Initiation Of Periodontitis Research Articles

Influence of periodontal microbial homeostasis on neurodegenerative diseases and its therapeutic perspectives

The oral cavity is the second largest reservoir of microorganisms in the human body, containing more than 700 species. Periodontal microorganisms are an important part of oral microorganisms. Plaque biofilm, the initiator of periodontal disease, contains an abundance of oral microorganisms. The special complex anatomy of the periodontium allows for a higher abundance of the periodontal microbiota. There are growing evidences show that the periodontal microbiota is not only closely associated with oral diseases, but also plays an important role in mouth-brain interactions. Dysbiosis of the periodontal microbiota may facilitate the progression of neurodegenerative diseases including Alzheimer disease, Parkinson disease, and multiple sclerosis. Here, this paper reviews the bidirectional role of periodontal microbiota between the oral cavity and the brain, that is, the bridge effect of periodontal microbiota involved in the interaction between the two diseases, enumerates the epidemiological and biological evidences that dysregulation of the periodontal microbiota induces and exacerbates neurodegenerative diseases, and analyzes their possible mechanisms. The positive implications of periodontal microbial homeostasis in the prevention and treatment of neurodegenerative diseases are described with the aim of providing new ideas and insights into the pathogenesis and therapeutic approaches for neurodegenerative diseases.

Clinical Study and Microbiological Analysis of Periodontopathogenic Microflora Analyzed among Children and Adolescents with Cardiovascular Diseases Compared to Group with Good General Status.

Periodontal diseases, as an important part of oral pathology, present different characteristics when affecting children and adolescents or young adults. Studies have shown that adolescence and childhood are closely related to a high risk of periodontal disease, but the follow-up for periodontal health or damage at this age has been insufficiently appreciated until now. The aim of this study was to identify subgingival microorganisms using a real-time polymerase chain reaction (PCR) in a group of children and adolescents aged 7-17 years with and without cardiovascular disease. The group of 62 subjects with gingival inflammation and poor hygiene was divided into two groups according to general condition: 31 subjects with carduivascular disease (group A) and 31 subjects without cardiovascular disease (group C). Subjects were examined in the initial consultation, the state of hygiene and periodontal inflammation was assessed using the plaque index (PI) and gingival index (GI), and samples were taken from the gingival sulcus using sterile paper cones to determine nine subgingival microorganisms. Nine subgingival microorganisms were identified: Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Treponema denticola (Td), Tannerella forsythias (Tf), Prevotella intermedia (Pi), Peptostreptococcus (Micromonas) micros (Pm), Fusobacterium nucleatum (Fn), Eubacterium nodatum (En), and Capnocytophaga gingivalis (Cg). The patients were included in a specialist treatment program which aimed to relieve the inflammatory condition, remove local irritative factors, and train the patients to perform proper oral hygiene at home by using primary and secondary oral hygiene products. Subjects were reevaluated 3 months after treatment, when measurements for the PI and GI and microbiological determinations were repeated. The results showed a predominance of subjects aged 16-17 years (12.4%). Among the subjects with marked gingival inflammation, the male gender was predominant (58.06%). The PI values changed considerably after treatment, with lower values in patients presenting a general condition without cardiovascular disease (PI = 8.10%) compared with the patients with cardiovascular disease (PI = 13.77%). After treatment, the GI showed considerable changes in both groups. Red, orange, and purple complex microorganisms were found before treatment and decreased considerably after treatment in both groups. The highest values were found for Treponema denticola (140,000 (1.4 × 105)) in patients with cardiovascular disease and generalized gingival inflammation. Of the pathogenic microorganisms, the most common was Tannerella forsythia in 52 patients before treatment, and red microorganisms considerably appeared in only 10 patients after treatment. Capnocytophaga gingivalis remained constant both in the diseased state and after treatment and was consistent with periodontal health. Children with cardiovascular diseases had a higher prevalence of gingival manifestations. The composition of the subgingival microbial plaque was directly influenced by the degree of oral hygiene, but the response to specialized treatment was also influenced by the general health status. The results of this study support the conclusion that periodontal pathogens appear and multiply in the absence of proper hygiene in childhood after the eruption of permanent teeth, and their action leads to the initiation of periodontal diseases.

To Evaluate the Association Between Serum Concentration of Vitamin D and Chronic Periodontitis in Non-menopausal Females: A Clinico Biochemical Study.

