanied these procedures, their usage has been limited by antibiotic resistance, as well as their partial effectiveness. Therefore, new strategies are needed to control local inflammation in the periodontium and host immune responses. In recent years, target molecules that modulate microbial signaling mechanisms, host inflammatory substances, and bone immune responses have received considerable attention by researchers.
There are few opinions about the disease. But As for as some group scientists go said [1] that we introduce three approaches that suggest a way forward for the development of new treatments for periodontal disease: (1) quorum quenching using quorum sensing inhibitors, (2) inflammasome targeting, and (3) use of FDA-approved anabolic agents, including Teriparatide and sclerostin antibody. Dental plaque, a biofilm comprised of a complex microbial community which grows on tooth surfaces, may trigger an inflammatory response in periodontal tissue [2]. Periodontal inflammation may be accompanied by bleeding, swelling, or pain. Gingivitis is a common reversible inflammation of the soft tissues of the gingiva that affects up to 95% of the world's population. Periodontitis is caused by bacterial invasion or bacterial toxins, but the pathology of the disease is mainly affected by host immune reaction [3,4]. The response of a particular host to these bacteria depends on genetic, immunological and environmental factors [5]. While gingivitis can be resolved with meticulous personal oral hygiene accompanied by plaque removal, periodontitis is an irreversible disease that affects 50% of the world's population.
Classification
Target
Mechanism
Quorum sensing Luxl/Lux R type system
Oligopeptide/two component
type system
Lux S encoded autoinducer-2
Quorum Acylase, Lactonase,
quenching Oxyreductase
S-adenosyl methionine
S-adenosyl cysteine
Inflammasome Sulforaphane
Glyburide
NSAIDs of fenamate class Sclerostin Sclerostin antibody
SOST gene
Usage of acyl homoserine lactones as an autoinducer in G(-) bacteria
Usage of amino acids and short peptide derivatives as an autoinducer in G(+) bacteria
Act on both G(+) and G(-) bacteria
Inactivation of AHL in G(—) bacterial by enzymatic degradation of signaling molecules
Inhibition of signal generation by blockage of AHL synthesis
Inhibits caspase-l proteolytic activation, IL-lp maturation and secretion downstream of several inflammasomes
Inhibit NLRP3 inflammasome activation and IL-lp secretion
Inhibit NLRP3 inflammasome activation
Neutralizing antibody to inhibit sclerostin action, ex) Romosozumab
Sclerostin in encoded by SOST gene
Table 1. Pharmaceutical targets for periodontal disease.
Moreover, prolonged and untreated gingival inflammation may eventually lead to alveolar bone destruction and tooth loss. For that reason, prevention, early diagnosis, and timely treatment are recommended as a matter of course. The current diagnostic classification of periodontitis is divided into four stages and of three grades according to severity and progression respectively [6]. Once a patient's case is classified, an appropriate periodontal treatment modality can be applied. To date, conventional periodontal treatments include non-surgical and surgical interventions [7] paired with adjunctive pharmaceuticals or nutraceuticals. In this review, we bring forth an overview of recent advances in the identification of therapeutic targets for the development of novel treatment modalities in periodontal disease. Table 1 summarizes the proposed pharmaceutical targets and mechanism of actions for periodontal disease [8].
Periodontitis is a bacterial-associated and host-mediated multifactorial inflammatory disease. Although the overall phenotype of chronic periodontitis may be similar across patients, the underlying causes of the disease varies from person to person. Traditional periodontal treatment fails primarily when local inflammation caused by bacterial invasion is met with an uncontrolled host immune response. Novel responses to periodontitis will require an understanding of individual molecular pathogenesis and the development of target-oriented therapeutic drugs.
