Interleukin-32 levels in gingival crevicular fluid and saliva of patients with chronic periodontitis after periodontal treatment.

BACKGROUND AND OBJECTIVE: The cytokine, interleukin (IL)-32, is a relatively new discovery. However, it is very powerful for stimulating tumor necrosis factor-alpha (TNF-α) under inflammatory conditions. The objective of this research was to explore fluctuations in the levels of TNF-α, IL-32 and IL-10, in both saliva and gingival crevicular fluid. The focus was on measurements taken before and after clinical treatment of chronic periodontitis. MATERIAL AND METHODS: For the purposes of the study, a total of 27 patients with chronic periodontitis and 27 controls (periodontally healthy) were recruited. Important clinical periodontal criteria were established before and 4 wk after the start of the research. The chronic periodontitis group was given an initial form of periodontal care. Samples of saliva and gingival crevicular fluid were collected exactly 4 wk preceding and 4 wk following the care. The levels of IL-10, IL-32 and TNF-α present in saliva and gingival crevicular fluid were recorded via the use of an ELISA. RESULTS: At baseline, the levels of TNF-α and IL-32 in the gingival crevicular fluid and saliva were significantly higher among patients in the chronic periodontitis group than among patients in the control group (p < 0.05). On the other hand, at baseline the levels of IL-10 were significantly lower in the gingival crevicular fluid and saliva of the chronic periodontitis group than the control group (p < 0.05). A significantly positive link was found between the TNF-α and IL-32 levels in the two study groups (p < 0.05). After treatment, the levels of TNF-α and IL-32 in saliva and gingival crevicular fluid were significantly lower in the chronic periodontitis group when compared with the baseline readings. However, the levels of IL-10 were significantly higher (p < 0.05). CONCLUSION: Ultimately, the level of IL-32 present in saliva and gingival crevicular fluid might be useful as an indicator of the condition and the expectations for its treatment and care. According to the results of the research, the proinflammatory impact of IL-32 could potentially be linked to the intensity and progression of periodontitis.

Fetuin-A, serum amyloid A and tumor necrosis factor alpha levels in periodontal health and disease.

OBJECTIVES: This study is evaluating fetuin-A, serum amyloid A (SAA) and tumor necrosis factor alpha (TNF-α) levels in gingival crevicular fluid (GCF) and serum samples in periodontal health and disease. MATERIAL AND METHODS: Sixty patients were divided into three groups: Group 1 periodontal health (n = 20), Group 2 gingivitis (n = 20) and Group 3 chronic periodontitis (CP) (n = 20). GCF and serum samples were evaluated using enzyme-linked immunosorbent assay kit. RESULTS: SAA and TNF-α levels in GCF and serum were significantly higher in patients with gingivitis and CP compared with controls (P < 0.016). Contrarily, fetuin-A levels in GCF and serum were significantly higher in controls than in patients with gingivitis and CP (P < 0.016). In CP group, a significant correlation was observed between GCF-SAA amount and the number of sites with 4 ≤ PPD ≤ 5 mm (P < 0.05). There was a significant correlation between GCF-fetuin-A levels and the number of sites with PPD ≥ 6 mm (P < 0.05). GCF-TNF-α was found to have a significant relationship with the number of sites with 4 ≤ PPD ≤ 5 mm and PPD ≥ 6 mm (P < 0.05). CONCLUSIONS: In conclusion, serum and total levels of SAA significantly increased, whereas fetuin-A levels significantly decreased, with increasing severity of PD.

Ankaferd blood stopper enhances healing after osseous grafting in patients with intrabony periodontal defects.

