Salivary Th17 cytokine, human ß-defensin 1-3, and salivary scavenger and agglutinin levels in Crohn's disease.

OBJECTIVES: Crohn's disease patients, who are prone to develop periodontal diseases, may carry genetic defects in their Th17 cytokine, human beta-defensin (hBD) 1-3, and salivary and scavenger agglutinin (SALSA) expressions. Biochemical composition of saliva reflects the oral consequences of systemic immune response modifications. Our aim was to evaluate the salivary Th17 cytokine, epithelial hBD 1-3, and SALSA levels in relation to Crohn's disease. MATERIALS AND METHODS: This cross-sectional study included 42 Crohn's disease patients and 34 systemically healthy controls. Periodontal and dental indexes were measured, and stimulated saliva samples were collected. Salivary Th17 cytokine levels were analyzed by multiplex technique, and hBD 1-3 and SALSA levels by enzyme-linked immunosorbent assay. RESULTS: There were 19 gingivitis and 11 initial periodontitis patients in the Crohn's disease group, and 15 gingivitis and 4 initial periodontitis in the control group. In comparison to controls, higher salivary Th17 cytokine levels were observed in Crohn's disease patients. No statistical difference was observed between Crohn's disease and control groups in terms of their salivary hBD 1-3 and SALSA levels. Based on the regression analysis, there is no independent association between Crohn's disease and salivary Th17 cytokine levels. CONCLUSIONS: Crohn's disease does not relate to salivary antimicrobial hBD 1-3 or SALSA levels. While Crohn's disease patients have higher salivary Th17 cytokine levels in comparison to systemically healthy controls, an independent association between Crohn's disease and Th17 cytokine profile is still missing. CLINICAL RELEVANCE: Diminished Th17 cytokine response in Crohn's disease, which might be related to genetic susceptibility, can be also visualized in saliva.

Dietary inflammatory index in relation to salivary cytokine concentrations and periodontitis: A cross-sectional analysis.

AIM: To examine the associations of dietary inflammatory index (DII) with salivary cytokine concentrations and periodontitis after controlling for body mass index (BMI), socio-demographic factors and lifestyle. MATERIALS AND METHODS: Subgroups from two Finnish surveys, DILGOM 2007 and Health 2000, were included (total n = 727). The DII scores were calculated based on a food frequency questionnaire. Periodontal status was assessed with a cumulative risk score in DILGOM 2007 and by pocket depth measurement in Health 2000. From saliva, interleukin (IL)-1ß, IL-1 receptor antagonist, IL-6, IL-8, IL-10 and tumour necrosis factor (TNF)-α concentrations were measured. RESULTS: The DII scores did not differ between non-periodontitis and periodontitis participants in pairwise comparison. After adjusting for energy intake, periodontal status, BMI, age, education level, smoking habit and physical activity, DII was not associated with salivary cytokine concentrations. After adjusting for salivary cytokine levels and other confounding factors, DII was associated with periodontitis in the Health 2000 subgroup but not in the DILGOM 2007 subgroup. CONCLUSIONS: The current data support the evidence that diet is not associated with salivary cytokine levels but may be associated with periodontitis. The association observed between diet and periodontitis is related to factors other than diet-dependent inflammatory tendency in the oral cavity.

Probiotics Support Resilience of the Oral Microbiota during Resolution after Experimental Gingivitis-A Randomized, Double-Blinded, Placebo-Controlled Trial.