According to conclusion which is based on few scientists's some information [1], the recent focus on inhibiting plaque biofilm formation with QSIs may result in the development of new drugs for periodontal treatment. Moreover, as inflammasomes and their components (NLR, ALR, and Pyrin) are associated with the onset of periodontal disease, drugs that directly target the inflammasome and relieve periodontal inflammation may be developed. Finally, two anabolic agents that inhibit bone loss and promote bone regeneration may be useful in treating advanced cases of periodontitis. Preclinical studies have shown that Teriparatide and sclerostin antibody are both effective in periodontitis. Of course, the safety and effectiveness of any of these drugs must be verified before being widely adopted. As this review has shown, however, there is a sound argument to be made that these potential treatments are ready for the next stage of testing; multicenter human clinical trial studies.
Inflammatory parodontal diseases, representing an important medical and social problem, are characterized by a wide prevalence, persistent progressive course with frequent exacerbations in people of all age groups. The significance of periodontal pathology is determined not only by the prevalence and severity of the disease, the negative impact on the body as a whole, but also by the insufficient effectiveness of the treatment [9,10]. In modern orthopedic dentistry, an urgent medical and social problem is inflammatory periodontal diseases (VZP), special attention should be paid to gingivitis and periodontitis, since these diseases are more common than others and affect the general condition of the oral cavity, the body as a whole, and the quality of life of the patient, in addition, this problem comes to the fore due to the high prevalence and low effectiveness of the therapy. The frequency of occurrence of VZD varies from 45 to 70 % according to research by scientists. At a high level, there is a steady trend towards a further increase in the incidence of periodontal tissues with a predominance of generalized periodontal disease and gingivitis in their structure, and the prevalence of this pathology among the adult population is increasing. There is an obvious increase in the frequency of prevalence of atypical forms of periodontitis, it should be noted that aggressive forms also belong to atypical forms of periodontitis.
According to the conclusions of I. V. Who periodontal diseases were detected in 75 % of patients, and chronic generalized periodontitis of moderate severity (69.9%) progressed. In
25.9% of patients, chronic generalized periodontitis of mild severity was detected, while severe pathological processes in periodontal tissues were detected only in 3.2 %. The most common pathological conditions in orthopedic dentistry that occur in patients today are defects in hard tooth tissues of various etiologies and partial tooth loss. Very often, VZP is combined with defects in the dentition, exerting a significant mutual influence on each other; the absence of teeth leads to an inferior chewing function and overload Unfortunately, there are many differences in the approaches to the complex therapy of VZP at the level of different periodontal schools, and even in different dental institutions in the same region, not to mention in our country as a whole. This is probably due to the fact that there are different approaches to the treatment of periodontal pathology, with different material and technical equipment, as well as with the difference between medical institutions from each other in terms of the qualifications of doctors. According to many scientists, the most effective treatment is the treatment of VZP by a periodontist; this treatment is usually limited to the removal of dental deposits, as well as the elimination of sub gingival granulations, if necessary. The existing modern methods of diagnosis and treatment of inflammatory reactions in the oral cavity, as a rule, do not take into account the presence of orthopedic structures and give general recommendations for periodontal diseases without taking into account the influence of the structural material of orthopedic structures on local immunity. In addition, the presence of concomitant diseases and various endogenous and exogenous risk factors affects both the course of inflammatory periodontal diseases, and the development of defects in the hard tissues of the teeth and secondary adentia. Therefore, it is necessary to take a serious approach to the choice of structural material for dentures, taking into account the severity of the disease and the changes occurring not only in the body, but also in the oral cavity, it is important to take into account and correlate the individual characteristics and immunological reactivity of the oral cavity in the treatment of such patients. Modern orthopedic dentistry allows achieving high functional and aesthetic results, but the influence of various structural materials used in fixed prosthetics on the clinical and immunological picture of the oral cavity was not given enough attention, the data are scattered and quite contradictory. It is necessary to understand that the choice of structural material can affect the course of periodontal disease, which in turn affects the quality of life of the patient and the overall result of prosthetics. The periodontal condition and clinical and immunological status should be taken