Subgingival instrumentation.

The S3-level clinical guidelines for the treatment of patients with periodontitis stages I-III published by the European Federation of Periodontology in 2020, suggest a pre-established stepwise approach for oral-healthcare professionals with precise therapeutic pathways. The second step of this approach consists of the subgingival instrumentation of periodontal pockets by non-surgical means to disrupt the microbial biofilm and remove soft and mineralized deposits This step aims to resolve periodontal inflammation by closure of periodontal pockets (probing pocket depth ≤ 4 mm, absence of bleeding on probing) employing different types of instruments and treatment protocols toward this end. Novel non-surgical treatment approaches that adopt micro instruments or subgingival application of biological agents have been recently tested. Subgingival instrumentation has been shown to effectively restore the subgingival microbiota to one associated with periodontal health and to modulate the inflammatory response. The outcomes of the subgingival instrumentation have to be evaluated in order to guide the therapist in providing additional but focused treatment in the remaining pockets OR at sites with residual inflammation. Of great importance is the impact that non-surgical periodontal treatment has on the patient's well-being, based on evidence that emerges from studies evaluating patient related outcomes and quality of life.

Association between bleeding periodontal pockets and eczemas: Results of the Northern Finland Birth Cohort 1966.

AIM: To investigate whether the periodontal condition as measured by bleeding periodontal pockets is associated with atopic dermatitis, seborrheic dermatitis, and eczema nummulare. MATERIALS AND METHODS: The study population (n = 1871) was obtained from the 46-year follow-up study of the Northern Finland Birth Cohort 1966 study (NFBC1966). The periodontal condition was measured by the number of sites with bleeding periodontal pockets that were ≥4 mm deep. The whole skin of the participants was clinically examined, and diagnoses of skin diseases were made according to the International Classification of Diseases. Prevalence rate ratios (PRR) and 95% confidence intervals (95% CIs) were estimated using Poisson regression models with robust error variance. RESULTS: In this cohort, comprising 46-year-old participants of NFBC1966, the presence of 1-3 and ≥4 bleeding-deepened periodontal pockets (≥4 mm deep) were associated with seborrheic dermatitis (PRR 1.9, 95% CI: 1.3-2.8 and PRR 2.2, 95% CI: 1.4-3.3, respectively) and with eczema nummulare (PRR 1.7, 95% CI: 0.9-3.1 and PRR 1.7, 95% CI: 0.9-3.3, respectively). For non-smokers, the corresponding estimates were 1.7 for seborrheic dermatitis (95% CI: 1.1-2.6) and 1.8 (95% CI: 1.1-3.1) and 1.4 for eczema nummulare (95% CI: 0.7-2.9) and 1.2 (95% CI: 0.5-2.9), respectively. No association was found between bleeding-deepened periodontal pockets and atopic dermatitis. Further adjustments for C-reactive protein, diabetes, and inflammatory diseases did not essentially change the risk estimates among either the total population or the non-smokers. CONCLUSION: Bleeding periodontal pockets appeared to be associated with the presence of seborrheic dermatitis and eczema nummulare.

Global Noncoding microRNA Profiling in Mice Infected with Partial Human Mouth Microbes (PAHMM) Using an Ecological Time-Sequential Polybacterial Periodontal Infection (ETSPPI) Model Reveals Sex-Specific Differential microRNA Expression.

