Mast cells – a role in periodontal diseases?

OBJECTIVES: Limited attention has been given to the role mast cells may play in periodontal diseases. BACKGROUND: Mast cells are indeed found abundantly below and within several types of mucosal epithelia. On the basis of their proteinase content, mast cells are divided into connective tissue (CT) and mucosal phenotypes. The CT phenotype contains both tryptase and chymase (MC(TC)), while the mucosal phenotype contains only tryptase (MC(T)). The in vivo significance of different mast cell phenotypes has not yet been fully established. Mast cells are able to phagocytose, process and present antigens as effectively as macrophages. RESULTS: Recently mast cells were found in high numbers in chronically inflamed gingival tissue taken from patients with chronic marginal periodontitis (CMP). The number of mast cells was found to be even higher in HIV(+) patients with CMP. Furthermore, mast cells also express strongly matrix metalloproteinases (MMPs), which are key enzymes in degradation of gingival extracellular matrix. Mast cells may release preformed cytokines directing local innate and adaptive immune responses. The present review will focus on possible roles for mast cells in periodontal diseases. CONCLUSIONS: We certainly feel that this is a key cell in inflamed periodontal tissue and its role in periodontitis needs to be revisited.     

Is there a role for antibiotics in periodontal treatment?

Plaque-induced inflammatory periodontal disease affects a significant number of the population, and raises the question as to why antibiotics are not universally used to treat a disease in which bacteria are the main aetiological agent. This article describes the reasons why antibiotics may not be effective in treating periodontitis, and why their use is not more widespread. However, antibiotics have been shown to be helpful in periodontal treatment in some cases, and evidence for this is presented and suggestions where their use may be indicated are made. CLINICAL RELEVANCE: To rationalize the selective use of antibiotics in the treatment of periodontitis and avoid inappropriate prescribing.     

Carboxypeptidase‐mediated metabolism of calcitonin gene‐related peptide in human gingival crevicular fluid – a rôle in periodontal inflammation?

Background: Metabolism by peptidases plays an important rôle in modulating the levels of biologically‐active neuropeptides. The metabolism of the anti‐inflammatory neuropeptide calcitonin gene‐related peptide (GCRP), but not the pro‐inflammatory neuropeptides substance P (SP) and neurokinin A (NKA) by components of the gingival crevicular fluid (GCF), could potentiate the inflammatory process in periodontitis. Aims: To characterise the extracellular hydrolysis of CGRP as a mechanism for the selective inactivation of this neuropeptide in GCF from periodontitis sites. Methods: Samples of GCF from periodontitis patients and periodontally‐healthy subjects were incubated with synthetic human SP, NKA or CGRP. Reaction between the GCF constituents and synthetic peptides was allowed to progress from 0–180 min. Results of neuropeptide metabolism at each time were analysed by matrix‐assisted laser desorption/ionisation mass spectrometry. Results: There was no evidence of metabolism of SP, NKA or CGRP by constituents of healthy GCF. Metabolism of synthetic SP and NKA was minimal even after extensive incubation with periodontitis GCF. However, loss of carboxy‐terminal amino acids was evident after only 1 min incubation with periodontitis GCF. The pattern of CGRP metabolism, which proceeded from the C‐terminus, indicated that the neuropeptide was degraded by a carboxypeptidase. After 180 min, there was extensive carboxypeptidase degradation of CGRP to an 11 amino acid peptide. Conclusions: It is concluded that carboxypeptidase activity in GCF from periodontitis patients is responsible for rapid breakdown of CGRP but not SP or NKA. The rapid action of this carboxypeptidase on the anti‐inflammatory neuropeptide CGRP is suggestive of a pathophysiological rôle for the enzyme in selectively degrading CGRP, thereby potentiating periodontal inflammation.     

Can application of exogenous fibronectin enhance periodontal regeneration?