into account together with the degree of severity of the pathological process, possible changes in the oral cavity by changing the local immune response to orthopedic structures, which, accordingly, affects the course of inflammatory periodontal diseases and the long-term duration of therapy. The purpose of the study. Inflammatory periodontal diseases with various orthopedic structures. According to the results of an in-depth clinical analysis of patients with defects in the dentition and hard tissues of the teeth and with inflammatory periodontal diseases, it is advisable to use a special dental card-a questionnaire of risk factors in the development of adentia and inflammatory periodontal diseases for individual choice of orthopedic design. Reasonable clinical and immunological diagnostic criteria allow improving the diagnosis and prognosis of the orthopedic treatment of patients with inflammatory periodontal diseases. An improved algorithm of complex orthopedic treatment of patients with defects of the dentition and hard tissues of the teeth and with inflammatory periodontal diseases has been developed and implemented in the clinical practice of the dentist. Diseases of the orthopedic profile play a significant role in the overall dental morbidity and account for 49.8%, and the analysis of the use of orthopedic structures indicates a tendency to increase the share of fixed prostheses from 24% to 60% over the past
5 years. The use of a therapeutic and diagnostic algorithm in patients with inflammatory periodontal diseases and various orthopedic structures improves the clinical condition and local immunological response of the oral cavity, which is confirmed by the normalization of humoral factors of oral protection. Allergization processes in the oral cavity, in comparison with all-ceramic orthopedic structures, and also have a significant effect on the activation of macrophage processes. [11-13].
Microbiological technique Microbiological perturbations Principal findings
Culture Reductions in total bacterial counts, Bacteroeides spp., Fusobacterium spp., P. gingivalis, P. intermedia, A. actinomycetemcomitans Study the timeframe of recolonisation patterns
PCR Reductions in P. gingivalis, T. forsythia. P. intermedia, A. actinomycetemcomitans. Increases in Actinomyces spp., Streptococcus spp., and Veillonellaparvula. Clinical improvements in parallel with microbiological reductions. Non-surgical periodontal therapy fails to eliminate the test putative pathogens
DNA-DNA Checkerboard Hybridisation Reductions in P. gingivalis, T. forsythia. P. intermedia, A. actinomycetemcomitans. Increase of A. Viscosus, Actinomyces Spp. Most significant microbial reductions are found within the first 3 months post-treatment, however sustained up to 12 months
Next Generation Sequencing Reductions in previous tested putative pathogens. Reductions in the levels of novel pathogens (i.e. F. alocis) Treatment disrupts inter-species connections
Table 1. Periodontal treatment effects on the microbial communities determined by bacterial identification techniques.
According to conclusion which is based on few scientists's some information [14], PDT could help improve the outcomes of periodontal parameters, compared with SRP alone in treatment of periodontitis. However, due to the limited evidence and heterogeneity in materials, methods and parameters of the included studies, superiority of adjunctive PDT over SRP alone is not certain. Further studies are required to reach a stronger conclusion.
So some group scientists made a conclusion [15] that advances in bacteria identification techniques contributed to a comprehensive evaluation of treatment effects, regarding perturbations of the microbial community and changes in re-colonization patterns. A landmark study examined the effects of treatment on bacteria succession, suggesting three distinct re-colonization patterns. A rapid reduction and slow return were noticed for the total bacterial counts and spirochaetes, while a rapid reduction accompanied by a rapid return was followed by Gram-negative anaerobic species. Streptococcus and Actinomyces species followed a different pattern of a rapid increase and slow reduction after therapy [16]. Several studies have assessed the microbiological effects of different designs of NSPT regimens regarding partial versus full-mouth treatment protocols in terms of re-colonization patterns and these findings are discussed in a comprehensive review [17]. Optimal treatment outcome is guaranteed by thorough plaque control, which ensues from highly motivated and skillful
patients in oral-hygiene practices for the long-term maintenance of plaque-free periodontal tissues following careful mechanical instrumentation [18]. Interestingly, in compact protocols of mechanical instrumentation and in the absence of oral-hygiene reinforcement, the 3 month reduction in numbers of P. gingivalis as determined by the checkerboard DNA-DNA hybridization technique and in plaque and bleeding indices were significantly smaller compared with the group that received re-iterated oral-hygiene instructions and motivation [19]. However, these inter-group differences disappeared at 6months following additional treatment given at 3 months. These data highlight the importance of professional removal of dental biofilm every 3 months in subjects with compromised plaque control. The microbiological effects of these treatment protocols are summarized in Table 2.
