Periodontal healing after application of enamel matrix derivative in surgical supra/infrabony periodontal defects in rats with streptozotocin-induced diabetes.

BACKGROUND AND OBJECTIVE: Epidemiologic and clinical studies have indicated that diabetes is a risk factor for periodontal disease progression and healing. The aim of the present study was to evaluate short-term healing after enamel matrix derivative (EMD) application in combined supra/infrabony periodontal defects in diabetic rats. MATERIAL AND METHODS: Thirty male Wistar rats were initially divided into two groups, one with streptozotocin-induced diabetes and another one with healthy (non-diabetic) animals. Bony defects were surgically created on the mesial root of the first maxillary molars. After root surface planing and EDTA conditioning, EMD was applied to the roots at one side of the maxillae, while those on the contralateral sides were left untreated. Animals were killed 3 wk after surgery, and block sections were prepared for histologic and histomorphometric analysis. RESULTS: There was statistically significant more gingival recession in diabetic animals than in non-diabetic animals. The length of the junctional epithelium was significantly shorter in the EMD-treated sites in both diabetic and normoglycemic rats. Sulcus depth and length of supracrestal soft connective tissue showed no statistically significant differences between groups. In all animals, new bone formation was observed. Although new bone occurred more frequently in healthy animals, the extent of new bone was not significantly different between groups. In none of the teeth, a layer of new cementum was detectable. EMD had no influence on bone or cementum regeneration. Adverse reactions such as excessive inflammation due to bacterial root colonization, ankylosis and bone fractures were exclusively observed in diabetic animals, irrespective of EMD treatment. CONCLUSION: Within the limits of the present study, it can be concluded that periodontal healing was impaired in streptozotocin-induced diabetic rats. EMD had no beneficial effects on new bone and cementum formation during short-term healing in this defect model and could not ameliorate the adverse effects in the systemically compromised animals.

Supplementation of green tea catechins in dentifrices suppresses gingival oxidative stress and periodontal inflammation.

OBJECTIVE: this study examined the effects of a dentifrice containing green tea catechins on gingival oxidative stress and periodontal inflammation using a rat model. DESIGN: twenty-four male Wister rats were randomly divided into four groups. The first group (Control group) received no treatment for 8 weeks. Periodontal inflammation was induced in the second group for 8 weeks. Periodontal inflammation was induced in the last two groups for 8 weeks and dentifrices with or without green tea catechins were topically applied to the gingival sulcus daily for 4 weeks prior to the end of the experimental period. RESULTS: rats that had experimental periodontal inflammation showed apical migration of the junctional epithelium, alveolar bone loss and inflammatory cell infiltration in the connective tissue subjacent to the junctional epithelium at 8 weeks, whilst the control group showed no pathologic changes. Topical application of a green tea catechin-containing dentifrice reduced inflammatory cell infiltration in the periodontal lesions to a greater degree than the control dentifrice at 8 weeks. The gingiva in which green tea catechin-containing dentifrice was applied also showed a lower level of expression of hexanoyl-lysine (a marker of lipid peroxidation), nitrotyrosine (a marker of oxidative protein damage), and tumour necrosis factor-α (an indicator of pro-inflammatory cytokines) at 8 weeks compared to gingiva in which the control dentifrice was applied. CONCLUSIONS: adding green tea catechins to a dentifrice may contribute to prevention of periodontal inflammation by decreasing gingival oxidative stress and expression of pro-inflammatory cytokines.

Muscarinic acetylcholine receptor activation increases transcellular transport of macromolecules across mouse and human intestinal epithelium in vitro.

The intestinal epithelium acts as a barrier restricting uptake of luminal macromolecules such as dietary antigens and microbes. Here, we examined the role of cholinergic signalling in the regulation of permeability to macromolecules. Mouse jejunum was mounted in Ussing chambers and permeability was determined by measuring the flux of the antigen-sized protein, horseradish peroxidase (HRP), across the tissue. Baseline HRP permeability was significantly reduced by neural blockade with tetrodotoxin or cholinergic muscarinic antagonism with atropine, suggesting that ongoing release of endogenous acetylcholine from enteric nerves regulates barrier function. Exogenous addition of the muscarinic agonist bethanechol caused significant increases in both HRP flux and the area of HRP-containing endosomes in enterocytes. Bethanechol-enhanced HRP flux was abrogated by the M3 receptor antagonist, 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), the phospholipase A(2) inhibitor quinacrine, and the cyclooxygenase inhibitor indomethacin. Complementary in vitro studies showed direct effects of bethanechol on T84 epithelial cells, where increased HRP uptake was associated with increased F-actin, and increased cytosolic phospholipase A(2) (cPLA(2)) phosphorylation. Taken together, these results provide evidence for cholinergic regulation of transepithelial transport of macromolecules, mainly mediated by activation of M3 receptors with subsequent involvement of phospholipase A(2) and cyclooxygenase products.