Periodontal disease's initiation and propagation is through a dysbiosis of the commensal oral microbiota. But recently, through the extraordinary progress, the interrelationship that exists between periodontal disease and systemic health has been unveiled. Through various studies, it has been revealed that vitamin D deficiency may be associated with a greater risk of developing chronic periodontitis and vitamin D supplementation may help to preserve periodontal health. To find a co-relation between 25-hydroxy vitamin D status and the severity of periodontal diseases. To evaluate and compare the effect of non-surgical periodontal therapy alone and in combination with vitamin D supplementation in reducing the severity of periodontal diseases. The present study was conducted on 90 non-menopausal female subjects who divided into 3 groups. Group I comprised of healthy controls. Group II comprised of patients with moderate chronic periodontitis who were assigned to receive only Scaling and root planing (SRP). While group III included patients with moderate chronic periodontitis who were assigned to receive SRP along with Vitamin D supplementation. The periodontal parameters and serum levels of 25- hydroxy vitamin D were recorded for all the participants at baseline. Group II and group III participants were reassessed at an interval of 3 months post-treatment. The results indicated that vitamin D deficiency affected periodontal health negatively. Statistically highly significant improvement was observed in Group III as compared to group II, signifying the efficacy of vitamin D supplementation adjunctive to SRP. Regular evaluation of Vitamin D levels and supplementation to treat the deficiency may have potential periodontal health benefits.

Zoledronic acid affects the process of Porphyromonas gingivalis infecting oral mucosal epithelial barrier: An in-vivo and in-vitro study.

Zoledronic acid (ZA), one of the commonly used bisphosphonates, is mainly used for bone-metabolic diseases. Studies proved that ZA has adverse effects on oral soft tissues. As the first line of innate immunity, the gingival epithelium could be infected by periodontal pathogens, which is a key process of the initiation of periodontal diseases. Yet, how ZA affects the periodontal pathogens infecting the epithelial barrier remains unclear. This study aimed to investigate the influences of ZA on the process of Porphyromonas gingivalis (P. gingivalis) infecting the gingival epithelial barrier via in-vitro and in-vivo experiments. In the in-vitro experiments, under the condition of different concentrations of ZA (0, 1, 10, and 100 μM), P. gingivalis was used to infect human gingival epithelial cells (HGECs). The infections were detected by transmission electron microscope and confocal laser scanning microscope. Besides, the internalization assay was applied to quantify the P. gingivalis, which infected the HGECs, in the different groups. To evaluate the expression levels of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, and IL-8, by infected HGECs, real-time quantitative reverse transcription-polymerase chain reactions were applied. In the in-vivo experiments, rats were given ZA solution (ZA group) or saline (control group) by tail intravenous injection for 8 weeks. Subsequently, we put ligatures around the maxillary second molars of all the rats and inoculated P. gingivalis to the gingiva every other day from day 1 to day 13. The rats were sacrificed on days 3, 7, and 14 for micro-CT and histological analyses. The in-vitro results manifested that the quantity of P. gingivalis that had infected HGECs increased with the ZA concentrations. Pro-inflammatory cytokines expression by HGECs were significantly increased by 100 μM ZA. In the in-vivo study, compared to the control group, more P. gingivalis was detected in the superficial layer of gingival epithelium in the ZA group. Besides, ZA significantly increased the expression level of IL-1β on day 14 and IL-6 on days 7 and 14 in gingival tissues. These findings suggest that the oral epithelial tissues of patients who receive high-dose ZA treatment may be more susceptible to periodontal infections, resulting in severe inflammatory conditions.

Oral Cavity Calprotectin and Lactoferrin Levels in Relation to Radiotherapy.

Background: Lactoferrin, an iron-binding glycoprotein, and calprotectin, a calcium binding protein, are sensitive markers of inflammation and their fecal levels increase during radiotherapy of prostate cancer patients. With this background, we analyzed mouthrinse calprotectin and lactoferrin levels of head- and neck-cancer patients before, during and after radiotherapy. Methods: Twenty cancer patients (mean age 55.85 ± 15.01, 80% male), who had been planned to undergo radiotherapy to the head and neck area, were included in this study. Mouthrinse samples were collected before radiotherapy, at the 3rd and 6th weeks of radiotherapy and 4 weeks after the radiotherapy. Mouthrinse samples were analyzed for calprotectin and lactoferrin using commercial ELISA kits. Results: Calprotectin levels increased significantly during radiotherapy (p = 0.022). Both markers, lactoferrin (p = 0.011) and calprotectin (p = 0.006), decreased significantly after the treatment. Conclusions: Present study results may suggest that the elevations in calprotectin and lactoferrin levels during radiotherapy reflect the increased and emerging inflammatory environment in the oral cavity, thus may increase the risk of periodontal disease initiation or progression.

