Health Professions Pharmacy

Oral and gingival health research

Description

This cluster of papers explores the risk factors, genetic mechanisms, and clinical aspects of gingival overgrowth induced by medications such as cyclosporin A, tacrolimus, and phenytoin. It delves into the molecular pathways, connective tissue metabolism, and the influence of growth factors and cytokines on the development and management of drug-induced and hereditary gingival fibromatosis. The cluster also investigates the prevalence, severity, and treatment options for gingival overgrowth in patients undergoing organ transplantation or medication therapy.

Keywords

Gingival Overgrowth; Drug-Induced; Hereditary Gingival Fibromatosis; Cyclosporin A; Tacrolimus; Collagen Metabolism; Matrix Metalloproteinases; Connective Tissue Growth Factor; Transforming Growth Factor-ß1; Periodontal Complications

The temporal aspects and mechanisms of the regulation of the matrix metalloproteinase (MMP) 72-kDa gelatinase/type IV collagenase (MMP-2) by transforming growth factor-beta 1 (TGF-beta 1) were investigated in early passage … The temporal aspects and mechanisms of the regulation of the matrix metalloproteinase (MMP) 72-kDa gelatinase/type IV collagenase (MMP-2) by transforming growth factor-beta 1 (TGF-beta 1) were investigated in early passage human gingival fibroblasts and compared with the regulation of the genes for collagenase (MMP-1) and TIMP, the tissue inhibitor of MMPs. Northern hybridization analyses revealed that 1.0 ng/ml TGF-beta 1 increased the abundance of MMP-2 mRNA/cell approximately 1.5-fold at 24 h, an increase similar to that observed in the level of [35S]methionine pulse-labeled MMP-2 at 24 h (1.9-fold). At 48 and 72 h, the increase in MMP-2 mRNA abundance remained elevated by 1.5-2.2-fold on a per cell basis whereas TIMP mRNA levels were elevated by up to 3.3-fold. In contrast, the relative levels of collagenase mRNA were reduced by 66-75%. The changes in the MMP-2, collagenase, and TIMP mRNA concentrations in response to TGF-beta 1 were blocked by cycloheximide indicating that protein synthesis was required to mediate the effects of TGF-beta 1 on these mRNA levels. TGF-beta 1 was also found to increase the half-life of the MMP-2 mRNA from approximately 46 to approximately 150 h but did not alter the stability of TIMP mRNA (t1/2 approximately 60 h). Nuclear run-off transcription assays revealed that MMP-2 gene transcription was increased approximately 5-fold 7 h following TGF-beta 1-treatment but returned to control levels by 24 h. In comparison, increased TIMP gene transcription was only detectable after 24 h whereas collagenase gene transcription, although low in control cells, was undetectable at 24 h. Gene transcription, mRNA levels, and message stability of the genes for the extracellular matrix proteins type I collagen and fibronectin were also increased by TGF-beta 1. Thus, the similarity in the control of MMP-2, alpha 1 (I) procollagen, and fibronectin expression at the transcriptional and post-transcriptional levels indicates that these genes may share regulatory elements. In comparison, TGF-beta 1 reduced the level of collagenase mRNA and increased the level of TIMP mRNA as a result of altered transcriptional activities, through pathways that required protein synthesis, and without changes in mRNA stability.
The primary aim of this study was to assess if the probiotic Lactobacillus reuteri could be effective in the treatment of gingivitis and further to evaluate the influence of the … The primary aim of this study was to assess if the probiotic Lactobacillus reuteri could be effective in the treatment of gingivitis and further to evaluate the influence of the probiotic on plaque and the lactobacilli population in the saliva. A randomised, placebo-controlled, double blind study was performed over 2 weeks. Fifty-nine patients with moderate to severe gingivitis were included and given one of two different Lactobacillus reuteri formulations (LR-1 or LR-2) at a dose of 2 x 10(8) CFU per day, or a corresponding placebo. At baseline (day 0) gingival index and plaque index were measured on two surfaces and saliva for lactobacilli determination was collected. The patients were instructed how to brush and floss efficiently and study treatment was started.The patients returned on day 14 for final assessment of gingivitis and plaque and saliva was collected. 20 patients were randomised to LR-1, 21 to LR-2 and 18 to placebo. Gingival index fell significantly in all 3 groups (p < 0.0001). LR-1, but not LR-2 improved more than placebo (p < 0.0001). Plaque index fell significantly in LR-1 (p < 0.05) and in LR-2 (p < 0.01) between day o and day 14 but there was no significant change in the placebo group. At day 14, 65% of the patients in LR-1 were colonised with Lactobacillus reuteri and 95% in the LR-2 group. Lactobacillus reuteri was efficacious in reducing both gingivitis and plaque in patients with moderate to severe gingivitis.