Periodontitis (PD) is a polymicrobial dysbiotic immuno-inflammatory disease. It is more prevalent in males and has poorly understood pathogenic molecular mechanisms. Our primary objective was to characterize alterations in sex-specific microRNA (miRNA, miR) after periodontal bacterial infection. Using partial human mouth microbes (PAHMM) (Streptococcus gordonii, Fusobacterium nucleatum, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia) in an ecological time-sequential polybacterial periodontal infection (ETSPPI) mouse model, we evaluated differential mandibular miRNA profiles by using high-throughput Nanostring nCounter® miRNA expression panels. All PAHMM mice showed bacterial colonization (100%) in the gingival surface, an increase in alveolar bone resorption (p < 0.0001), and the induction of a specific immunoglobin G antibody immune response (p < 0.001). Sex-specific differences in distal organ bacterial dissemination were observed in the heart (82% male vs. 28% female) and lungs (2% male vs. 68% female). Moreover, sex-specific differential expression (DE) of miRNA was identified in PAHMM mice. Out of 378 differentially expressed miRNAs, we identified seven miRNAs (miR-9, miR-148a, miR-669a, miR-199a-3p, miR-1274a, miR-377, and miR-690) in both sexes that may be implicated in the pathogenesis of periodontitis. A strong relationship was found between male-specific miR-377 upregulation and bacterial dissemination to the heart. This study demonstrates sex-specific differences in bacterial dissemination and in miRNA differential expression. A novel PAHMM mouse and ETSPPI model that replicates human pathobiology can be used to identify miRNA biomarkers in periodontitis.

Approximal plaque pH lowering after sugar intake in a periodontally infected dentition.

OBJECTIVES: The aim of this study was to evaluate the effect of periodontal inflammation on the approximal plaque pH after a sucrose rinse. MATERIALS AND METHODS: Thirty-two periodontitis patients (aged 38-72 years; 9M/23F) were included. All patients were in need of periodontal surgery. Two non-adjacent interdental spaces, one healthy (no bleeding on probing [BoP] and probing pocket depth [PPD] < 4 mm) and one periodontally diseased (BoP and PPD ≥5 mm) were selected. Before and after surgery, the approximal plaque pH was measured before and after 2, 5 and 10 min after a 1-min rinse with sucrose solution. RESULTS: In periodontally diseased interdental spaces, a significant pH drop was seen 5 min after rinsing. In healthy spaces and after surgery, a significant pH drop was seen after 2 min. A multilevel regression analysis showed that greater probing pocket depths were significantly associated with pH change measured 5 min after rinsing (p < .05). Further on, the approximal pH drop after a sucrose rinse tended to be delayed in dentitions with ≥10% of PPD ≥5 mm (p = .052). CONCLUSIONS: The results suggest that an ongoing periodontal inflammation could temporarily neutralize acidic metabolic products after a sugar challenge. This may further suggest that plaque pH measured after a sugar rinse might be used to identify an ongoing periodontal disease.

Alveolar bone histological necrosis observed prior to extractions in patients, who received bone-targeting agents.

OBJECTIVE: We reported the alveolar bone histology prior to dental extractions in cancer patients, who received bone-targeting agents (BTA). SUBJECTS AND METHODS: Fifty-four patients were included. Patients underwent extractions, and bone biopsies were taken. RESULTS: Extractions were performed due to pain, swelling, purulence, fistula, and numbness, not responding to treatment, in 40 patients (group A); extractions due to asymptomatic, non-restorable teeth, were performed in 14 patients (group B). Complete alveolar jaw bone histological necrosis was observed in 28 of 40 (70%) patients of group A and none of group B (p < .001). The development of clinical osteonecrosis (MRON) was assessed in 44 patients; 10 patients, who were also treated with Low Level Laser Treatments-LLLT, were excluded from this analysis, as the alternative therapies were a confounding factor. Twelve patients, with alveolar bone histological necrosis prior to extraction, developed medication-related osteonecrosis of the jaw (MRONJ) compared with two patients with vital or mixed vital/non-vital bone (p < .0007). BTAs >1 year and concurrent targeted therapy were also significantly associated with MRONJ (p = .016 and p = .050). CONCLUSION: Pain, swelling, purulence, fistula, and numbness were significantly associated with complete bone histological necrosis prior to extractions and increased MRONJ development. Research is justified to explore whether histological necrosis represents an early stage of osteonecrosis.

Long-term metabolic syndrome is associated with periodontal pockets and alveolar bone loss.