The present study aims to test whether probiotics protect against experimental gingivitis incited by 14 days of oral hygiene neglect and/or subsequently support the restoration of oral homeostasis. Eighty systemically and orally healthy participants refrained from oral hygiene procedures for 14 days, followed by 14 days with regular oral hygiene procedures. Additionally, participants consumed either probiotics (n = 40) or placebo (n = 40) throughout the trial. At baseline, day 14, and day 28, supragingival plaque score and bleeding-on-probing percentage (BOP %) were registered, and supragingival plaque and saliva samples were collected. The supragingival microbiota was characterized using 16S sequencing, and saliva samples were analyzed for levels of pro-inflammatory cytokines and proteases. At day 28, the relative abundance of Lautropia (p = 0.014), Prevotella (p = 0.046), Fusobacterium (p = 0.033), and Selenomonas (p = 0.0078) genera were significantly higher in the placebo group compared to the probiotics group, while the relative abundance of Rothia (p = 0.047) species was associated with the probiotics group. Streptococcus sanguinis was associated with the probiotics group, while Campylobacter gracilis was associated with the placebo group. No difference was observed in salivary cytokines, albumin, or any enzyme activity. The present study suggests that probiotics support the resilience of the oral microbiota in the resolution period after gingivitis.

Probiotics Partly Suppress the Impact of Sugar Stress on the Oral Microbiota-A Randomized, Double-Blinded, Placebo-Controlled Trial.

The aim was to test if probiotics counteract oral dysbiosis during 14 days of sugar stress and subsequently help restore oral homeostasis. Eighty healthy individuals received either probiotics (n = 40) or placebo lozenges (n = 40) for 28 days and rinsed with a 10% sucrose solution 6-8 times during the initial 14 days of the trial. Saliva and supragingival samples were collected at baseline, day 14, and day 28. Saliva samples were analyzed for levels of pro-inflammatory cytokines, albumin, and salivary enzyme activity. The supragingival microbiota was characterized according to the Human Oral Microbiome Database. After 14 days of sugar stress, the relative abundance of Porphyromonas species was significantly higher (p = 0.03) and remained significantly elevated at day 28 in the probiotic group compared to the placebo group (p = 0.004). At day 28, the relative abundance of Kingella species was significantly higher in the probiotic group (p = 0.03). Streptococcus gordinii and Neisseria elongata were associated with the probiotic group on day 28, while Streptococcus sobrinus was associated with the placebo group on day 14 and day 28. On day 28, the salivary albumin level was significantly lower in the probiotic group. The present study demonstrates a potential stabilizing effect on the supragingival microbiota mediated by consumption of probiotics during short-term sugar stress.

Salivary IL-33 and sST2 levels in relation to TLR2 rs111200466 polymorphism and periodontitis.

OBJECTIVES: Toll-like receptor-2 (TLR2) signalling pathway is involved in the regulation of interleukin (IL)-33 and its receptor suppression of tumorigenicity-2 (ST2). This study aimed to compare salivary IL-33 and soluble ST2 (sST2) levels of periodontitis patients with those of periodontally healthy individuals in relation to their TLR2 rs111200466 23-bp insertion/deletion polymorphism within the promoter region. MATERIALS AND METHODS: Unstimulated saliva samples were collected, and periodontal parameters were recorded from 35 periodontally healthy individuals and 44 periodontitis patients. Non-surgical treatments were applied to periodontitis patients, and sample collections and clinical measurements were repeated 3 months following therapy. Salivary IL-33 and sST2 levels were measured with enzyme-linked immunosorbent assay kits, and TLR2 rs111200466 polymorphism was detected by polymerase chain reaction. RESULTS: Elevated salivary IL-33 (p = 0.007) and sST2 (p = 0.020) levels were observed in periodontitis patients, in comparison to controls. sST2 levels declined 3-months following treatment (p < 0.001). Increased salivary IL-33 and sST2 levels were found to be associated with periodontitis, with no significant relation to the TLR2 polymorphism. CONCLUSION: Periodontitis, but not TLR2 rs111200466 polymorphism, is associated with elevated salivary sST2 and possibly IL-33 levels, and periodontal treatment is effective in reducing salivary sST2 levels.

Radiotherapy Increases aMMP-8-Levels and Neutrophil/Lymphocyte Ratio Rapidly in Head and Neck Cancer Patients: A Pilot Study.