The Action of Gene Polymorphism in the pathogenesis of periodontal diseases: A Narrative Review

Presently, it is known that pathogenic bacteria are the key factors for the initiation of periodontal disease, but the host response and the severity of clinical expression are largely determined by genetic susceptibility and environmental factors. There is evidence that the individual response to the environment and variations in the immune response in periodontitis are associated with genetic factors. The gene polymorphisms like interleukin-1 beta (IL-1b), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-a) genes and their factors that determine the production of various cytokines which play an important role in the pathophysiology of inflammation and periodontal diseases. A sequel of this realization is that if the genetic basis of periodontal disease susceptibility can be understood, such information may have diagnostic and therapeutic value. This review focus to upgrade the general practitioners and periodontist about various genetic polymorphisms associated with periodontal diseases to aid in a better approach to the condition in the future.

Genomic Medicine in Periodontal Disease: Old Issue, New Insights.

Genetic variability is the main cause of phenotypic variation. Some variants may be associated with several diseases and can be used as risk biomarkers, identifying animals with higher susceptibility to develop the pathology. Genomic medicine uses this genetic information for risk calculation, clinical diagnosis and prognosis, allowing the implementation of more effective preventive strategies and/or personalized therapies. Periodontal disease (PD) is the inflammation of the periodontium induced mainly by bacterial plaque and is the leading cause of tooth loss. Microbial factors are responsible for the PD initiation; however, several studies support the genetic influence on the PD progression. The main purpose of the present publication is to highlight the main steps involved in the genomic medicine applied to veterinary patients, describing the flowchart from the characterization of the genetic variants to the identification of potential associations with specific clinical data. After investigating which genes might potentially be implicated in canine PD, the RANK gene, involved in the regulation of osteoclastogenesis, was selected to illustrate this approach. A case-control study was performed using DNA samples from a population of 90 dogs - 50 being healthy and 40 with PD. This analysis allowed for the discovery of four new intronic variations that were banked in GenBank (g.85A>G, g.151G>T, g.268A>G and g.492T>C). The results of this study are not intended to be applied exclusively to PD. On the contrary, this genetic information is intended to be used by other researchers as a foundation for the development of multiple applications in the veterinary clinical field.

The influence of smoking on the periodontal biome. A review.

Abstract Periodontal disease is believed to be an opportunistic infection due to the interaction of bacterial plaque and the patient’s response that may be influenced by environmental, genetic, and other risk factors. In addition to the fact that smoking is considered a risk factor in many systemic diseases, it has also been associated with the initiation of periodontal disease. Smoking is one of the modifiable risk factors and has a significant influence on the development, progress, and results of the treatment of periodontal disease. The current state in the field of study suggests that smoking aids the colonization of periodontal microorganisms, accelerating the onset of periodontal disease. Biological modifications in pathogens, such as Porphyromonas gingivalis, along with poor immune response, influence the variations of subgingival flora in smoking patients. Only with an individual approach can the risk factors of each patient be identified and satisfactory results obtained. The aim of this paper is to present a comprehensive review of the influence of smoking on periodontal microbiome and the importance of adopting the appropriate treatment method according to the influence of this risk factor on healing.

The Need for Oral Hygiene Care and Periodontal Status among Hospitalized Gastric Cancer Patients.

Poor oral hygiene leads to the accumulation of dental plaque, thus contributing to the initiation of periodontal disease (PD). Local infections can lead to systemic inflammatory responses, which are essential mediators for the evolution of systemic conditions or cancer tumorigenesis. Often, patients hospitalized with life-threatening and incapacitating disorders such as gastric cancer (GC) might lose interest in keeping their mouth healthy. This study evaluates oral hygiene, periodontal status, and the need for oral care and medical personnel to assist in achieving it in patients hospitalized with GC. This study was carried out on 25 patients with a diagnosis of GC, divided into two groups (GP—14 patients from the Gastroenterology Department, and SP—11 patients from the 1st Department of Surgery). Patients were examined on the day of admission (T0), the day of the medical procedure of endoscopy or surgery (T1), and the day of discharge (T2), recording the number of absent teeth, dental plaque (PI), bleeding on probing (BOP), probing depths (PPD), frequency of toothbrushing, and if the oral hygiene had been self-performed or assisted. Data were subjected to statistical analysis. Our results showed that, in both the GP and the SP group, there were strong and statistically significant correlations between PI and BOP measured on the last day of hospitalization and the period of hospitalization after the medical procedure. Longer hospital stays and the presence of surgery were risk factors for changing toothbrushing frequency. Results also highlight the need for a dentist to diagnose and eventually treat periodontal disease before and after hospitalization, and for a trained nurse who should help take care of the patient’s oral hygiene during hospitalization.