AIM: To investigate whether the metabolic syndrome (MetS) is associated with deepened periodontal pockets and alveolar bone loss. MATERIALS AND METHODS: This study was based on a subpopulation of the Northern Finland Birth Cohort 1966 survey (n = 1964). The criteria of the AHA/NHLBI were used to determine MetS. The analyses were based on the metabolic data at ages 31 and 46, and probing pocket depth and alveolar bone level data at age 46. Relative risks (RR, 95% CI) were estimated using Poisson regression models. RESULTS: Relative risks for PD ≥ 4 mm and BL ≥ 5 mm were higher in individuals with an exposure to MetS ≥ 15 years (RR 1.8, 95% CI 1.6-2.1 and RR 1.5, 95% CI 1.3-1.9, respectively) than in those whose exposure was <15 years (RR 1.2, 95% CI 1.1-1.3 and RR 1.1, 95% CI 1.0-1.3, respectively). Consistently stronger associations were found in never smokers. Women showed stronger associations of MetS with PD ≥ 4 mm than men. The association with BL ≥ 5 mm was observed only in men. CONCLUSION: A long-term exposure by MetS was associated independently and in an exposure-dependent manner with periodontal pockets and alveolar bone level.

An appraisal of the role of specific bacteria in the initial pathogenesis of periodontitis.

BACKGROUND: Historically, inflammatory periodontal diseases (gingivitis and periodontitis) have been recognized as being primarily of bacterial origin. Bacteria are necessary for disease development, but the presence of specific bacteria does not guarantee progression to periodontitis. Periodontitis is a multifactorial disease; specific bacteria are associated with disease, but may not be the target of treatment. Gingivitis and periodontitis are inflammatory conditions associated with bacterial overgrowth. AIM: To analyse evidence for established thought that specific bacteria directly participate in the pathogenesis of periodontitis and question the long-held tenet that penetration of the periodontal connective tissues by bacteria and their products is a significant phase in the initial development of periodontitis. METHODS: The literature was searched for studies on initiation of gingivitis and periodontitis by specific pathogens. The search results were insufficient for a systematic review and have been summarized in a commentary instead. RESULTS: There is very little evidence in the literature to support the commonly held concept that specific bacteria initiate periodontitis. CONCLUSION: We present evidence for a paradigm supporting the central role of inflammation, rather than specific microbiota, in the early pathogenesis of periodontitis, and discuss whether controlling the inflammation can influence the character and composition of the periodontal infection.

The implication of probiotics in the prevention of dental caries.

The current oral health crisis, whose causes are varied and complex, necessitates timely oral evaluation and early detection and treatment of oral health problems. Dramatic changes in eating habits and lifestyles are associated with the recent decline in oral health. Probiotics are "good" bacteria that support digestion and a healthy immune system and offer various health benefits to the host. Traditionally, probiotics have been used to improve gut health; the most common uses have historically been as a treatment or prevention of gastrointestinal infections and disease. During the last decade, studies have additionally suggested the intake of probiotics for oral health purposes. Probiotic use provides an effective strategy to combat oral disease, including the development of dental caries and periodontal infection. The aim of this review is to describe the beneficial roles of probiotic bacteria in the oral cavity and the potential mechanisms by which these bacteria exert their effects on oral health.

In-vitro activity of sodium-hypochlorite gel on bacteria associated with periodontitis.