Radiotherapy for head and neck carcinoma (HNC) has both curative and palliative purposes. This study investigated mouthrinse aMMP-8 levels, molecular forms of MMP-8, blood neutrophil counts and neurophil/lymphocyte ratios before and 3 weeks after HNC radiotherapy started. Thirteen HNC patients undergoing radiotherapy were included. Mouthrinse samples (before and 3 weeks after HNC radiotherapy had started) were assayed quantitatively by aMMP-8 point-of-care-kit (PerioSafe®/ORALyzer®) and by western immunoblot. Total neutrophil counts and neutrophil/lymphocyte ratios were evaluated in the hemogram results. Three weeks after HNC radiotherapy started, significant increases in aMMP-8 levels and neutrophil/lymphocyte ratios were observed. No significant difference was found in total neutrophil counts. Elevations of the activated and fragmented MMP-8 levels after HNC radiotherapy application were observed on western immunoblot analysis. The increase in the aMMP-8 levels and neutrophil/lymphocyte ratios indicate inflammation both locally and systemically suggesting increased risk for periodontitis due to the HNC radiotherapy.

Localization and expression profiles of gingival monocyte chemoattractant protein-1-induced protein-1 (MCPIP-1) and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1).

OBJECTIVES: The purposes of this study were to localize monocyte chemoattractant protein-1-induced protein-1 (MCPIP-1) and its suppressor mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1) in gingival tissues and to profile their protein expression levels in relation to the clinical inflammation, Porphyromonas gingivalis colonization, and interleukin (IL)-8 levels. MATERIALS AND METHODS: Study samples were collected from two independent study populations: (1) Gingival tissues were collected from eight periodontally healthy individuals and eight periodontitis patients to localize MCPIP-1 and MALT-1 immunohistochemically, and (2) forty-one gingival tissue samples with marginal, mild, or moderate to severe inflammation were collected from 20 periodontitis patients to determine MCPIP-1 and MALT-1 levels using immunoblots, P. gingivalis levels with qPCR, P. gingivalis gingipain activities with fluorogenic substrates, and IL-8 levels with multiplex technique. RESULTS: MCPIP-1 was detectable in the epithelium and in connective tissue, being especially prominent around the blood vessel walls in healthy periodontal tissues. MALT-1 was observed at all layers of gingival epithelium and especially around the accumulated inflammatory cells in connective tissue. No difference in gingival tissue MCPIP-1 and MALT-1 levels was observed in relation to the severity of gingival inflammation. MALT-1 levels were elevated (p = 0.023) with the increase in tissue P. gingivalis levels, and there was an association between MALT-1 and IL-8 levels (ß = 0.054, p = 0.001). CONCLUSIONS: Interactions of MALT-1 levels with gingival tissue P. gingivalis counts and IL-8 levels suggest that activation of MALT-1 can take part in P. gingivalis-regulated host immune responses. CLINICAL RELEVANCE: Pharmacological targeting the crosstalk between immune response and MCPIP-1/MALT-1 may have benefits in periodontal treatment.

Anti-Apoptotic and Pro-Apoptotic Bcl-2 Family Proteins in Peri-Implant Diseases.

