Gingival crevicular fluid oxidative stress level in patients with periodontal disease and hyperlipidemia.

This study aimed to assess the impact of hyperlipidemia on healthy and diseased periodontal tissue by evaluating oxidative stress biomarkers in gingival crevicular fluid (GCF). Clinical periodontal parameters and blood serum lipid, GCF malondialdehyde (MDA), protein carbonyl (PC), and total antioxidant capacity (TAOC) levels were evaluated in six age and sex-matched groups (n = 15 each) of normolipidemic and hyperlipidemic individuals as follows: normolipidemic + periodontally healthy (H), normolipidemic + gingivitis (G), normolipidemic + chronic periodontitis (CP), hyperlipidemic + periodontally healthy (HH), hyperlipidemic + gingivitis (HG), and hyperlipidemic + CP (HCP). GCF MDA, and PC levels varied among groups, with patients with periodontitis having the highest MDA and PC levels [CP > G > H (p < 0.01) and HCP > HG > HH (p < 0.01)] and the lowest TAOC levels [CP < G < H (p < 0.01) and HCP < HG < HH (p < 0.01)]. Furthermore, paired comparisons showed MDA and PC levels to be higher and TAOC levels to be lower in HCP compared with NCP (p < 0.01). In patients with hyperlipidemia, GCF, MDA, and PC levels positively correlated with clinical assessments and serum triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL) levels and negatively correlated with serum high-density lipoprotein cholesterol (HDL) levels, whereas GCF TAOC levels negatively correlated with clinical assessments and serum TG, TC, and LDL levels, but positively correlated with serum HDL levels (p < 0.01). In normolipidemic patients, GCF, MDA, and PC levels positively correlated with clinical assessments and serum TG levels and negatively correlated with serum HDL levels, whereas GCF TAOC levels negatively correlated with clinical assessments and serum TG levels and positively correlated with serum HDL levels (p < 0.01). In conclusion, abnormal serum lipid subfractions could be considered a risk factor for enhancing oxidative stress in GCF in the presence of periodontal disease.

Effects of grape seed extract on periodontal disease: an experimental study in rats.

OBJECTIVE: This study aimed to demonstrate the effect of grape seed extract (GSE) on periodontitis. MATERIAL AND METHODS: Ligature induced periodontitis was created in 40 rats and they were assigned to four equal groups. One group was fed laboratory diet (group A) while three groups received GSE additionally. Silk ligatures were placed around the cervical area of the mandibular first molars for four weeks to induce periodontitis. The GSE groups were reallocated regarding GSE consumption as: for two weeks before ligation (group B; totally eight weeks), from ligation to two weeks after removal of the ligature (group C; totally six weeks), and for two weeks from ligature removal (group D; totally two weeks). Sections were assessed histologically and immunohistochemically. Inflammatory cell number (ICN), connective tissue attachment level (CAL), osteoclast density (OD), IL-10 and TGF-ß stainings in gingival epithelium (GE), connective tissue (GC), and periodontal ligament (PL) were used as the study parameters. RESULTS: Lower ICN, higher CAL, and lower OD were observed in the GSE groups (p<0.05). IL-10 was more intensive in the GSE groups and in the GEs (p<0.05). Group B showed the highest IL-10 for PL (p<0.05). TGF-ß was higher in the GEs of all groups (p<0.017). CONCLUSIONS: The results suggest anti-inflammatory activities of GSE, but further investigations are needed for clarification of these activities.

Gingival crevicular fluid oxidative stress level in patients with periodontal disease and hyperlipidemia