OBJECTIVES: The aim of the present study was to assess the antimicrobial activity of a sodium hypochlorite formulation including its components against bacteria associated with periodontal disease. MATERIALS AND METHODS: Sodium hypochlorite formulation (NaOCl gel), its components sodium hypochlorite (NaOCl), and the activating vehicle were compared with 0.1 % chlorhexidine digluconate (CHX) solution. The antimicrobial activity was proven by determination of minimal inhibitory concentrations (MIC), minimal bactericidal concentrations, and killing assays. Furthermore, the influence on formation as well as on a 4-day-old 6-species biofilm was tested. RESULTS: Except for one strain (Parvimonas micra ATCC 33270 in case of NaOCl gel), the MICs both of the CHX solution and NaOCl gel did not exceed 10 % of the formulations' concentration. In general, MICs of the NaOCl gel were equal as of the CHX solution against Gram-negatives but higher against Gram-positive bacteria. CHX but not NaOCl gel clearly inhibited biofilm formation; however, the activity of NaOCl gel was more remarkable on a 4-day-old biofilm. NaOCl killed bacteria in the biofilm and interfered with the matrix. CONCLUSIONS: The NaOCl gel acts antimicrobial in particular against Gram-negative species associated with periodontitis. Moreover, its component NaOCl hypochlorite is able to alter biofilm matrices. CLINICAL RELEVANCE: The NaOCl gel may represent a potential alternative for adjunctive topical antimicrobial treatment in periodontitis.

Natural killer T cells mediate alveolar bone resorption and a systemic inflammatory response in response to oral infection of mice with Porphyromonas gingivalis.

BACKGROUND AND OBJECTIVE: T and B cells are known to be involved in the disease process of periodontitis. However, the role of natural killer T cells in the pathogenesis of periodontitis has not been clarified. MATERIALS AND METHODS: To examine the role of these cells, C57BL/6J (wild-type), CD1d(-/-) and α-galactosylceramide (αGC)-stimulated wild-type mice were orally infected with Porphyromonas gingivalis strain W83. RESULTS: Apart from CD1d(-/-) mice, the level of alveolar bone resorption was elevated by the infection and was further accelerated in αGC-stimulated mice. The infection induced elevated levels of serum amyloid A and P. gingivalis-specific IgG in the sera, although the degree of elevation was much smaller in the CD1d(-/-) mice. Infection-induced RANKL elevation was only observed in αGC-stimulated mice. Although the cytokines produced by splenocytes were mainly T-helper 1 type in wild-type mice, those in αGC-stimulated mice were predominantly T-helper 2 type. In the liver, the infection demonstrated no effect on the gene expression for interferon-γ, interleukin-4 and RANKL except αGC-stimulated mice in which the infection upregulated the gene expressions. CONCLUSION: This study is the first to show that natural killer T cells upregulated systemic and local inflammatory responses induced by oral infection with P. gingivalis, thereby contributing to the progression of alveolar bone resorption.

Association between periodontal condition and hypertension in a non-smoking population aged 30-49 years: results of the Health 2000 Survey in Finland.

AIM: The aim of this cross-sectional study was to investigate whether periodontal condition is associated with hypertension and systolic blood pressure. MATERIALS AND METHODS: The study population consisted of dentate, non-diabetic, non-smoking individuals aged 30-49 years (n = 1296) in the national Health 2000 Survey in Finland. The number of teeth with deepened (≥4 mm) and deep (≥6 mm) periodontal pockets and the number of sextants with gingival bleeding were used as explanatory variables. Hypertension and systolic blood pressure were used as outcome variables. RESULTS: There was no consistent association between the number of teeth with deepened (≥4 mm) (OR 0.98, 95% CI 0.95-1.01) or deep (≥6 mm) (OR 1.01, 95% CI 0.90-1.12) periodontal pockets and hypertension after adjusting for confounding factors. Nor was there any essential association between the number of bleeding sextants and hypertension. CONCLUSIONS: Periodontal pocketing and gingival bleeding did not appear to be related to hypertension in non-diabetic, non-smoking individuals aged 30-49 years. Further studies using experimental study designs would be required to determine the role of infectious periodontal diseases in the development or progression of hypertension.

Body mass index and periodontal infection in a sample of non-smoking older individuals.