BACKGROUND AND OBJECTIVE: The aim of this clinical study were to compare the clinical efficacy of ankaferd blood stopper (ABS) when used in combination with autogenous cortical bone graft (ACB) in the treatment of intrabony periodontal defects. MATERIAL AND METHODS: The study was planned as a split-mouth design. Fifteen patients with chronic periodontitis at 30 sites (six men, nine women; 42 ± 7 years) were included. Treatment sites had probing pocket depths (PPD) of ≥ 6 mm and osseous defect depths of ≥ 4 mm as radiographically assessed. Following the initial periodontal therapy, patients were randomly assigned to two treatments in contralateral areas of the dentition: ACB + ABS or ACB alone. At baseline and 6 mo after surgery, clinical parameters of plaque index, gingival index, PPD, clinical attachment level and gingival recession (GR) were recorded. The primary outcome variable was the change in clinical attachment level between baseline and 24 wk after surgery. Gingival crevicular fluid samples were collected immediately before surgery and at 2, 4, 6, 12 and 24 wk after the surgery. Gingival crevicular fluid volume was calculated and vascular endothelial growth factor levels in gingival crevicular fluid were measured. RESULTS: PPD decreased, clinical attachment level improved and gingival index decreased significantly in response to both modes of treatment (p < 0.05). Both treatment modalities resulted in a significant gain in radiographic bone levels compared to baseline (p < 0.05). Intergroup comparisons showed that there was a significantly higher gain in clinical attachment level in the ABS/ACB group compared to ACB group (p < 0.05) with significantly less GR (p < 0.05). Similarly, vascular endothelial growth factor concentration in gingival crevicular fluid was significantly higher in the ABS/ACB group at postoperative weeks 2 and 4 compared to the ACB group (p < 0.01). CONCLUSIONS: The findings suggest that ABS enhances the soft tissue healing during the periodontal defect fill by the ACB by stimulating angiogenesis and vascular endothelial cell function, prevents GR and thereby increases the clinical attachment gain.

Glutathione levels in plasma, saliva and gingival crevicular fluid after periodontal therapy in obese and normal weight individuals.

BACKGROUND AND OBJECTIVE: The purpose of this study was to investigate the effects of obesity on reduced and oxidized glutathione (GSH and GSSG) levels in the gingival crevicular fluid, plasma and saliva of patients with chronic periodontitis and to evaluate the changes after nonsurgical periodontal therapy. MATERIAL AND METHODS: The study included 60 patients: 30 patients with chronic periodontitis (15 obese patients and 15 normal weight patients) and 30 healthy control subjects (15 obese patients and 15 normal weight patients). Gingival crevicular fluid, plasma and saliva samples were collected, and clinical periodontal measurements were recorded at baseline and at the first month after periodontal therapy from patients with chronic periodontitis. GSH and GSSG levels were analyzed with spectrophotometry. RESULTS: The GSH levels in the plasma, saliva and gingival crevicular fluid in obese individuals with chronic periodontitis were lower than in normal weight individuals at baseline (p < 0.01). There was a significant difference in the GSH/GSSG ratio in plasma and gingival crevicular fluid between the obese and normal weight groups at baseline (p < 0.01). The GSH levels in plasma, gingival crevicular fluid and saliva were significantly increased in both chronic periodontitis groups after nonsurgical periodontal therapy (p < 0.01). A significant positive correlation was found between GSH levels in saliva, plasma and gingival crevicular fluid in all groups (p < 0.001). CONCLUSIONS: The study revealed that obesity in patients with chronic periodontitis is associated with decreased GSH levels and the GSH/GSSG ratio. Moreover, nonsurgical periodontal therapy may be helpful for improvement in glutathione values in obese and normal weight individuals with chronic periodontitis.

Chemerin and interleukin-6 levels in obese individuals following periodontal treatment.

OBJECTIVE: To investigate changes in the levels of gingival crevicular fluid (GCF) chemerin and interleukin-6 (IL-6) in both obese/non-obese individuals with periodontitis following non-surgical periodontal therapy. METHODS: Individuals (n = 80) were split into four groupings according to periodontal/anthropometric parameters: (i) periodontal healthy without obesity; (ii) chronic periodontitis (CP) without obesity; (iii) periodontal healthy with obesity; and (iv) CP with obesity. Individuals with periodontitis were treated with non-surgical periodontal therapy. Both GCF sampling procedures and clinical periodontal measures were performed prior to treatment and 6 weeks thereafter. Enzyme-linked immunosorbent assay was utilized to measure both chemerin and IL-6 levels. RESULTS: Greater values for chemerin and IL-6 were observed in obese individuals compared to their non-obese controls and in individuals with CP compared to their periodontal healthy controls (P < 0.008), which decreased following therapy (P < 0.05). A positive correlation was found between chemerin and IL-6 in obese groups (P < 0.05). A comprehensive overview of all groups showed a statistically significant positive correlation among chemerin, along with IL-6, waist-to-hip ratio, body mass index, and clinical attachment levels (P < 0.05). CONCLUSION: It could be concluded that chemerin levels may act as both diagnostic and prognostic indicators. Chemerin may also play an integral part in the pathologic mechanisms that relate adipokines to both periodontal disease and obesity.