Abstract: This study aimed to assess the impact of hyperlipidemia on healthy and diseased periodontal tissue by evaluating oxidative stress biomarkers in gingival crevicular fluid (GCF). Clinical periodontal parameters and blood serum lipid, GCF malondialdehyde (MDA), protein carbonyl (PC), and total antioxidant capacity (TAOC) levels were evaluated in six age and sex-matched groups (n = 15 each) of normolipidemic and hyperlipidemic individuals as follows: normolipidemic + periodontally healthy (H), normolipidemic + gingivitis (G), normolipidemic + chronic periodontitis (CP), hyperlipidemic + periodontally healthy (HH), hyperlipidemic + gingivitis (HG), and hyperlipidemic + CP (HCP). GCF MDA, and PC levels varied among groups, with patients with periodontitis having the highest MDA and PC levels [CP > G > H (p < 0.01) and HCP > HG > HH (p < 0.01)] and the lowest TAOC levels [CP < G < H (p < 0.01) and HCP < HG < HH (p < 0.01)]. Furthermore, paired comparisons showed MDA and PC levels to be higher and TAOC levels to be lower in HCP compared with NCP (p < 0.01). In patients with hyperlipidemia, GCF, MDA, and PC levels positively correlated with clinical assessments and serum triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL) levels and negatively correlated with serum high-density lipoprotein cholesterol (HDL) levels, whereas GCF TAOC levels negatively correlated with clinical assessments and serum TG, TC, and LDL levels, but positively correlated with serum HDL levels (p < 0.01). In normolipidemic patients, GCF, MDA, and PC levels positively correlated with clinical assessments and serum TG levels and negatively correlated with serum HDL levels, whereas GCF TAOC levels negatively correlated with clinical assessments and serum TG levels and positively correlated with serum HDL levels (p < 0.01). In conclusion, abnormal serum lipid subfractions could be considered a risk factor for enhancing oxidative stress in GCF in the presence of periodontal disease.

The Effects of Smoking on the Osmotic Pressure of Human Dental Pulp Tissue.

OBJECTIVE: We aimed to investigate the effect of smoking on the osmotic pressure (OP) of human dental pulp tissue. MATERIALS AND METHODS: Sixty male dental patients (smokers and nonsmokers) scheduled for root canal treatment for prosthodontics were included in the study. Fifteen patients (1 premolar tooth/patient) were allocated to each of the following groups according to their smoking habits, i.e. group 1: ≤10 cigarettes/day, group 2: 11-20 cigarettes/day, group 3: >20 cigarettes/day and group 4: nonsmoking controls. Apical pulp tissues were removed via coronal access. Pulp tissue supernatants were obtained to measure the pulpal OP by means of a semimicro digital osmometer. One-way analysis of variance and the post hoc Duncan test were used to analyze the differences in OP between groups. Regression analysis was used to determine the relationship between the number of cigarettes smoked daily and the pulpal OP. RESULTS: The mean (± SD) OP value decreased as cigarette consumption increased: group 4 (268.00 ± 10.09 mosm/kg) > group 1 (259.20 ± 7.16 mosm/kg) > group 2 (248.90 ± 2.23 mosm/kg) > group 3 (239.90 ± 7.40 mosm/kg). The OP differed significantly between groups (p < 0.01), and a significant negative correlation was found between cigarette consumption and pulpal OP (r = -0.809, p < 0.01). CONCLUSION: In this study, the OP decreased as the number of cigarettes smoked increased. In clinical examination, there may be misdiagnosis of pulpal conditions in smokers (even in healthy pulp tissue) due to the effect of altered OP on pulpal tissue reactions.

Gingival crevicular fluid levels of neuropeptides following dental restorations.

PURPOSE: Local neuropeptide release has a critical role in the initiation and progression of an inflammatory response. This study investigated the effects of different restorative materials on periodontium in this regard, by evaluating their neuropeptide-producing effects on gingival crevicular fluid (GCF). METHODS: The study included 14 patients suitable for metal-ceramic, composite and amalgam restorations. Four weeks after periodontal therapy, the restorations were performed. Study groups were constituted regarding the tooth/restoration surfaces contacting gingiva in each patient: 1 ceramic surface of a metal-ceramic crown (ceramic group), its opposite metal surface (metal group), 1 composite surface (composite group), its opposite enamel surface (opposite-composite group), 1 amalgam surface (amalgam group), its opposite enamel surface (opposite-amalgam group) and 1 nonrestored enamel surface (enamel group). Four weeks after dental restorations, clinical data and GCF were obtained from the group sites. Clinical data, GCF volume and its proinflammatory cytokine profile were utilized to evaluate the periodontal health. GCF levels of substance P (SP), neurokinin A (NKA) and calcitonin-gene related peptide (CGRP) were determined by ELISA for revealing the neuropeptide levels. RESULTS: GCF volume was found to increase in all groups compared with the enamel group (p<0.05). SP and NKA levels were higher in the ceramic, composite and amalgam groups than those in the enamel group (p<0.05). SP and NKA levels were also higher in the composite and amalgam groups than those in the opposite-composite/amalgam groups (p<0.05). CONCLUSIONS: These results suggest that ceramic, composite and amalgam materials may uniquely trigger local neuropeptide release in periodontium.