BACKGROUND: Although fibronectin (FN) is an important extracellular glycoprotein involved in periodontal wound healing, it is not clear whether the application of exogenous fibronectin (ExoFN) offers any clinical benefit. The purpose of this preliminary in vitro study was to determine the binding of FN from three different sources, viz. endogenous EDTA-plasma, endogenous serum and exogenous commercial purified human fibronectin in PBS buffer, to demineralized and non-demineralized root powder. METHOD: The binding of FN to a known quantity of mineralized and non-demineralized root powder by overnight incubation at 15 degrees C was studied by enzyme immunoassay (EIA) technique. The criteria for optimal performance of EIA procedure for the determination of FN was established. Particle size of powdered root structure was standardized using a Vibratory Sieve Shaker. RESULTS: The EDTA-plasma and the serum FN exhibited binding of (17.8 +/- 2.1 microg) and (6.5 +/- 4.5 microg), respectively, to the non-demineralized root powder. However, the binding was only significant for the EDTA-plasma FN (p < 0.01) when compared to controls. In the demineralized group there was no ascertainable binding of FN from either endogenous or exogenous sources. ExoFN in buffer exhibited no binding at all to the non-demineralized or demineralized root powder. CONCLUSION: The preliminary data suggest that additional plasma and serum factors may facilitate the binding of FN to root powder. High levels of FN in blood do not necessarily indicate that FN is available for binding to the root surface during periodontal surgery.     

Is there a temporal trend in the reported treatment efficacy of periodontal regeneration? A meta‐analysis of randomized‐controlled trials

Background/Aim: The aim of study was to conduct a meta‐analysis to investigate whether or not there was a temporal trend in the treatment efficacy reported in the randomized‐controlled trials (RCTs) on guided tissue regeneration (GTR) or enamel matrix protein derivatives (EMD) in the treatment of infrabony defects. Material and Methods: The treatment outcomes were changes in probing pocket depth (PPD) and clinical attachment level (CAL). Weighted multilevel and ordinary regression analyses were performed to test the temporal relationship between treatment effect difference or treatment effectiveness and publication years. Results: For PPD reduction, non‐significant positive relationships were found in the treatment effect difference or treatment effect of both GTR and flap operation. For CAL gain, a small positive relationship was found in the treatment effect difference, but a significant positive trend in the treatment effect of flap operation was found. No significant temporal trend was found in the treatment effect difference for EMD. Conclusions: There was no evidence to support or refute a temporal trend in the treatment effect of regenerative procedures, but a positive trend was observed in the control group. These results suggest that only RCTs should be included in the meta‐analysis, as the treatment effect of the control group may not be constant.     

T cells,teeth and tissue destruction – what do T cells do in periodontal disease?

The microbial plaque biofilm resides adjacent to the tissue‐destructive inflammatory infiltrate in periodontitis. Although not sufficient, this biofilm is necessary for this inflammatory response. Patients with periodontitis generate antibodies specific for bacteria in the biofilm – although the role of these antibodies is not clear, there is, undoubtedly, an adaptive immune response in periodontitis. T lymphocytes are central to adaptive immunity, and provide help for B cells to generate specific antibodies. T‐cell receptor recognition of peptide antigen in the context of major histocompatibility complex can result in T‐cell activation. The activation and differentiation of the T‐cell can take many forms, and hence numerous types of T cells have been described. The role of adaptive immune responses, and the T‐cell component thereof, in periodontitis remains relatively poorly defined. This review aims to broadly summarize findings about T cells and their role in periodontitis, focusing primarily on studies of human disease with a short discussion of some animal studies.     

The cause of drooling in children with cerebral palsy – hypersalivation or swallowing defect?

Summary. Objective. To determine whether or not drooling in children with cerebral palsy is due to hypersalivation. Population and methods. The study population consisted of 10 children with cerebral palsy who were identified as having severe drooling, and a matched control group composed of 10 unaffected children who had no known physical or mental disabilities. Salivary flow rate was compared between the cerebral palsied children and the control group using the chin‐cup collection drool quantification method described by Sochanjwskyj. Components of the system included a cup‐like collection device, a vacuum pump, plastic tubing, an airtight collection chamber, and calibrated test tubes held against the subject's chin with elastic straps attached to an orthodontic head bonnet. Statistical analysis was completed using the Student's t‐test and Fisher's Exact Probability test. Results. The ages of the population ranged from 5·2 to 15·6 years, mean age (± SE) of 10·56 ± 1·13 years. There was no statistically significant difference in the rate of salivary flow rate between the two groups’ mean ± SE: cerebral palsy group 0·220 ± 0·018; control group 0·334 ± 0·052 (P = 0·053). The results were further confirmed by comparing the buffering capacity (P = 1·00) and concentrations of the sodium (P = 0·065) and potassium ions (P = 0·058) in the saliva of the study groups. Conclusions. Children with cerebral palsy who drool do not appear to produce excess saliva. Their salivation is similar to the control children.     