OBJECTIVE: The aim of this study was to investigate the association between BMI and periodontal infection in a sample of non-smoking individuals aged 75 years or older. SUBJECTS AND METHODS: The study sample included 157 non-smoking dentate persons (110 women, 47 men, mean age 80.6 years) belonging to the Geriatric Multidisciplinary Strategy for the Good Care of Older People study in Kuopio, Finland. The data were gathered by interview together with geriatric and oral clinical examination. The outcome variable was the number of teeth with periodontal pockets measuring 4 mm or more in depth. Poisson regression models were used to estimate relative risk (RR) and 95% confidence intervals (CI). RESULTS: After adjustment for confounding factors, the relative risk for the number of teeth with deepened periodontal pockets (≥4 mm) was 0.7 (CI: 0.6-0.9) among those with a BMI 25-29.99 and 1.1 (CI: 0.8-1.4) among those with a BMI ≥30, compared with those having a BMI <25. CONCLUSION: Within the limitations of this study, including small sample size, possibility of confounding and other biases, the results do not provide evidence that elevated body weight would be a risk for periodontal infection among older people.

Relationship between Carotid Intima-Media Thickness, Periodontal Disease, and Systemic Inflammation Biomarkers in an Adult Population.

A positive relationship has been reported between advanced periodontitis and carotid intima-media thickness (cIMT) measurement. The aim of this study was to investigate this relationship with parameters for periodontitis, such as PISA and systemic inflammation biomarkers. An observational descriptive cross-sectional study was conducted. A blood sample was collected from 75 subjects to analyze glucose, total cholesterol, HDL, LDL, and cytokine values. Increased cIMT was found in 32% of the patients with fewer teeth. Patients with periodontitis had a larger periodontal inflamed surface area (PISA) (p = 0.000) and had a 1.42-times-higher risk of having increased cIMT values compared to periodontally healthy individuals, though without a statistically significant association. Higher values in the left cIMT, IL-8, and TNF-α were found in men than in women with significant differences. In the multivariate analysis involving cytokines, age continues to be linked to increased cIMT values. INF-γ showed a trend towards a protective effect; as the IMT-M decreases, there is an increase in the expression of INF-γ, and a higher proportion of subjects with elevated INF-γ concentrations demonstrated normal IMT-C. This study did not find a statistically significant association between cIMT and periodontal disease, but the risk of having increased cIMT is 1.42-times higher for individuals with periodontitis.

Role of insulin sensitivity and beta cell function in the development of periodontal disease in adults without diabetes.

AIM: The goal of this study was to explore whether insulin resistance and beta cell function are related to periodontal pocket formation, indicative of infectious periodontal disease in non-smoking adults without manifest diabetes. MATERIAL AND METHODS: We analysed data from a Health 2000 Survey consisting of dentate subjects without any indication of diabetes, aged between 30 and 64, who had never smoked and who had participated in the Follow-up Study on Finnish Adults' Oral Health about 4 years later (n = 157). The Homeostasis Model Assessment Indices were used to measure insulin resistance (HOMA-IR) and ß-cell function (HOMA-B). The development of periodontal disease was measured by means of the incidence of deepened periodontal pockets (4 mm deep or deeper) during the follow-up period. Incidence rate ratios (IRR) were estimated using Poisson regression models. RESULTS: Both HOMA-IR and HOMA-B indices were associated with periodontal pocket formation during the 4-year follow-up. CONCLUSION: The results of this follow-up study suggest that impaired glucose metabolism measured as insulin resistance and altered beta cell function predict the breakdown of periodontal tissues. Further studies about their role in the pathogenesis of periodontal diseases are needed.

Cerebral Venous Thrombosis Mimicking Limbic Encephalitis.

Cerebral venous thrombosis (CVT) is challenging to diagnose, as it presents with variable symptoms. We encountered a complicated case of CVT that mimicked limbic encephalitis due to sensory aphasia. Based on the characteristic magnetic resonance imaging findings, this 72-year-old Japanese man was later confirmed to have CVT, the cause of which was periodontitis due to Eikenella corrodens, a Gram-negative facultative anaerobic that is part of the mouth's normal flora. The symptoms improved without sequelae following anticoagulation treatment and antibiotics. Clinicians should consider CVT as a differential diagnosis when unexplainable neurological symptoms suggesting limbic encephalitis are observed.