The impact of dietary induced hyperparathyroidism on healthy and diseased periodontia: an experimental study in rats.

BACKGROUND AND OBJECTIVE: Nutrition may be a potential modifying factor in periodontal conditions. The present study investigated this phenomenon for dietary induced hyperparathyroidism (dHPT) by revealing the histopathological and histomorphometrical profiles of healthy and diseased periodontia in dHPT. METHODS: Dietary induced hyperparathyroidism was induced in 12 rats by dietary calcium/phosphorous imbalance and 12 rats were fed standard diet (SD). Periodontitis was induced on the right mandibular molar teeth (mmt) of these rats by injecting an endotoxin + saline solution whereas injecting pure saline to the left mmt. Thus, four study groups were created: dHPT + saline (group 1), dHPT + endotoxin (group 2), SD + endotoxin (group 3) and SD + saline (group 4). Histological sections were obtained from the second mmt and examined using light microscope. RESULTS: Group 1 demonstrated inflammatory and degenerative alterations in periodontium without pocket formation. Periodontitis was evident in groups 2 and 3. Group 2 revealed the highest amounts of gingival inflammatory cell and vessel counts (group 2 > group 3 > group 1 > group 4), attachment and bone losses (group 2 > group 3 > groups 1 > group 4) and osteoclast count (group 2 > group 3 > group 1 > group 4) (p < 0.05). CONCLUSION: These results propose that dHPT may impair the health status of periodontium and may worsen the pathobiology of periodontal diseases.

Excessive fluoride intake alters the MMP-2, TIMP-1 and TGF-ß levels of periodontal soft tissues: an experimental study in rabbits.

OBJECTIVES: This study evaluated the influence of fluoride on periodontal soft tissues by investigating any alterations in their MMP-2, TIMP-1 and TGF-ß profiles secondary to excessive fluoride intake. MATERIAL AND METHODS: Fluorosis was induced in 18 rabbits (test group) through consumption of fluoride added to drinking water, whereas 10 rabbits consumed regular tap water as daily supply (control group). Following fluorosis verification, animals were sacrificed and their 1st mandibular molar teeth were utilized in the assessments. MMP-2, TIMP-1 and TGF-ß were separately investigated for gingival epithelium (GE), gingival connective tissue (GC) and periodontal ligament (PL) to evaluate periodontal soft tissues. Histological sections were prepared from the groups, the parameters were determined by immunohistochemistry, and their levels were calculated by quantification of the immunostainings. RESULTS: Staining intensity of MMP-2 in GC and PL (p < 0.01); TIMP-1 and TGF-ß of GE, GC and PL (p < 0.01) were higher in the test group compared to those of the control group. Intra-group staining of TIMP-1 was higher than MMP-2 in all test group compartments (p < 0.01) and in the control group GE (p < 0.01). TIMP-1 was also higher than TGF-ß in the GE and PL of the test group (p < 0.05) and in the GE of the control group (p < 0.01). CONCLUSION: These results suggest that excessive fluoride intake may affect periodontal soft tissues by increasing MMP-2, TIMP-1 and TGF-ß, and thereby altering the MMP-2/TIMP-1 and TIMP-1/TGF-ß ratios. CLINICAL RELEVANCE: Excessive fluoride consumption may alter the periodontal tissue homeostasis which may be detrimental in the maintenance of periodontal health.

Local peptidergic innervation of gingiva in smoking and non-smoking periodontitis patients.