OBJECTIVES: Intrinsic apoptosis, which is regulated by Bcl-2 family proteins, has an important role in chronic inflammatory diseases. The aim of the study was to identify the tissue levels and ratios of anti- and pro-apoptotic Bcl-2 family proteins in peri-implant diseases. MATERIALS AND METHODS: Twenty-three individuals with peri-implant mucositis, 25 individuals with peri-implantitis, and 24 controls were included. The following clinical parameters were recorded: keratinized mucosa width, modified bleeding index, probing depth, modified plaque index, modified gingival index, and keratinized tissue thickness. Marginal alveolar bone assessments were performed by a software program. Granulation tissues were collected during treatments of peri-implant diseases. The control tissue samples were collected during the second stage of implant surgery. The tissue levels of Bcl-2 family pro-apoptotic (Bak, Bax, active caspase-3) and anti-apoptotic (Bcl-2, Bcl-xL, Mcl-1) proteins were determined by multiplex immunoassay method. RESULTS: The pro-apoptotic proteins; Bak, Bax and anti-apoptotic proteins Bcl-2, Bcl-xL, Mcl-1 were detected significantly higher in controls compared with patients with peri-implant mucositis and peri-implantitis (p < .001), respectively. The higher active caspase-3 levels were also detected in controls in comparison with peri-implant mucositis (p = .018) and peri-implantitis (p = .005). Anti-apoptotic: pro-apoptotic protein ratios (Bcl-2:Bax, p < .001; Bcl-2:Bak, p = .01; Bcl-xL: Bax, p = .006, Bcl-xL:Bak, p = .011; Mcl-1:Bak, p < .001) were significantly increased in diseased groups. A positive correlation was demonstrated between clinical variables and anti-apoptotic: pro-apoptotic ratios. CONCLUSION: Our findings indicate dysregulation of the Bcl-2 family proteins in peri-implant diseases. This unregulated response may disturb the homeostasis of peri-implant tissue.

Salivary levels of BAFF, TWEAK, and soluble CD163 and salivary arginase activity before and after periodontal treatment.

OBJECTIVE: To monitor salivary B-cell activating factor (BAFF), tumor necrosis factor-like weak inducer of apoptosis (TWEAK), and soluble (s)CD163 levels and arginase activity in periodontitis patients following nonsurgical periodontal treatment. BACKGROUND: BAFF, TWEAK, and sCD163 and arginase are associated with activities of B cells and macrophages, which are important regulators of periodontal immune-inflammatory response and healing following treatment. Increased salivary BAFF and sCD163 levels and arginase activity in periodontitis have been demonstrated, but their changes following treatment have not been evaluated before. MATERIALS AND METHODS: Forty-four Stage III/IV periodontitis patients and 35 periodontally healthy controls were included in the study. Full-mouth periodontal measurements were recorded and unstimulated saliva was obtained from all participants at baseline. Sample collection and measurements were repeated in periodontitis patients at 2, 6, 12, and 24 weeks following full-mouth scaling and root debridement, whereas controls were only seen at baseline. BAFF, TWEAK, and sCD163 levels were analyzed with bead-based multiplexed immunoassay. Arginase activity was measured with Chinard's method. RESULTS: BAFF (p < .001) and sCD163 (p = .003) levels and arginase activity (p < .015) were higher in periodontitis patients compared to healthy controls. BAFF levels (p < .001) and arginase activity (p < .001) of periodontitis patients were reduced at 2 weeks posttreatment and continued to decrease up to 6 (p = .038) and 12 weeks (p = .024), respectively. The reduction of sCD163 levels became significant (p = .003) at 24 weeks posttreatment. CONCLUSIONS: The decrease in salivary BAFF levels 2 weeks after periodontal treatment indicates a change in cell signaling toward limited B-cell activation. Decreasing arginase activity similarly reflects a significant reduction in inflammatory response. The reduction in sCD163 levels that are observed at 24 weeks may reflect a longstanding anti-inflammatory macrophage activation, given their multiple functions in immune response, inflammation, and healing.

Human ß-Defensins in Diagnosis of Head and Neck Cancers.

Head and neck cancers are malignant growths with high death rates, which makes the early diagnosis of the affected patients of utmost importance. Over 90% of oral cavity cancers come from squamous cells, and the tongue, oral cavity, and salivary glands are the most common locations for oral squamous cell carcinoma lesions. Human ß-defensins (hBDs), which are mainly produced by epithelial cells, are cationic peptides with a wide antimicrobial spectrum. In addition to their role in antimicrobial defense, these peptides also take part in the regulation of the immune response. Recent studies produced evidence that these small antimicrobial peptides are related to the gene and protein expression profiles of tumors. While the suppression of hBDs is a common finding in head and neck cancer studies, opposite findings were also presented. In the present narrative review, the aim will be to discuss the changes in the hBD expression profile during the onset and progression of head and neck cancers. The final aim will be to discuss the use of hBDs as diagnostic markers of head and neck cancers.