Obesity-Related Gut Microbiota Aggravates Alveolar Bone Destruction in Experimental Periodontitis through Elevation of Uric Acid.

ABSTRACTObesity is a risk factor for periodontal disease (PD). Initiation and progression of PD are modulated by complex interactions between oral dysbiosis and host responses. Although obesity is associated with increased susceptibility to bacterial infection, the detailed mechanisms that connect obesity and susceptibility to PD remain elusive. Using fecal microbiota transplantation and a ligature-induced PD model, we demonstrated that gut dysbiosis-associated metabolites from high-fat diet (HFD)-fed mice worsen alveolar bone destruction. Fecal metabolomics revealed elevated purine degradation pathway activity in HFD-fed mice, and recipient mice had elevated levels of serum uric acid upon PD induction. Furthermore, PD induction caused more severe bone destruction in hyperuricemic than normouricemic mice, and the worsened bone destruction was completely abrogated by allopurinol, a xanthine oxidase inhibitor. Thus, obesity increases the risk of PD by increasing production of uric acid mediated by gut dysbiosis.

Periodonal desiease – local antiseptic therapy: problem of efficiency. Literature review

The purpose of this reviewarticle is to analyze the current data on the use of antiseptics in the treatment of periodontitis, development of resistance of periodontopathogens to antiseptic agents using the example of chlorhexidine, cetylpyridinium chloride and hexetidine. Periodontal pathogens are an integral part of the commensal microflora of the oral cavity, but under certain conditions and under the influence of etiological factors, their number begins to progressively grow, which increases the risk of initiation of periodontal diseases through the formation of aggressive biofilm on the teeth.Materials and methods. Тhe study of publications was produced in the electronic databases such as PubMed and Google Scholar in the course of a systematic review of the literature. Included articles contain information about antiseptic agents which are chlorhexidine, cetylpyridinium chloride and hexetidine, as well as their effect on periodontopathogens and the possibility of developing resistance in them against these antiseptics.Results. 127 articles were viewed during the review. After analyzing the literature for inclusion criteria, the total number of publications has become 94.Conclusions. Аccording to the analyzed data, we have found that antiseptic treatment of the oral cavity and lesions in periodontitis is an integral part of the treatment of this inflammatory disease, as an addition to the mechanical treatment protocol. Chlorhexidine in local forms of delivery has shown particular activity against periodontopathogens.

Oral Hygiene as a Risk Factor in Periodontitis

Dental plaque is the etiological factor for initiation of periodontal disease due to secretion of toxins andproteolytic enzymes by the microbial accumulation in the cervical region of teeth & sub gingival area.Gingival inflammation will progress into the continuing destruction of supporting tissues like resorptionof alveolar bone Joss of attachment increase pocket depth if we don’t remove the microbial dental plaque,by daily oral hygiene practice through mechanical tooth brushing of the person himself &periodic clinicalexamination to remove the plaque .calculus &other retentive factors to maintain the oral hygiene in a goodmanner.The oral hygiene is considered as a risk factor in the prevention or progression of periodontal diseasedepending on daily removing of dental plaque by the person & professional recalling system clinically.

