Umur Sakallıoğlu

Healing of periodontal defects treated with enamel matrix proteins and root surface conditioning: an experimental study in dogs

Application of enamel matrix proteins has been introduced as an alternative method for periodontal regenerative therapy. It is claimed that this approach provides periodontal regeneration by a biological approach, i.e. creating a matrix on the root surfaces that promotes cementum, periodontal ligament (PDL) and alveolar bone regeneration, thus mimicking the events occurring during tooth development. Although there have been numerous in vitro and in vivo studies demonstrating periodontal regeneration, acellular cementum formation and clinical outcomes via enamel matrix proteins usage, their effects on the healing pattern of soft and hard periodontal tissues are not well-established and compared with root conditioning alone. In the present study, the effects of Emdogain (Biora, Malmö, Sweden), an enamel matrix derivative mainly composed of enamel matrix proteins (test), on periodontal wound healing were evaluated and compared with root surface conditioning (performed with 36% orthophosphoric acid) alone (control) histopathologically and histomorphometrically by means of the soft and hard tissue profile of periodontium. An experimental periodontitis model performed at premolar teeth of four dogs were used in the study and the healing pattern of periodontal tissues was evaluated at days 7, 14, 21, 28 (one dog at each day), respectively. At day 7, soft tissue attachment evaluated by means of connective tissue and/or epithelial attachment to the root surfaces revealed higher connective tissue attachment rate in the test group and the amount of new connective tissue proliferation in the test group was significantly greater than the control group (p<0.01). New bone formation by osteoconduction initiated at day 14 in the test and control group. At day 21, the orientation of supra-alveolar and PDL fibers established, and new cementum formation observed in both groups. At day 28, although regenerated cementum was cellular in all of the roots in the control samples, an acellular type of cementum (1.32+/-0.83 mm in length and 3.16+/-0.23 microm in width) was also noted in six roots of test samples with an inconsistent distribution on the root surfaces. The amount of new cementum was significantly higher in the test group than the control group samples (p<0.01). The width of the cellular cementum in the control group was more than the cellular cementum in the test group, but the difference was not statistically significant (p>0.05). A firm attachment of acellular cementum to the root dentin with functional organization of its collagen fibers was noted, and, the accumulation and organization of cellular cementum in the control group was more irregular than the cellular cementum formed in the test group. The amount of new bone was 2.41+/-0.75 mm in the test and 1.09+/-0.46 mm in the control group at day 28. The rate of bone maturation (the number of osteons) was found higher in the test group (10.75+/-0.85) than the control group (5.50+/-0.86). Under the limitations of the study, our results reveal that when compared with root surface conditioning, enamel matrix proteins have more capacity for stimulating periodontal regeneration via their positive effects on root surfaces, i.e. inhibition of gingival epithelium down growth and stimulation of connective tissue proliferation and attachment to the root surfaces during wound healing. An acellular type of cementum regeneration and new alveolar bone formation by an accelerated osteoconductive mechanism are also achieved with application of enamel matrix proteins.

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.

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.

Dietary-induced hyperparathyroidism affects serum and gingival proinflammatory cytokine levels in rats.

BACKGROUND Poor diet and inadequate nutrition are suggested to affect the periodontium as well as impair the systemic health. This study investigated the systemic and periodontal effects of dietary-induced hyperparathyroidism (dHPT) by evaluating serum and gingival proinflammatory cytokine levels. METHODS Twenty-four Sprague-Dawley rats were used in the study. dHPT was induced in 12 rats by calcium/phosphorus imbalance, and 12 rats were fed a standard diet (SD). Afterward, endotoxin-induced periodontitis was induced on the right mandibular molar teeth (mmt). Four study groups were created: dHPT + mmt without periodontitis (group 1), dHPT + mmt with periodontitis (group 2), SD + mmt with periodontitis (group 3), and SD + mmt without periodontitis (group 4). Interleukin (IL)-1beta and tumor necrosis factor-alpha (TNF-alpha) levels were measured by enzyme-linked immunosorbent assay to evaluate the proinflammatory cytokine profiles. Serum cytokines were analyzed in the blood samples collected prior to periodontitis induction, whereas gingival cytokines were analyzed in the gingival supernatants of the four groups. RESULTS Serum cytokines were higher in dHPT rats than in SD rats (P <0.001), with a positive correlation between parathormone and the cytokines (P <0.001). Gingival cytokines were highest in group 2 and lowest in group 4 (group 2 > group 3 > group 1) (P <0.001). There was a positive correlation between parathormone and the gingival cytokines in group 1 (P <0.001 for IL-1beta; P <0.01 for TNF-alpha). CONCLUSION The results suggested that increased serum proinflammatory cytokine production may be a complication of dHPT, and this may affect healthy and diseased periodontia by increasing gingival proinflammatory cytokine levels.

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.

Excessıve fluorıde ıntake alters the MMP-2, TIMP-1 and TGF-β levels of perıodontal soft tıssues: an experımental study ın rabbıts

ObjectivesThis study evaluated the influence of fluoride on periodontal soft tissues by investigating any alterations in their MMP-2, TIMP-1 and TGF-β profiles secondary to excessive fluoride intake.Material and methodsFluorosis 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-β 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.ResultsStaining intensity of MMP-2 in GC and PL (p < 0.01); TIMP-1 and TGF-β 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-β in the GE and PL of the test group (p < 0.05) and in the GE of the control group (p < 0.01).ConclusionThese results suggest that excessive fluoride intake may affect periodontal soft tissues by increasing MMP-2, TIMP-1 and TGF-β, and thereby altering the MMP-2/TIMP-1 and TIMP-1/TGF-β ratios.Clinical relevanceExcessive fluoride consumption may alter the periodontal tissue homeostasis which may be detrimental in the maintenance of periodontal health.

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.