Assessment of periostin levels in serum and gingival crevicular fluid of patients with periodontal disease.

BACKGROUND AND OBJECTIVE: Periostin, a secreted adhesion molecule essential for periodontal tissue integrity, is highly expressed in the periodontal ligament and plays a critical role in tooth and bone development. The purpose of this study was to investigate periostin levels in the gingival crevicular fluid and serum of patients with periodontal disease and compare them with those of healthy individuals. MATERIAL AND METHODS: Eighty individuals (41 males and 39 females; age range: 25-48 years) were enrolled in the study. Individuals were divided into three groups following clinical and radiographic examinations: the periodontal-healthy group (n = 20), gingivitis group (n = 30) and chronic periodontitis group (n = 30). Gingival crevicular fluid and serum samples were collected and periostin levels were determined using the enzyme-linked immunosorbent assay. RESULTS: The total amount and concentration of periostin decreased in gingival crevicular fluid with the progression and severity of the disease from healthy controls to gingivitis and to chronic periodontitis groups and differed significantly (p < 0.05). However, there was no significant difference in serum periostin concentration within all groups (p > 0.05). Periostin in gingival crevicular fluid negatively correlated with the gingival index in the periodontal disease groups, whereas it is inversely correlated with the clinical attachment level only in the periodontitis group (p < 0.05). When all the clinical groups were examined together, the periostin concentration negatively correlated with clinical attachment level and gingival index; moreover, total periostin positively correlated with periostin concentration and clinical attachment level (p < 0.05). CONCLUSIONS: The periostin levels in gingival crevicular fluid decreased proportionally with the progression and severity of periodontal disease, and negatively correlated with the clinical parameters. Within the limits of the study, the periostin level in gingival crevicular fluid can be considered a reliable marker in the evaluation of periodontal disease susceptibility and activity.

Activity of platelet activating factor acetylhydrolase following phase I periodontal therapy.

OBJECTIVE: Elevated levels of platelet activating factor (PAF), a potent inflammatory mediator in periodontal disease and decreased PAF levels following periodontal surgical therapy have been previously detected in gingival tissues and gingival crevicular fluid (GCF). Platelet activating factor acetylhydrolase (PAF-AH) is a calcium-independent phospholipase A2 that catalyses the hydrolysis of PAF, thereby inactivating this mediator The hypothesis, a relationship between activity of PAF-AH and healing following periodontal therapy, was tested by detecting activity of PAF-AH in GCF samples collected from sites that had undergone phase I periodontal therapy with generalized chronic periodontitis. METHODS: Twenty patients with generalized chronic periodontitis were divided into two groups (n = 10): group 1 with probing pocket depth (PPD) 4-5 mm and group 2 with PPD > or = 6-8 mm. Clinical parameters were recorded and GCF was sampled before phase I periodontal therapy and at the 2nd, 7th, 14th, 21st and 28th day follow-up evaluation visits. Activity of PAF-AH in GCF was analysed by enzyme-linked immunosorbent assay (ELISA). RESULTS: Probing pocket depth at the 21st and 28th day in group 1, and PPD at the 14th, 21st and 28th day in group 2 were significantly decreased when compared to the baseline values (p < 0.001). Activity of PAF-AH (micromol/ml) was significantly decreased at the 7th, 14th, 21st and 28th day following phase I periodontal therapy in both groups 1 and 2 compared to the baseline values (p < 0.05). CONCLUSION: Platelet activating factor acetylhydrolase is detectable in GCF by ELISA and showed a continuous decrease following phase I periodontal therapy. Changes in the PAF-AH activity would be a progressive marker of periodontal healing to evaluate the success of periodontal therapies.