The efficacy of NSPT in terms of clinical and microbiological improvements has long been established. The microbial effects of NSPT, as described above, can be summarized by a decrease of motile anaerobes and spirochaetes and an increase of cocci and motile bacteria. A predominantly Gram-negative anaerobic microbial community is reversed into a Grampositive one following treatment. In other words, putative periodontal pathogens decrease, giving rise to beneficial species more compatible with health. Interestingly, studies employing contemporary molecular techniques offered valuable information regarding previously uncultivated species that play a key role in periodontal pathogenesis such as Filifactor alocis. On the other hand, Veillonella species oral clone X042, a Gram-negative bacterium, was the most common member of the subgingival bacterial community and was associated with periodontal health. These data suggest that the aetiopathogenesis of periodontitis appears to be more complex than initially thought and monitoring the levels of these bacteria - subgingivally and in saliva - may prove clinically useful. With regard to the keystone pathogen P. gingivalis , a number of studies have demonstrated the ability of periodontal treatment to decrease the levels of this pathogen in a relatively short period of 6 weeks post-treatment [19,20].
The main outcome of NSPT is not the eradication of specific pathogens but rather the establishment of a healthy ecosystem by altering the microbial community in numbers and composition and contributing to the maturation of the host response. The ecosystem appears to return to one comparable to periodontal health. Thus, the main therapeutic target is to turn the clock back and return the current status to the one before disease was initiated, implying that the subgingival microbiota has to go through prolonged modifications in composition and quantities to reach the status required for disease occurrence.
Conclusion: Treatment may be performed by a periodontist, a dentist or a dental hygienist. The goal of periodontitis treatment is to thoroughly clean the pockets around teeth and prevent damage to surrounding bone. You have the best chance for successful treatment when you also adopt a daily routine of good oral care, manage health conditions that may impact dental health and stop tobacco use. Apart from the fact, in this article we have reviewed the current status of periodontal diseases. We also discussed the treatment options for this diseases. We have analyzed the opinions and conclusions of several scientists on this topic. We believe that this article can be an impetus for further in-depth research.
REFERENCES
1. Recent Advances of Therapeutic Targets for the Treatment of Periodontal Disease. Woo Jin Kim, Yunjo Soh and Seok-Mo Heo. Biomol Ther (Seoul). 2021 May 1; 29(3): 263-267. doi: doi: 10.4062/biomolther.2021.001.
2. Loos B. G., Van Dyke T. E. The role of inflammation and genetics in periodontal disease. Periodontol. 2000. 2020;83:26-39. doi: 10.1111/prd.12297.
3. Marchesan J. T., Girnary M. S., Moss K., Monaghan E. T., Egnatz G. J., Jiao Y., Zhang S., Beck J., Swanson K. V. Role of inflammasomes in the pathogenesis of periodontal disease and therapeutics. Periodontol. 2000. 2020;82:93-114. doi: 10.1111/prd.12269.
4. Marchesan J. T., Jiao Y., Moss K., Divaris K., Seaman W., Webster-Cyriaque J., Zhang S., Yu N., Song C., Bencharit S., Teles R., Offenbacher S. Common polymorphisms in IFI16 and AIM2 genes are associated with periodontal disease. J. Periodontol. 2017;88:663-672. doi: 10.1902/jop.2017.160553.
5. Ominsky M. S., Vlasseros F., Jolette J., Smith S. Y., Stouch B., Doellgast G., Gong J. H., Gao Y. M., Cao J., Graham K., Tipton B., Cai J., Deshpande R., Zhou L., Hale M. D., Lightwood D. J., Henry A. J., Popplewell A. G., Moore A. R., Robinson M. K., Lacey D. L., Simonet W. S., Paszty C. Two doses of sclerostin antibody in cynomolgus monkeys increases bone formation, bone mineral density, and bone strength. J. Bone Miner. Res. 2010;25:948-959. doi: 10.1002/jbmr.14.