Nicotine effects on polymorphonuclear cell apoptosis and lipopolysaccharide‐induced monocyte functions. A possible role in periodontal disease?

Apoptosis provides a mechanism for clearance of unwanted cells in a variety of situations in which programmed or physiological cell death occurs; but the premature death of defensive cells could promote infection, inflammation and concomitant disease. We detected high values of apoptosis in polymorphonuclear cells (PMN) elicited from crevicular sulci of smokers affected by adult periodontitis. To learn more about the effects of nicotine on the periodontal environment, we studied its ability to modulate the apoptosis of two phagocytic lines, PMN and mononuclear cells, which are continuously recruited from gingival vessels to prevent or control plaque extension. Brief exposure of PMN to nicotine concentrations ranging from 0.01 to 0.3% shortened, in a dose-dependent relationship, the lag culture time required to observe at fluorescent microscopy the morphological traces of apoptosis. These observations were confirmed by specific tools of apoptosis: DNA fragmentation on gel electrophoresis and expression of the apoptosis-signaling receptor Fas/Apo-1. The apoptotic effect excited by nicotine on these first line defensive cells may be an important feature of the pathogenesis of periodontal disease. As for mononuclear leukocytes, nicotine was unable to induce apoptotic modifications on cells observed up to 72 h culture time, but the drug inhibited IL-1beta release and procoagulant activity (PCA) expression. The conflicting role played by these lipopolysaccharide (LPS)-induced monocyte functions in the inflammatory process is a further intrigue in the mechanism by which nicotine compromises the oral health.     

Occlusion on implants – is there a problem?

Oral rehabilitation restores form and function and impacts on general health. Teeth provide a discriminating sense of touch and directional specificity for occlusal perception, management of food with mastication and swallowing, and awareness of its texture and hardness. Peripheral feedback for control of jaw muscles includes the enamel-dentine-pulp complex and mechanoreceptors in the periodontal tissues. The implications of feedback from periodontal and other intra-oral mechanoreceptors as well as changes in central representation are significant for function and adaptation to oral rehabilitation. With implants, in the absence of the periodontium and periodontal mechanoreceptor feedback, fine motor control of mastication is reduced, but patients are still able to function adequately. Further, there is no significant difference in function with full-arch fixed prostheses on teeth in comparison with implants. Predictable implant outcomes depend on bone support. Optimum restoration design appears to be significant for bone remodelling and bone strains around implants with occlusal loading. Finite element analysis data confirmed load concentrations at the coronal bone around the upper section of the implant where bone loss is commonly observed clinically. Load concentration increased with steeper cusp inclination and broader occlusal table and decreased with central fossa loading and narrower occlusal table size. It is recommended that occlusal design should follow a narrow occlusal table, with central fossa loading in intercuspal contact and low cusp inclination to minimise lateral loading in function and parafunction. Acknowledging these features should address potential problems associated with the occlusion in implant therapy.     

Zimmermann–Laband syndrome with bilateral developmental cataract – a new association?

An unusual case of Zimmermann-Laband syndrome in a young male child with an unreported association of bilateral developmental cataract is presented. The pathognomonic triad of gingival fibromatosis, aplastic or hypoplastic distal phalanges with absent nails, and enlargement of soft tissues of the face were obvious, besides the known moderate learning disability and mild hearing loss. The case is discussed in the light of relevant literature. To the best of our knowledge, this is the first report of early developmental cataracts in association with the Zimmermann-Laband syndrome. Besides detection and timely recognition of the syndrome to allow adequate dental care, ophthalmic screening at periodic intervals is merited to improve the overall quality of life for these patients.