BACKGROUND: The present study aimed to investigate the local peptidergic innervation of diseased and healthy periodontia in smokers and non-smokers. METHODS: Fifteen smokers and 12 non-smokers, all with localized chronic periodontitis, participated in the study. Periodontally diseased and healthy tooth sites were selected in smokers (groups 1 and 2, respectively) and non-smokers (groups 3 and 4, respectively). Local peptidergic innervation was assessed by the concentrations of two neuropeptides, substance P (SP) and calcitonin gene-related peptide (CGRP), in the gingival biopsies obtained from the groups. Clinical data and biopsies were collected from the same two tooth sites in each group. SP and CGRP levels were measured by enzyme immunosorbent assay in the supernatants of gingival samples. RESULTS: Increased probing depth and attachment loss were found in group 1 compared to group 3 (P<0.05). SP was higher in group 1 compared to groups 2, 3, and 4, and it was higher in group 3 compared to groups 2 and 4 (P<0.05). CGRP was higher in group 1 than in groups 2, 3, and 4, but it was lower in group 3 than in groups 2 and 4 (P<0.05). CONCLUSION: The study results suggested that 1) although smoking may affect the neurogenic inflammation in the presence of periodontitis by increasing local peptidergic innervation, this effect may not be seen in periodontal health, and 2) SP may be regarded as an indicator of periodontitis, whereas CGRP may be important in the acute and/or initial periodontal inflammation.

Fluid dynamics of gingiva in diabetic and systemically healthy periodontitis patients.

OBJECTIVES: The influence of diabetes mellitus (DM) on the fluid dynamics of periodontium has not been reported in periodontal disease. The objectives of this study were (i) to investigate the alterations in the fluid dynamics of periodontium in diabetic periodontitis patients, and present the association of this phenomenon with the metabolic control of DM; (ii) to reveal any correlation between the fluid dynamics of periodontium and clinical signs of periodontal disease in DM and periodontitis. DESIGN: Fifteen well-controlled diabetic chronic periodontitis patients (Group 1), 14 systemically healthy chronic periodontitis patients (Group 2), and 14 systemically and periodontally healthy individuals were included in the study. Gingival crevicular fluid volume (GCF-V) and gingival tissue osmotic pressure (GOP) were used as the parameters of periodontal fluid dynamics. GCF-V was measured by a Periotron device, while GOP was measured by a digital osmometer. Silness-Löe plaque index (PI), Löe-Silness gingival index (GI) and clinical attachment loss (AL) levels were recorded to determine the periodontal health status. RESULTS: PI, GI and AL were higher in Groups 1 and 2 than in Group 3 (P<0.05), but similar between Groups 1 and 2 (P>0.05). Increased GCF-V and GOP were observed in Groups 1 and 2 compared with Group 3 (P<0.01), and the increase in Group 1 was greater than that in Group 2 (P<0.01). There were strong positive correlations between GCF-V and GOP in all three groups: between GI and GCF-V and GI and GOP in Groups 1 and 2; and between AL and GCF-V and AL and GOP in Groups 2 and 3. CONCLUSION: The results suggest that (i) DM may have an additive influence on the fluid dynamics of periodontium in the presence of periodontal disease; (ii) this phenomenon may not be prevented by the metabolic control of DM; (iii) the clinical signs of periodontal disease may be affected by the fluid dynamics of periodontium in both DM and periodontitis.

Gingival levels of monocyte chemoattractant protein-1 (MCP-1) in diabetes mellitus and periodontitis: an experimental study in rats.

The objectives of this study were to investigate and compare the monocyte chemoattractant protein-1 (MCP-1) levels of gingival tissues in diabetes mellitus (DM) and periodontitis and to reveal the effects of MCP-1 on periodontal inflammation and destruction in these diseases. DM was created in 15 rats (group 1) by streptozotocin injection, and periodontitis was obtained by ligature induction in 15 rats (group 2). Fifteen systemically and periodontally healthy rats were used as control (group 3). Gingival MCP-1 levels were measured by enzyme-linked immunosorbent assay (ELISA). Periodontal inflammation was quantified by the inflammatory cell infiltration in the gingival samples, whereas periodontal destruction was assessed by the alveolar bone loss in the experimental regions. MCP-1 concentrations were higher in groups 1 and 2 than in group 3 (p < 0.001). Increased gingival inflammatory cell infiltration and alveolar bone loss were observed in groups 1 and 2 compared to group 3 (p < 0.001). There were positive correlations among the MCP-1 level, gingival inflammatory cell infiltration, and alveolar bone loss in groups 1 and 2 (p < 0.001). Our results suggest that (1) DM may lead to enhanced MCP-1 production in periodontal tissues likewise for periodontitis and (2) there may be a positive correlation between the MCP-1 concentration and diseased nature of periodontium in both diseases.