The latent forms of stromelysin and collagenase from human gingival fibroblasts were purified to homogeneity. These latent proenzymes underwent serial small reductions in Mr upon activation by treatment with either … The latent forms of stromelysin and collagenase from human gingival fibroblasts were purified to homogeneity. These latent proenzymes underwent serial small reductions in Mr upon activation by treatment with either 4-aminophenylmercuric acetate or trypsin. Similar shifts in Mr and activation kinetics were observed upon identical treatments of either recombinant prostromelysin or procollagenase. Prostromelysin showed a lag between activation and Mr fall, suggesting an initial activation by conformational change. Collagenase activity was enhanced up to 12-fold by either natural or recombinant stromelysin in the presence of trypsin or 4-aminophenylmercuric acetate. Stromelysin caused a further apparent decrease in the Mr of procollagenase. Since these important connective-tissue-degrading enzymes are usually co-ordinately produced by cells, a cascade mechanism is proposed in which collagenase is activated by stromelysin.
Abstract No Abstract Available. From the Departments of Orthodontics, Pedodontics and Anatomy, Dental faculty, University of Oslo, Oslo, Norway. Abstract No Abstract Available. From the Departments of Orthodontics, Pedodontics and Anatomy, Dental faculty, University of Oslo, Oslo, Norway.
Ciclosporine-A (CSA) has been in clinical use as an immunosuppressive drug in transplant recipients for over a decade. Unfortunately, CSA also has major side-effects (including nephrotoxic ones). In an attempt … Ciclosporine-A (CSA) has been in clinical use as an immunosuppressive drug in transplant recipients for over a decade. Unfortunately, CSA also has major side-effects (including nephrotoxic ones). In an attempt to find safer agents, tacrolimus (TAC) has been introduced recently. Despite major differences in the chemical structure, TAC and CSA seem to have many effects in common. This phenomenon can be explained by the inhibition of the calcineurin pathway characteristic for both drugs. The aim of our brief review was to compare personal observations regarding side-effects encountered under CSA or TAC therapy with data reported previously. We found that the profile of side-effects both under CSA and TAC was nearly identical. In particular, morphologic changes associated with toxic drug effects in the kidney were indistinguishable from one another, i.e. tubular lesions, arteriolopathy, HUS-like changes in glomeruli and vessels. The prevalence of defined nephrotoxic lesions was very similar. Some differences were found regarding the prevalence of clinical side effects. Hypertension, hypertrichosis and gingival hyperplasia were less pronounced in the TAC group and an elevated blood glucose level in the CSA group. We conclude that TAC and CSA are closely related immunosuppressive drugs with regard to adverse effects.
This review describes the clinical status (based on available information) of experimental drugs that inhibit enzymes called proteases, or more precisely a sub-class of proteases called peptidases that catalyse the … This review describes the clinical status (based on available information) of experimental drugs that inhibit enzymes called proteases, or more precisely a sub-class of proteases called peptidases that catalyse the hydrolysis of polypeptide main chain amide bonds. These peptidases are classified by the key catalytic residue in the active site of the enzyme that effects hydrolysis, namely aspartic, serine, cysteine, metallo or threonine proteases. In this review we show structures for 108 inhibitors of these enzymes and update the clinical disposition of over 100 inhibitors that have been considered worthy enough by pharmaceutical, biotechnology or academic researchers and their financial backers to be trialed in humans as prospective medicines. We outline some of their chemical and pharmacological characteristics and compare the current status of protease inhibitors in the clinic with what was observed about 5 years ago (Leung et al, J. Med. Chem. 2000, 43, 305-341). We assess the progress of protease inhibitors into man, predict their futures, and outline some of the hurdles that have been overcome and that still remain for this promising class of new therapeutic agents. Keywords: protease, proteinase, peptidase, inhibitor, review, clinic
To study the relation between expression of the putative myofibroblast marker alpha-smooth muscle actin and the remodelling of extracellular matrix, immunocytochemical, gel electrophoresis, and collagen gel contraction studies were performed … To study the relation between expression of the putative myofibroblast marker alpha-smooth muscle actin and the remodelling of extracellular matrix, immunocytochemical, gel electrophoresis, and collagen gel contraction studies were performed on two human fibroblast subtypes. Double immunolabelling for total actins and alpha-smooth muscle (sm) actin as well as affinity labelling of filamentous and monomeric actins in gingival fibroblasts demonstrated that alpha-sm was colocalized in stress fibres and in regions with high levels of monomeric actin throughout the cytoplasm. alpha-sm comprised up to 14% of total cellular actin as assessed by 2D gel electrophoresis. Thirteen different gingival and seven different periodontal ligament fibroblast lines constitutively expressed on alpha-sm actin. These cells exhibited up to 60% inter-line variations of fluorescence due to alpha-sm actin and up to 70% and 45% inter-line variation in the rate of collagen gel contraction. Quantitative, single cell fluorimetry of alpha-sm actin immunoreactivity demonstrated a linear relation between gel contraction and alpha-sm actin (correlation coefficients of 0.71 for gingival and 0.61 for periodontal ligament cells), but there was no detectable relationship between total actin content and gel contraction. In contrast, flow cytometry demonstrated that 99% of the total gated cells from cell lines exhibiting rapid gel contraction showed