Salivary and serum levels of neutrophil proteases in periodontitis and rheumatoid arthritis.

OBJECTIVE: The aim was to profile serum and salivary levels of active-matrix metalloproteinase (aMMP)-8, tissue inhibitor MMP (TIMP)-1, aMMP-8/TIMP-1 ratio, total MMP (tMMP)-9, tMMP-9/TIMP-1 ratio, myeloperoxidase (MPO), and human neutrophil elastase (HNE) in periodontitis and rheumatoid arthritis (RA). MATERIALS AND METHODS: Rheumatoid arthritis patients with periodontitis (RA + P, n = 26), periodontally healthy RA patients (RA, n = 23), systemically healthy periodontitis patients (P, n = 24), and controls (C, n = 24) were included. aMMP-8 levels were determined by a time-resolved immunofluorescence assay (IFMA), TIMP-1, tMMP-9, MPO, and HNE levels were measured by enzyme-linked immunosorbent (ELISA) assays. RESULTS: Higher salivary aMMP-8 (p < 0.001), aMMP-8/TIMP-1 ratio (p = 0.043), tMMP-9 (p = 0.011), tMMP-9/TIMP-1 ratio (p = 0.022), MPO (p = 0.026) and HNE (p < 0.001) levels were detected in P relative to the controls. Salivary TIMP-1 was increased in RA patients regardless of periodontal status (RA + P vs. P: p = 0.038; RA vs. C: p = 0.020). Serum neutrophil proteases were increased in RA groups (RA + P, RA) compared to systemically healthy groups (P, C) (p < 0.05). CONCLUSIONS: Serum levels of neutrophil proteases were increased in RA study groups; however rheumatologic status seemingly does not affect salivary levels of these proteins.

Salivary Human ß-Defensin 1-3 and Human α-Defensin-1 Levels in Relation to the Extent of Periodontal Disease and Tooth Loss in the Elderly.

The oral innate immune response may diminish with aging. In the present study, the aim was to examine human ß-defensin (hBD) 1-3 and human neutrophil peptide (HNP)-1 levels in the saliva of an elderly population to establish the extent of periodontal disease and tooth loss. A total of 175 individuals aged ≥ 65 years were divided into five groups based on the number of teeth with a pocket depth ≥ 4 mm as follows: 17 pocket-free individuals (Control), 55 individuals having 1-6 pocket teeth (PerioA), 33 individuals having 7-13 pocket teeth (PerioB), 29 individuals having at least 14 pocket teeth (PerioC), and 41 edentulous individuals. Their salivary defensin levels were measured with ELISA kits. The salivary HNP-1 levels were significantly higher in the Perio groups (PerioB: p < 0.001 and PerioC: p < 0.001) in comparison to the Control. The associations between salivary HNP-1 levels and the number of pocket teeth remained significant after adjustments for age, gender, level of education, and number of teeth. The salivary HNP and hBD levels differed in terms of their correlation to the extent of periodontal disease and tooth loss in the elderly.

Salivary IgA and IgG Antibody Responses against Periodontitis-Associated Bacteria in Crohn's Disease.