The expression of vascular endothelial growth factor in a rat model at destruction and healing stages of periodontal disease.

BACKGROUND: The major role of vascular endothelial growth factor (VEGF), an angiogenic mediator, in promoting the progression or the healing of periodontal disease is still unclear. The aim of this study was to evaluate the VEGF expression in the destruction and healing stages of periodontal disease and to investigate the association between VEGF expression and vascularization with regard to the number and diameters of blood vessels. METHODS: Thirty rats were distributed equally into two test groups and a control group. Experimental periodontal disease was induced in the test groups by silk ligatures, which were kept in position for 40 days. On the 40th day, ligatures were removed from the healing group, whereas ligatures were left in position in the destruction group. On the 60th day, rats were sacrificed; histomorphometric and biochemical analyses were carried out to determine the number and diameters of blood vessels and the assessment of VEGF concentration by enzyme-linked immunosorbent assay, respectively. RESULTS: There was a statistically significant increase in the number of blood vessels in the healing group and in the diameters of blood vessels in the destruction group compared to the control group (P <0.001). In vivo VEGF expressions were highest in the healing group (P <0.001) and correlated significantly with the number of blood vessels (r(2) = 0.814; P = 0.001). CONCLUSION: VEGF expression may be related more to the healing stage of periodontal disease than to the destruction stage of the lesion.

Osmotic pressure and vasculature of gingiva in experimental diabetes mellitus.

BACKGROUND: Alterations in tissue osmotic pressure (OP) and vasculature are considered to be the inevitable aspects of an inflammatory process that subsequently alter the fluid dynamics of the tissues involved. The aim of this study was to reveal a profile of OP and vascular changes in periodontally healthy gingival tissues and analyze the relationship between them in diabetes mellitus (DM) to evaluate the possible effects of DM on the fluid dynamics of the periodontium. METHODS: Experimental DM was created by intraperitoneal streptozotocin injection in 10 periodontally healthy rats. These rats were used as the test group, and 10 systemically and periodontally healthy rats served as the control group. Gingival tissue samples obtained from the groups were used for the test procedures. OP was measured in the supernatants of these samples by a semimicrodigital osmometer. Vasculature was assessed as the alterations in vascularization (vessel number [VN]) and vasodilatation (vessel diameter [VD]) by histomorphometric means. RESULTS: There was a gross increase in the OP level of the test group (172.7 +/- 59.7 mOsm/kg) compared to the control group (11.4 +/- 4.2 mOsm/kg; P <0.001). VN was found to be significantly larger in the test group (12.7 +/- 2.8) than in the control group (6.8 +/- 1.1; P <0.001). VD was found to be smaller in the test group (10.1 +/- 2.8 microm) than in the control group (15.5 +/- 2.4 microm), and this difference was statistically significant (P <0.001). A positive correlation between OP and VN (r = 0.77; P <0.001) and a negative correlation between OP and VD (r = 0.1; P >0.05) were observed in the test group. CONCLUSION: Our results reveal that the fluid dynamics of periodontal soft tissues may be affected by the diabetic conditions in this diabetic model because of the increased OP and VN during the pathogenesis of the disease.

Vascular endothelial growth factor (VEGF) levels of gingiva and gingival crevicular fluid in diabetic and systemically healthy periodontitis patients.