Is periodontal infection a risk factor for thromboembolic disease? A systematic review.

Background: Venous thromboembolism (VTE) is a rising major health problem comprising pulmonary embolism (PE) and deep vein thrombosis. It is of concern due to premature mortality, increased morbidity, and associated healthcare costs and hospitalization. Periodontitis can increase the risk of VTE by way of systemic inflammation induced by infection that can contribute to hypercoagulability and platelet aggregation. This systematic review aims to synthesize all the evidence concerning periodontal infection as a risk factor for thromboembolic disease. Materials and Methods: A search for articles published from 1967 till December 2020 was conducted in the PubMed (MEDLINE), Scopus, and EMBASE data bases. Results: Five hundred and five articles were retrieved after running search strategies in PubMed, Scopus, and EMBASE search databases. Based on the inclusion criteria, three clinical studies, two case series, and ten case reports were included for qualitative analysis. The presence of periodontal disease was reported to influence the occurrence of venous thromboembolic disease with a statistical significance of <0.010. Case series and case reports of septic PE due to periodontal disease showed complete resolution of lung lesions and subsiding of symptoms after dental treatment and antimicrobial therapy. Conclusions: The results of this systematic review suggested for an association between periodontal disease and the incidence of thromboembolic disease. As most of the included/available studies are case series and case reports, the strength of evidence is weak. Evidence generated from well-designed longitudinal controlled clinical trials may be helpful to further assess the strength of the association.

Aberrant pulmonary immune response of obese mice to periodontal infection.

Obesity and periodontitis constitute mutual risk factors in respiratory disorders; this study aimed to explore the pulmonary immune response to periodontal infection using combined animal models with diet-induced obesity (DIO). Thirty-two C57 BL/6J mice were randomly divided into low-fat (LF) or high-fat (HF) diet groups and fed an LF diet as a control or an HF diet to induce obesity. The 30-week mice in the diet group were divided into periodontal ligation group (10 days using Porphyromonas gingivalis ATCC 33277) or sham-ligation group. The expressions of the macrophage-specific maker (F4/80), macrophage chemotactic protein1 (MCP1), and inflammatory cytokines in lung tissues were analyzed. The mRNA and protein levels of F4/80, MCP1, interleukin (IL)-1ß, and IL-6 expressions were significantly upregulated by obesity in lung tissues. However, the mRNA and protein levels of F4/80, MCP1, and IL-6 were downregulated by periodontitis in DIO mice relative to that of the HF control group. Periodontitis increased tumor necrosis factor-α level of lung tissues under LF, while IL-10 was not affected by obesity regardless of periodontitis. Periodontitis may aggravate pulmonary immune response in obese rodents. This may relate to the imbalance of the pro- and anti-inflammatory cytokine status of lung lesions, which tends to attenuate the infiltration of alveolar macrophages.

Application of antimicrobial photodynamic therapy to treat subgingival multidrug-resistant bacterial infections in ICU patients.

BACKGROUND: Drug-resistant bacterial infections have received much attention in recent years. Antimicrobial photodynamic therapy (aPDT) is an effective antimicrobial strategy. This study aimed to evaluate the therapeutic effect of methylene blue (MB)-mediated aPDT against subgingival multidrug-resistant (MDR) bacterial infections in intensive care unit (ICU) patients. METHODS: Eighty-three patients who were hospitalized in the ICU of the Second Affiliated Hospital of Nanchang University from July 2019 to June 2021 were selected. The intraoral partitioned control test was conducted. Teeth that met the criteria were selected from different quadrants of the same patient, randomly divided into three groups, namely, A, B, and C, and treated with aPDT, chlorhexidine gargle, or normal saline. The counts of MDR bacteria in the gingival crevicular fluid were assessed in the different groups at different time points before and after treatment. RESULTS: The MDR bacterial count decreased immediately after aPDT and was significantly different from that in the chlorhexidine gargle rinse group and the normal saline rinse group (P<0.05). There was no significant difference among the three groups at 6, 12, and 24 hours after treatment (P>0.05). CONCLUSION: aPDT can be used to treat subgingival MDR bacterial infections, but the long-term effects of treatment need to be further studied.