Elevated serum immunoglobulin (Ig) antibody levels are observed in Crohn's disease patients. The aim of this study was to evaluate the salivary IgA and IgG antibody levels against Porphyromonas gingivalis, Tannerella forsythia, Aggregatibacter actinomycetemcomitans, and Prevotella intermedia in Crohn's disease patients. Eighty-eight participants (47 Crohn's disease patients and 41 systemically healthy age- and gender-matched controls) were included in the study. Oral and medical health statuses were recorded and salivary samples were collected. Salivary P. gingivalis, T. forsythia, A. actinomycetemcomitans, and P. intermedia carriage were analyzed with DNA sequencing technique, salivary levels of IgG1, IgG2, IgG3, IgG4, and IgM were measured with the Luminex® xMAP™ technique, and salivary IgA and IgG antibody levels against P. gingivalis, T. forsythia, A. actinomycetemcomitans, and P. intermedia were detected by ELISA. As result, higher salivary IgG2 (p = 0.011) and IgG3 (p = 0.006), P. gingivalis IgA (p < 0.001), A. actinomycetemcomitans IgG (p = 0.001), and P. intermedia IgG (p < 0.001) antibody levels were detected in the Crohn's disease group compared to the controls. Salivary P. gingivalis carriage was lower in the Crohn's disease group in comparison to the controls (p = 0.024). In conclusion, salivary IgA antibody responses against P. gingivalis and IgG antibody responses against P. intermedia have independent associations with Crohn's disease.

Salivary macrophage activation-related chemokines and mitogen-activated kinase kinase-degrading proteolytic activity in type 1 diabetes mellitus.

BACKGROUND: This cross-sectional study aimed to evaluate salivary concentrations of macrophage activation-related chemokines and mitogen-activated kinase kinase (MAPKK)-degrading proteolytic activity in children and adolescents with and without type 1 diabetes mellitus (T1DM). METHODS: A total of 122 children and adolescents (65 T1DM patients, 50.8% female, mean age:10.9 years; 57 systemically healthy controls, 36.8% female, mean age: 9.5 years) were included in the study. Salivary concentrations of interferon gamma inducible protein-10 (IP-10), monocyte chemoattractant protein (MCP)-1, MCP-2, MCP-3, MCP-4, macrophage-derived chemokine (MDC), macrophage migration inhibitory factor (MIF), monokine induced by interferon gamma (MIG), and macrophage inflammatory protein-1 alpha (MIP-1α) were quantified using a bead-based technique. MAPKK-degrading proteolytic activity was detected using fluorescent peptide substrates. RESULTS: The T1DM group had higher plaque index (PI%, p = 0.032) and bleeding on probing (BOP%, p = 0.045) scores, and lower decayed, missing, filled teeth (dmft/DMFT, p = 0.002) index scores compared to the healthy controls. Compared to the controls, salivary MCP-1 (p = 0.007), MCP-3 (p < 0.001), MIG (p = 0.007), and MIP-1α (p = 0.033) concentrations were elevated whereas MCP-4 concentrations decreased (p < 0.001) in the T1DM group. After adjusting for age, PI%, BOP%, and dmft/DMFT scores, significant differences in salivary concentrations of MIG (p = 0.033) and MIP-1α (p = 0.017) were observed between the groups. Moreover, protease activities directed to the cleavage sites of MEK23-18 (p = 0.001), MKK6b7-22 (p = 0.007), MKK451-66 (p = 0.005), MKK7b37-52 (p = 0.034), and MKK7b69-84 (p = 0.009) were elevated in the T1DM group. CONCLUSION: T1DM disrupts the salivary macrophage activation-related chemokine profile and dysregulates proteolytic MAPKK cleavage. These findings can be an outcome of the impaired systemic immune response in T1DM.

Serum, saliva, and gingival tissue human ß-defensin levels in relation to retinoic acid use.