It has been demonstrated that diabetes mellitus (DM) may have an inductive effect on the vascular endothelial growth factor (VEGF) levels of periodontium during periodontal disease. The aim of this study is to confirm this phenomenon, investigating whether it is also valid for diabetic periodontitis patients under good metabolic control. Sixteen type II DM patients, all with a glycosylated hemoglobin (HbA1c) value less than 7 (test), and 15 systemically healthy (control) chronic periodontitis patients were included in the study. The VEGF concentrations in the gingival supernatants and gingival crevicular fluid (GCF) samples of the study groups were measured by enzyme-linked immunosorbent assay. The data were analyzed by Student's t test in statistical means. The VEGF levels were significantly higher in the gingival supernatants of the test group (55.89 +/- 8.11 pg/ml) than that of the control group (24.81 +/- 2.04 pg/ml; p < 0.01). However, there was no statistically significant difference in the VEGF levels of GCF between the study groups (38.96 +/- 4.89 pg/ml in the test and 32.20 +/- 4.02 pg/ml in the control group; p > 0.05). Our study confirms that DM affects the VEGF levels of periodontal soft tissues in periodontal disease, and our results also suggest that this effect may not be influenced by the metabolic control of DM.

Increased expression of vascular endothelial growth factor in cyclosporin A-induced gingival overgrowth in rats.

BACKGROUND: Gingival overgrowth is a side effect associated with cyclosporin A (CsA) therapy. The lesion is characterized by increased epithelial thickness, enlargement of connective tissue, and increased vascularization. The aim of this experimental study was to examine the role of vascular endothelial growth factor (VEGF) in the pathogenesis of CsA-induced gingival overgrowth. METHODS: Twenty male Wistar rats were divided into two groups of 10 animals each. For the development of gingival overgrowth, one group received CsA therapy subcutaneously in a daily dose of 10 mg/kg for 60 days, and the other group was used as a control. At the end of the experimental period, rats were subsequently decapitated, and the mandibles with the surrounding gingiva and soft tissue were removed. Half of each sample was used for histomorphometric analysis, and the other half was used for biochemical analysis. Histomorphometric analysis included the measurements of the number and diameter of blood vessel profiles under a microscope, and biochemical analysis included the assessment of VEGF concentration by enzyme-linked immunosorbent assay (ELISA). RESULTS: The histomorphometric findings showed that the number of blood vessel profiles increased in the CsA group compared to the control group (P <0.001), although the increase in the diameter of blood vessel profiles was not significant (P >0.05). The biochemical findings showed that in vivo VEGF expression was higher in the CsA group compared to the control group (P <0.001). CONCLUSION: The results of this study suggest that increased VEGF expression may be associated with the pathogenesis of CsA-induced gingival overgrowth.

Pemphigus vulgaris and complications of systemic corticosteroid therapy: a case report.

Pemphigus refers to a group of diseases characterized by painful lesions caused by intraepidermal acantholytic structures in the skin and mucous membrane. The exact nature of the disease remains unknown. Pemphigus is a rare chronic mucocutaneous disease characterized by intra-epithelial bulla formation, due to autoantibodies directed against proteins of the desmosome-tonofilament complex between keratinocytes. The bullous lesions are painful, slow to heal and with a tendency to become invasive. Any part of the oral cavity may be affected, with the soft palate, buccal mucosa and lips being the most common sites. The high doses and prolonged administration of corticosteroids often required to control the disease result in several side effects, many of which are serious or life-threatening. In the present case, steroid treatment was begun at 180 mg/day and subsequently increased to 250 mg/day and 350 mg/day. Oral lesions were treated locally with 0.2% chlorhexidine gluconate in addition to systemic corticosteroids containing an immunosuppressive. Oral lesions were observed to recur without healing completely. Respiratory problems occured, necessitating direct lung radiographs and computerised tomography. Pulmonary embolism was diagnosed and the patient was transferred to the vascular surgery department. Unfortunately the patient died due to pulmonary embolism on the seventh day. Pemphigus vulgaris (PV) is a chronic autoimmune mucocutaneous disease that often primarily involves the oral cavity. Therefore, early diagnosis of oral symptoms is crucial for the successful treatment of PV. Although there is no consensus regarding the initial steroid dosage needed to induce remission, it is suggested that high doses of corticosteriods may cause fatal complications.