Diet-Induced Non-alcoholic Fatty Liver Disease and Associated Gut Dysbiosis Are Exacerbated by Oral Infection.

Increasing evidence indicates that chronic inflammation due to periodontal disease is associated with progression of non-alcoholic fatty liver disease (NAFLD) caused by a Western diet. NAFLD has also been associated with oral infection with the etiological agent of periodontal disease, Porphyromonas gingivalis. P. gingivalis oral infection has been shown to induce cardiometabolic disease features including hepatic lipid accumulation while also leading to dysbiosis of the gut microbiome. However, the impact of P. gingivalis infection on the gut microbiota of mice with diet-induced NAFLD and the potential for those changes to mediate NAFLD progression has yet to be determined. In the current study, we have demonstrated that P. gingivalis infection induced sustained alterations of the gut microbiota composition and predicted functions, which was associated with the promotion of NAFLD in steatotic mice. Reduced abundance of short-chain fatty acid-producing microbiota was observed after both acute and chronic P. gingivalis infection. Collectively, our findings demonstrate that P. gingivalis infection produces a persistent change in the gut microbiota composition and predicted functions that promotes steatosis and metabolic disease.

Oral Phenotype and Salivary Microbiome of Individuals With Papillon-Lefèvre Syndrome.

Papillon-Lefèvre syndrome (PLS) is an autosomal recessive rare disease, main characteristics of which include palmoplantar hyperkeratosis and premature edentulism due to advanced periodontitis (formerly aggressive periodontitis). This study aimed to characterize the oral phenotype, including salivary parameters, and the salivary microbiome of three PLS sisters, comparatively. Two sisters were toothless (PLSTL1 and PLSTL2), and one sister had most of the teeth in the oral cavity (PLST). Total DNA was extracted from the unstimulated saliva, and the amplicon sequencing of the 16S rRNA gene fragment was performed in an Ion PGM platform. The amplicon sequence variants (ASVs) were obtained using the DADA2 pipeline, and the taxonomy was assigned using the SILVA v.138. The main phenotypic characteristics of PLS were bone loss and premature loss of primary and permanent dentition. The PLST sister presented advanced periodontitis with gingival bleeding and suppuration, corresponding to the advanced periodontitis as a manifestation of systemic disease, stage IV, grade C. All three PLS sisters presented hyposalivation as a possible secondary outcome of the syndrome. Interestingly, PLST salivary microbiota was dominated by the uncultured bacteria Bacterioidales (F0058), Fusobacterium, Treponema, and Sulfophobococcus (Archaea domain). Streptococcus, Haemophilus, and Caldivirga (Archaea) dominated the microbiome of the PLSTL1 sister, while the PLSTL2 had higher abundances of Lactobacillus and Porphyromonas. This study was the first to show a high abundance of organisms belonging to the Archaea domain comprising a core microbiome in human saliva. In conclusion, a PLST individual does have a microbiota different from that of the periodontitis' aggressiveness previously recognized. Due to an ineffective cathepsin C, the impairment of neutrophils probably provided a favorable environment for the PLS microbiome. The interactions of Bacteroidales F0058, Caldivirga, and Sulfophobococcus with the microbial consortium of PLS deserves future investigation. Traditional periodontal therapy is not efficient in PLS patients. Unraveling the PLS microbiome is essential in searching for appropriate treatment and avoiding early tooth loss.