BACKGROUND: Retinoic acid is an active derivative of vitamin A and regulates the differentiation, proliferation, and antimicrobial peptide expression profiles of human cells. The aim of the present study was to analyze the effect of systemic retinoic acid use on serum, saliva, and gingival tissue levels of human ß-defensin (hBD)-1, hBD-2, and hBD-3. METHODS: A total of 69 participants (34 systemic retinoic acid users and 35 healthy controls) were enrolled in this study. Plaque index, probing pocket depth, bleeding on probing (BOP), and clinical attachment loss were measured. Saliva and serum hBD-1, hBD-2, and hBD-3 levels were quantified by enzyme-linked immunosorbent assay. Gingival tissue hBD-1, hBD-2, and hBD-3 levels were determined by immunohistochemistry. A univariate general linear model was used in adjusted comparisons of hBD1, hBD-2, and hBD-3. P values of < 0.05 were considered statistically significant. RESULTS: Reduced salivary levels of hBD-2 (P = 0.042), but not hBD-1 or hBD-3, were detected in systemic retinoic acid users compared to non-user controls. There was a significant difference in the adjusted (for BOP%) salivary hBD-2 concentrations between retinoic acid and control groups (P = 0.031). No difference was observed in serum or tissue levels of hBD-1, hBD-2, or hBD-3 between the two study groups. CONCLUSION: Systemic retinoic acid use was associated with suppressed salivary hBD-2 level, which was independent of gingival inflammation.

Baseline interleukin-10, CD163, and tumor necrosis factor-like weak inducer of apoptosis (TWEAK) gingival tissue levels in relation to clinical periodontal treatment outcomes: A 12-week follow-up study.

BACKGROUND: The aim of this study was to examine the relationship between healing response after non-surgical periodontal treatment and baseline gingival tissue levels of M2 macrophage activation-related proteins CD163, interleukin (IL)-10, interferon (IFN)-γ, and tumor necrosis factor-like weak inducer of apoptosis (TWEAK), and the CD163/TWEAK ratio. METHODS: Eighty-eight gingival tissue samples from 44 Stage III/IV, Grade C periodontitis patients (18 smokers) and 41 tissue samples from 41 periodontally healthy participants (18 smokers) were evaluated. Clinical parameters were recorded in periodontally healthy individuals at baseline and in periodontitis patients at pre-treatment and 2, 6, and 12 weeks following therapy. IL-10, IFN-γ, CD163, and TWEAK levels were analyzed with Luminex technique. RESULTS: Tissue levels (median, 1st -3rd quartile) of IL-10 (pg/ng protein), CD163 (pg/µg protein) and TWEAK (pg/µg protein) were as follows: IL-10 periodontitis: 2.08, 0.86-5.32 and periodontally healthy: 5.22, 3.20-10.25; CD163 periodontitis: 8.85, 4.92-14.06 and periodontally healthy: 18.36, 12.51-34.02; TWEAK periodontitis: 0.08, 0.05-0.11 and periodontally healthy: 0.16, 0.12-0.21. IL-10, CD163, and TWEAK levels were higher (P < 0.001) in periodontally healthy tissues than in periodontitis tissues. Pocket closure at 12 weeks was associated with elevated baseline gingival CD163 levels (P = 0.047) and CD163/TWEAK ratio (P = 0.001). Elevated baseline gingival CD163/TWEAK ratio was associated with pocket reduction at 6 (P = 0.022) and 12 weeks (P = 0.002). CONCLUSION: Associations of pocket closure with pre-treatment gingival tissue CD163 levels and CD163/TWEAK ratio indicate that baseline M2 macrophage activation profile may play a role in periodontal wound healing.

Analysis of Chemical Structure and Antibiofilm Properties of Exopolysaccharides from Lactiplantibacillus plantarum EIR/IF-1 Postbiotics.