Activity of platelet activating factor acetylhydrolase following phase I periodontal therapy / Actividad de la acetilhidrolasa del factor activador de las plaquetas tras la fase I de la terapia periodontal

OBJECTIVE: Elevated levels of platelet activating factor (PAF), a potent inflammatory mediator, in perio-dontal disease and decreased PAF levels following periodontal surgical therapy have been previously detected in gingival tissues and gingival crevicular fluid (GCF). Platelet activating factor acetylhydrolase (PAF-AH) is a calcium-independent phospholipase A2 that catalyses the hydrolysis of PAF, thereby inactivating this mediator. The hypothesis, a relationship between activity of PAF-AH and healing following periodontal therapy, was tested by detecting activity of PAF-AH in GCF samples collected from sites that had undergone phase I periodontal therapy with generalized chronic periodontitis. METHODS: Twenty patients with generalized chronic periodontitis were divided into two groups (n = 10): group 1 with probing pocket depth (PPD) 4-5 mm and group 2 with PPD > 6-8 mm. Clinical parameters were recorded and GCF was sampled before phase I periodontal therapy and at the 2nd, 7th, 14th, 21st and 28th day follow-up evaluation visits. Activity of PAF-AH in GCF was analysed by enzyme-linked immunosorbent assay (ELISA). RESULTS: Probing pocket depth at the 21st and 28th day in group 1, and PPD at the 14th, 21st and 28th day in group 2 were significantly decreased when compared to the baseline values (p < 0.001). Activity of PAF-AH (µmol/ml) was significantly decreased at the 7th, 14th, 21st and 28th day following phase I periodontal therapy in both groups 1 and 2 compared to the baseline values (p < 0.05). CONCLUSION: Platelet activating factor acetylhydrolase is detectable in GCF by ELISA and showed a continuous decrease following phase I periodontal therapy. Changes in the PAF-AH activity would be a progressive marker of periodontal healing to evaluate the success of periodontal therapies.

OBJETIVO: Niveles elevados del factor activador de las plaquetas (PAF) - un potente mediador inflamatorio en la enfermedad periodontal - y niveles disminuidos de PAF tras la terapia quirúrgica periodontal, han sido detectados previamente en los tejidos gingivales y el fluido crevicular gingival (FCG). La acetilhidrolasa del factor activador de las plaquetas(PAF-AH) es una fosfolipasa A2 independiente del calcio, que cataliza la hidrólisis de PAF, inactivando así este mediador. La hipótesis - la existencia de una relación entre la actividad de PAF-AH y la curación tras la terapia periodontal - fue sometida a comprobación mediante la detección de la actividad de PAF-AH en muestras de FCG recogidas de sitios que pasaron por la fase I de la terapia periodontal por periodontitis crónica generalizada. MÉTODOS: Veinte pacientes con periodontitis crónica generalizada fueron divididos en dos grupos (n = 10): grupo 1 con una profundidad de bolsa al sondeo (PPD) de 4-5 mm, y grupo 2 con PPD = 6-8 mm. Se registraron los parámetros clínicos, y se obtuvieron muestras de FCG antes de la fase I de la terapia periodontal, y en las visitas de evaluación de seguimiento los días 2, 7, 14, 21 y 28. La actividad de PAF-AH en FCG se analizó mediante ensayo por inmunoabsorción ligada a enzimas (ELISA). RESULTADOS: La profundidad de bolsa al sondeo los días 21 y 28 en el grupo 1, y PPD los días 14, 21 y 28 en el grupo 2 se vieron disminuidas significativamente cuando se les comparó con los valores iniciales (p < 0.001). La actividad de PAF-AH (µmol/ml) disminuyó significativamente los días 7, 14, 21 y 28 tras la fase I de la terapia periodontal en ambos grupos 1 y 2 en comparación con los valores al inicio del estudio (p< 0.05). CONCLUSIÓN: La acetilhidrolasa del factor activador de las plaquetases detectable en FCG mediante ELISA, y mostró una disminución continua tras la fase I de la terapia periodontal. Los cambios en la actividad de la PAF-AH sería un marcador progresivo de la curación periodontal para evaluar el éxito de las terapias periodontales.