Effect of enamel matrix protein derivative on healing of surgical supra-infrabony periodontal defects in the rat molar: a histomorphometric study.

BACKGROUND: Enamel matrix protein derivative (EMD) has proven to enhance periodontal regeneration in human and animal studies. The present histomorphometric study evaluated healing of combined supra-infrabony periodontal defects with EMD. METHODS: The study comprised two groups of 10 Wistar rats each, 7 to 8 months old. Bony defects were created on the mesial aspect of the mesial root of the first maxillary molar. The root surface was planed and 24% EDTA gel applied for 2 minutes and then rinsed with water. In the study group, EMD was applied, and in the control group, only propylene glycol alginate was applied. Animals were sacrificed 12 weeks after surgery, and block sections were removed, demineralized, and embedded in paraffin. For histomorphometric analysis, three sections from the central area of the defect were selected. Root, surgical defect, epithelial attachment, sulcus, supracrestal connective tissue, ankylosis, and the length and area of new cementum and new bone were measured. RESULTS: No statistically significant differences between the two groups were found for root and defect measures. The remaining parameters were calculated as a percentage of the defect. In the study group, smaller gingival recession (P = 0.05), deeper gingival sulcus (P = 0.05), and shorter junctional epithelium (P = 0.01) were found. New cementum was observed in the study group only (P = 0.02). Ankylosis was six times larger in the control group but not statistically significant. New bone formation was similar in both groups. CONCLUSION: Enamel matrix protein derivative enhanced periodontal healing in this model by reducing gingival recession and junctional epithelium along the root surface and enhancing the formation of new cementum.

Effect of an oily calcium hydroxide suspension (Osteoinductal) on healing of intrabony periodontal defects. A pilot study in dogs.

The aim of the present study was to evaluate histologically in dogs the effect of treating intrabony defects with an oily calcium hydroxide suspension (OCHS). Intrabony defects were surgically created bilaterally at the distal aspects of the maxillary first premolars and at the mesial aspects of the third premolars in two mongrel dogs. Subsequently, the defects were randomly treated with (a) access flap surgery followed by the application of an OCHS or (b) access flap surgery alone. After 8 weeks of healing, the animals were killed. Dissected blocks containing the experimental specimens were fixed in formalin, decalcified in EDTA, and embedded in paraffin. The formation of new cementum and bone was assessed histomorphometrically. In the control group, healing was predominantly characterized by the formation of a long junctional epithelium along the root surface and limited periodontal regeneration at the most apical part of the defect. The OCHS-treated defects consistently revealed periodontal regeneration (i.e., new periodontal ligament, new cementum with inserting collagen fibers, and new bone). Within the limits of the present study, it can be concluded that OCHS may favor periodontal regeneration in acute-type intrabony periodontal defects.

Restoration of periodontal attachment employing enriched collagen solution in the dog.

Three wall intrabony defects were produced in 11 dogs using a round bur followed by curettes and hoes. A copper band was fixed to the tooth with stainless steel ligature wire. Six weeks later, the copper band was removed and the defect was treated with an enriched collagen solution (ECS) prepared from acid-extracted dog skin collagen. Thirty-three defects were treated with ECS and 33 defects were controls. Healing was assessed histologically 4 and 6 weeks after treatment for the presence of new cementum, periodontal ligament and alveolar bone, as well as arrested epithelial downgrowth along the dental root. Unlike the controls, treatment with ECS resulted in restoration of periodontal attachment after 4 weeks. This included formation of new cementum, new alveolar bone and dense connective tissue fiber running between bone and cementum. Control sections showed epithelial migration along the root, separating it from the adjacent connective tissue and thus preventing new attachment.