Oral Microbiome Signatures in Diabetes Mellitus and Periodontal Disease

Disturbances in the oral microbiome are associated with periodontal disease initiation and progression and diabetes mellitus (DM), but how this contributes to the cause-and-effect relationship between periodontal disease and DM is poorly understood. We examined the bacterial composition in plaque samples from 128 South Africans with periodontal disease across glycemic statuses using 16S rDNA sequencing of regions 2, 3, 4, 6-7, 8, and 9. Of the 9 phyla identified, Firmicutes, Proteobacteria, Bacteroidetes, Fusobacteria, and Actinobacteria made up >98%. Fusobacteria and Actinobacteria were significantly more abundant in subjects with diabetes, while Proteobacteria were less abundant. However, in the presence of gingival bleeding and DM, as compared with DM without gingival bleeding, Actinobacteria were markedly reduced while Bacteroidetes were more abundant. In contrast, no differences in Actinobacteria or Bacteroidetes abundance were observed between DM with and without pocket depth (PD) ≥4 mm. At the genus level, similar changes in relative abundance were observed in the presence of DM and periodontal disease. Our findings remained in conditional logistic regression models adjusted for age, sex, waist circumference, and the 5 most dominant phyla. For example, Actinobacteria significantly increased the odds of diabetes by 10% in subjects with gingival bleeding, while Fusobacteria increased this odd by 14%; yet, among subjects with PD ≥4 mm, Fusobacteria decreased the odds of DM by 47%. Our findings have confirmed the alterations in the composition of the oral microbiota across glycemic statuses as well as different stages of periodontal disease. However, it is not clear whether these differences were the consequence of hyperglycemia or the presence of periodontal diseases. Therefore, we recommend further investigations in a longitudinal study design.

Association of Khat chewing, smoking, age and sex with periodontal status among Yemeni adults

Objective: Periodontal diseases are very common dental disease. Many risk factors may play significant role in the periodontal disease initiation and progression. This study was performed to evaluate the effects of khat chewing, smoking, age and gender on periodontal status among Yemeni adults. Material and Methods: This cross-sectional study was performed on 1231 patients attending the outpatient dental polyclinics of University of Science and Technology during the academic years 2017/2018.. All completed sheets were collected throughout the year by the supervisors. Data cleaning, descriptive statistics, and inferential statistics were then performed. Results: Khat chewers were more frequent than non-chewers counterparts (60.7% vs. 39.3%). The prevalence of smoking was 25.5% (297 patients). Study results indicated that periodontitis is more associated with female gender and participants aged more than 35 years old. Results also showed that female and age older participants aged more than 35 years were significantly associated with gingival recession. Mean number of the teeth with gingival recession in male patients were higher than in females. Male gender and patients aged more than 35 years old were significantly associated with furcation involvement. Conclusion: The present study has shown females gender and age older than 35 seem to be risk factors of periodontal diseases. Males has more teeth affected by gingival recession and more furcation involvement.KeywordsPeriodontal disease; Khat chewing; Smoking; Yemen; Risk factors.

Filifactor alocis and Dialister pneumosintes in a Mexican population affected by periodontitis and rheumatoid arthritis: An exploratory study.

Filifactor alocis and Dialister pneumosintes have been associated with the initiation and progression of periodontitis (PE). We determined and compared the frequency of both bacteria in patients with PE, rheumatoid arthritis (RA), and PE/RA simultaneously. Detection was performed by polymerase chain reaction in the subgingival biofilm. Bacteria were more frequent in patients with PE, and clinical periodontal parameters such as pocket depth (PD) and clinical attachment loss (CAL) were significantly higher in patients with PE/RA. F. alocis and D. pneumosintes could influence PD and CAL, hence participating in the initiation and progression of PE in patients with RA.

Regulation of defensive function on gingival epithelial cells can prevent periodontal disease.

SummaryPeriodontal disease is a bacterial biofilm-associated inflammatory disease that has been implicated in many systemic diseases. A new preventive method for periodontal disease needs to be developed in order to promote the health of the elderly in a super-aged society. The gingival epithelium plays an important role as a mechanical barrier against bacterial invasion and a part of the innate immune response to infectious inflammation in periodontal tissue. The disorganization of cell–cell interactions and subsequent inflammation contribute to the initiation of periodontal disease. These make us consider that regulation of host defensive functions, epithelial barrier and neutrophil activity, may become novel preventive methods for periodontal inflammation. Based on this concept, we have found that several agents regulate the barrier function of gingival epithelial cells and suppress the accumulation of neutrophils in the gingival epithelium. We herein introduce the actions of irsogladine maleate, azithromycin, amphotericin B, and Houttuynia cordata (dokudami in Japanese), which is commonly used in traditional medicine, on the epithelial barrier and neutrophil migration in gingival epithelial cells in vivo and in vitro, in order to provide support for the clinical application of these agents to the prevention of periodontal inflammation.

Periodontal diseases.