Previous studies have indicated that the exopolysaccharides of lactic acid bacteria exhibit antibiofilm activity against non-oral bacteria by preventing their initial adhesion to surfaces and by downregulating the expression of genes responsible for their biofilm formation. The aims of this study were to (1) characterize the exopolysaccharides (EPSs) of Lactobacillus plantarum EIR/IF-1 postbiotics, (2) test their antibiofilm effect on dual biofilms, and (3) evaluate their bacterial auto-aggregation, co-aggregation, and hydrocarbon-binding inhibitory activity. The EPSs were characterized by FTIR, HPLC, and thermogravimetric analysis. Bacterial auto- and co-aggregation were tested by Kolenbrander's method and hydrocarbon binding was tested by Rosenberg's method. Dual biofilms were formed by culturing Fusobacterium nucleatum ATCC 25586 with one of the following bacteria: Prevotella denticola ATCC 33185, P. denticola AHN 33266, Porphyromonas gingivalis ATCC 33277, P. gingivalis AHN 24155, and Filifactor alocis ATCC 35896. The EPSs contained fractions with different molecular weights (51 and 841 kDa) and monosaccharides of glucose, galactose, and fructose. The EPSs showed antibiofilm activity in all the biofilm models tested. The EPSs may have inhibited bacterial aggregation and binding to hydrocarbons by reducing bacterial hydrophobicity. In conclusion, the EPSs of L. plantarum EIR/IF-1, which consists of two major fractions, exhibited antibiofilm activity against oral bacteria, which can be explained by the inhibitory effect of EPSs on the auto-aggregation and co-aggregation of bacteria and their binding to hydrocarbons.

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.

Tissue Levels of CD80, CD163 and CD206 and Their Ratios in Periodontal and Peri-Implant Health and Disease.

This study aimed to compare tissue levels of CD80 (pro-inflammatory macrophage-related surface marker), CD163, and CD206 (anti-inflammatory macrophage-related surface markers), and their ratios in periodontal and peri-implant health and disease. Altogether, 36 tissue samples were obtained from 36 participants with clinically healthy gingiva (n = 10), healthy peri-implant mucosa (n = 8), periodontitis lesions (n = 9), and peri-implantitis lesions (n = 9). CD80, CD163, and CD206 levels were assessed with immunoblotting. CD163 levels were found to be decreased (p = 0.004), and the CD80/CD163 ratio was found to be elevated (p = 0.002) in periodontitis lesions compared to healthy gingiva. Peri-implantitis lesions showed a tendency towards a higher CD80/CD163 ratio than in healthy peri-implant mucosa with a borderline difference (p = 0.054). No statistically significant difference was detected in CD80, CD163, and CD206 levels of periodontitis lesions when compared to peri-implantitis, and in healthy gingiva when compared to healthy peri-implant mucosa. A disruption in CD80/CD163 balance seems to be related to the pathogenesis of periodontitis and peri-implantitis, being less prominent in the latter. The reason behind this phenomenon may be either suppressed CD163 expression or reduced CD163+ anti-inflammatory macrophage abundance.

Effects of sugar-free polyol chewing gums on gingival inflammation: a systematic review.

OBJECTIVES: A systematic review of published data was conducted with the aim of assessing the effects of sugar-free polyol chewing gums on gingival inflammation. MATERIALS AND METHODS: Electronic and hand searches were performed to find clinical studies concerning the effects of sugar-free chewing gums on gingival scores. Prospective randomized controlled clinical trials published between 1971 and 2021 were included in the review. RESULTS: The initial search identified 46 erythritol, 102 xylitol, 23 sorbitol, and nine maltitol chewing gum articles. After applying inclusion and exclusion criteria, seven xylitol chewing gum studies, one sorbitol, and one maltitol chewing gum study with either high or fair quality were reviewed. In five out of the seven xylitol studies, xylitol gum decreased gingival scores. In two studies, xylitol decreased gingival scores compared to a polyol gum, and in three studies compared to no gum/gum base. As for sorbitol and maltitol, only sorbitol gum chewing showed a small decrease in gingival scores compared to the controls. CONCLUSIONS: Habitual xylitol gum chewing may reduce gingival inflammation. The low number of studies and their heterogeneity provide clear indications that the effects of sugar-free polyol chewing gums on gingival inflammation need further, well-controlled studies. CLINICAL RELEVANCE: Sugar-free chewing gums, especially xylitol gum, may function as adjuncts to toothbrushing for reducing gingival inflammation, but the evidence so far is inconclusive.