6. Padhi D., Jang G., Stouch B., Fang L. A., Posvar E. Single-dose, placebo-controlled, randomized study of AMG 785, a sclerostin monoclonal antibody. J. Bone Miner. Res. 2011;26:19-26. doi: 10.1002/jbmr.173.
7. Venkatramanan M., Sankar Ganesh P., Senthil R., Akshay J., Veera Ravi A., Langeswaran K., Vadivelu J., Nagarajan S., Rajendran K., Shankar E. M. Inhibition of quorum sensing and biofilm formation in Chromobacterium violaceum by fruit extracts of Passiflora edulis. ACS Omega. 2020;5:25605-25616. doi: 10.1021/acsomega.0c02483.
8. Ren Y. S., Han X. L., Ho S. P., Harris S. E., Cao Z. G., Economides A. N., Qin C. L., Ke H. Z., Liu M., Feng J. Q. Removal of SOST or blocking its product sclerostin rescues defects in the periodontitis mouse model. FASEB J. 2015;29:2702-2711. doi: 10.1096/fj.14-265496.
9. Arutyunov, S. D. features of chronic inflammatory diseases of periodontal tissues in patients with acute myocardial infarction / M. P. Pimenov, S. D. Arutyunov // Russian dental journal. - 2014. - No. 3. - P. 42-46.
10. Atrushkevich, V. G. the Role of disorders of vitamin D metabolism in the pathogenesis of inflammatory periodontal diseases (review) / V. G. Atrushkevich, M. S. Zablocka, N. In. Toroptsova // Periodontology. - 2012. - Vol. 17, No. 1. - p. 3-10.
11. The biocompatibility and the effect on the growth activity of the cell culture of fibroblasts metal free ceramic and metal-ceramic prostheses / A. V. Zharov, E. E. Nikonchuk, E. Y. Kuanova [et al.] / / Kuban scientific medical Bulletin. - 2013. - № 6 (141). - S. 100102.
12. Blashkova, S. L. Diagnostic criteria for risk of development of inflammatory periodontal diseases in individuals undergoing orthodontic treatment / S. L. Blashkova, I. G. Mustafin, G. R. haliullina // Periodontics. - 2015. - Vol. 20, No. 3 (76). - p. 57-60.
13. Gaffarov S. A., Saidov A. A., Yakubova F.Kh. An integrated approach to the diagnosis and treatment of a dysfunction of the temporomandibular joint in children and adolescents / / Journal of critical reviews, 2020.Vol 7, Issue 17 - - P. 77-85.
14. Understanding the microbial components of periodontal diseases and periodontal treatment-induced microbiological shifts Free Ioannis. Fragkioudakis, Marcello P. Riggio, Danae Anastasia. 09 December 2020. doi: 10.1099/jmm.0.001247.
15. Slots J, Mashimo P, Levine MJ, Genco RJ. Periodontal therapy in humans: I. microbiological and clinical effects of a single course of periodontal scaling and root planing, and of adjunctive tetracycline therapy. J Periodontol 1979; 50:495-509.
16. Apatzidou DA. Modern approaches to non-surgical biofilm management. Front Oral Biol 2012; 15:99-116.
17. Apatzidou DA, Kinane DF. Nonsurgical mechanical treatment strategies for periodontal disease. Dent Clin North Am 2010; 54:1-12.
18. Apatzidou DA, Zygogianni P, Sakellari D, Konstantinidis A. Oral hygiene reinforcement in the simplified periodontal treatment of 1 hour. J Clin Periodontol 2014; 41:149-156.
19. Cobb CM. Non-Surgical pocket therapy: mechanical. Ann Periodontol 1996; 1:443-490.
20. Belstr0m D, Grande MA, Sembler-M0ller ML, Kirkby N, Cotton SL et al. Influence of periodontal treatment on subgingival and salivary microbiotas. J Periodontol 2018; 89:531539.