Periodontal diseases comprise a wide range of inflammatory conditions that affect the supporting structures of the teeth (the gingiva, bone and periodontal ligament), which could lead to tooth loss and contribute to systemic inflammation. Chronic periodontitis predominantly affects adults, but aggressive periodontitis may occasionally occur in children. Periodontal disease initiation and propagation is through a dysbiosis of the commensal oral microbiota (dental plaque), which then interacts with the immune defences of the host, leading to inflammation and disease. This pathophysiological situation persists through bouts of activity and quiescence, until the affected tooth is extracted or the microbial biofilm is therapeutically removed and the inflammation subsides. The severity of the periodontal disease depends on environmental and host risk factors, both modifiable (for example, smoking) and non-modifiable (for example, genetic susceptibility). Prevention is achieved with daily self-performed oral hygiene and professional removal of the microbial biofilm on a quarterly or bi-annual basis. New treatment modalities that are actively explored include antimicrobial therapy, host modulation therapy, laser therapy and tissue engineering for tissue repair and regeneration.

Combined effects of starvation and butyrate on autophagy‐dependent gingival epithelial cell death

Bacteria in the dental biofilm surrounding marginal gingival grooves cause periodontal diseases. Numerous bacteria within the biofilm consume nutrients from the gingival crevicular fluid. Furthermore, some gram-negative bacteria in mature dental biofilms produce butyrate. Thus, gingival epithelial cells in close proximity to mature dental biofilms are at risk of both starvation and exposure to butyrate. In the present study, we determined the combined effects of starvation and butyrate exposure on gingival epithelial cell death and the underlying mechanisms. The Ca9-22 cell line was used as an in vitro counterpart of gingival epithelial cells. Cell death was measured as the amount of total DNA in the dead cells using SYTOX Green dye, which penetrates through membranes of dead cells and emits fluorescence when it intercalates into double-stranded DNA. AMP-activated protein kinase (AMPK) activity, the amount of autophagy, and acetylation of histone H3 were determined using western blot. Gene expression levels of microtubule-associated protein 1 light chain 3b (lc3b) were determined using quantitative reverse transcription-polymerase chain reaction. Butyrate-induced cell death occurred in a dose-dependent manner whether cells were starved or fed. However, the induction of cell death was two to four times higher when cells were placed under starvation conditions compared to when they were fed. Moreover, both starvation and butyrate exposure induced AMPK activity and autophagy. While AMPK inactivation resulted in decreased autophagy and butyrate-induced cell death under conditions of starvation, AMPK activation resulted in butyrate-induced cell death when cells were fed. Combined with the results of our previous report, which demonstrated butyrate-induced autophagy-dependent cell death, the results of this study suggest that the combination of starvation and butyrate exposure activates AMPK inducing autophagy and subsequent cell death. Notably, this combination markedly induced LC3B production and the induction was attenuated by AMPK inhibition. LC3B knockdown, in turn, significantly decreased butyrate-induced cell death. Therefore, AMPK-dependent LC3B induction apparently plays an important role in butyrate-induced cell death. There was a lack of correspondence between the levels of AMPK activation and LC3B induction; this may reflect the histone deacetylase-inhibitory capacity of butyrate on histone proteins. Taken together, starvation and butyrate exposure promote autophagy via AMPK signaling, while the histone deacetylase-inhibitory effects of butyrate alter chromatin to transcriptionally active state, resulting in strong LC3B induction and subsequent cell death. These findings may help improve the understanding of the cellular processes underlying periodontal disease initiation.

Unravelling the Oral Ascendancy of Female Sex Hormones on Periodontium

Bacterial plaque has been established as the primary etiologic factor for the initiation of periodontal disease. It has also been shown that without a susceptible host the periodontal pathogens are necessary but not sufficient for disease to occur. The notable periodontal changes related specifically to female sex steroid levels, primarily those manifested as pathologic alterations in the gingiva, attest to the dramatic potential these hormones possess to impact the oral tissues beyond normal homeostatic functions. Hormonal changes in women present a unique challenge for decision making in periodontal therauptics.

Impact of Hashimoto’s Thyroiditis (Ht) On Periodontal Treatment – A Case Report

Periodontitis is a multifactorial disease with microbial dental plaque as the initiator of periodontal disease. However the manifestation and progression of the disease is influenced by a wide variety of determinants and factors. The strongest type of causal relationship is the association of systemic disease and periodontal disease. Similarly, we present a case of Hashimoto's thyroiditis which altered the periodontal therapy. Hashimoto's thyroiditis is an autoimmune disease seen in children and women. A female patient diagnosed as chronic periodontitis was treated with periodontal flap surgical procedure with bone grafting as and where required. The 3 month reassessment showed fair prognosis obvious changes. However a year later the patient's periodontal status was severely deteriorated. Medical reports revealed Hashimoto's thyroiditis. A possible association of Periodontitis and Hashimoto's thyroiditis is considered in the case report.