alpha-sm actin staining above background fluorescence as compared to only 35% of cells with slow rates of gel contraction. Contracting collagen gels stained with FITC-phalloidin showed cells with well-developed stress fibres that were progressively more compact and elongated during the time of maximal gel contraction. To examine the dependence of gel contraction on assembly of monomeric actin into actin filaments, cells were electroporated in the presence of phalloidin or cytochalasin D. Collagen gels exhibited up to 100% inhibition of gel contraction that was dose-dependent. Gel contraction was inhibited 93% by electroinjection of cells with alpha-sm actin antibody prior to incubation, but the antibody did not inhibit actin assembly after attachment and spreading on substrates. These data indicate that gel contraction is dependent on alpha-sm actin expression and that alpha-sm actin is a functional marker for a fibroblast subtype that rapidly remodels the extracellular matrix.
Colonization or emergence of microbial pathogens may result in tissue destruction by activation of one or more of five distinct host degradative pathways (matrix metalloproteinase pathway, plasminogen‐dependent pathway, phagocytic pathway, … Colonization or emergence of microbial pathogens may result in tissue destruction by activation of one or more of five distinct host degradative pathways (matrix metalloproteinase pathway, plasminogen‐dependent pathway, phagocytic pathway, PMN‐serine proteinase pathway and osteoclastic bone resorption) or by direct cleavage of extracellular matrix constituents by microbial proteinases. Activation of endogenous destructive pathways may be mediated by immune responses resulting in expression of degradative cellular phenotypes among both immigrant and resident cell populations. In addition, expression of degradative phenotypes may be triggered by direct influences on host cells of microbial products (LPS, enzymes, toxins). A body of evidence suggests that each of these mechanisms involves local production of proinflammatory cytokines and growth factors. The matrix metalloproteinase pathway is centrally involved in dissolution of all unmineralized connective tissues and perhaps in resorption of bone as well. The matrix metalloproteinase family consists of nine or more genetically distinct Zn ++ endopeptidases which collectively cleave all of the constituents of the extracellular matrix. Recent studies have uncovered many essential elements of a complex, but still incomplete, regulatory network that governs tissue destruction. Proinflammatory cytokines and growth factors induce signalling pathways several of which are dependent on protein kinase C and result in transient expression of the transcription factors c‐jun and c‐fos. Initiation of transcription of most matrix metalloproteinase genes requires binding of the transcription factor AP‐1 (c‐jun/c‐fos) to a specific promoter sequence but attainment of maximal transcription rates is dependent on interaction with other promoter elements as well. Several matrix metalloproteinases have been detected in crevicular fluids and tissues of inflamed human gingiva as have the proinflammatory cytokines (IL‐1 and TNF‐α) which regulate their transcription. Although the mere presence of enzymes and cytokines does not necessarily impart function per se, these observations suggest that some level of spatial or temporal linkage exists between metalloproteinase/cytokine expression and gingival inflammation.
Abstract In the Medical Clinic at the University of Basle, the immunosuppressive drug cyclosporin‐A has been employed recently for kidney transplant patients. A side effect of this drug appears to … Abstract In the Medical Clinic at the University of Basle, the immunosuppressive drug cyclosporin‐A has been employed recently for kidney transplant patients. A side effect of this drug appears to be pronounced gingival enlargement. This report documents 3 such cases, with a discussion of etiology and possible treatment modalities
Background: The prevalence of gingival overgrowth induced by chronic medication with calcium channel blockers is uncertain. Although there have been several studies examining this question, the results are conflicting, with … Background: The prevalence of gingival overgrowth induced by chronic medication with calcium channel blockers is uncertain. Although there have been several studies examining this question, the results are conflicting, with previous estimates ranging from 20% to 83%. There have been only 2 studies examining the prevalence of overgrowth induced by diltiazem and amlodipine, with estimates of 74% and 3.3%, respectively. Methods: The current study aimed to address the problems associated with these studies by examining a sample of patients taking one of 3 calcium channel blockers, who were drawn from a community‐based population in northeastern England. Nine hundred eleven (911) subjects were recruited from general medical practices in the area. Of these, 442 were taking nifedipine, 181 amlodipine, and 186 diltiazem. In addition, 102 control subjects were examined. Drug and demographic data for each subject were recorded. The periodontal condition of all subjects was assessed including plaque index, papillary bleeding index, and a photograph of the anterior gingivae for subsequent analysis of overgrowth severity. Results: More than six percent (6.3%) of subjects taking nifedipine were seen to have significant overgrowth. This overgrowth was statistically greater than the amount of overgrowth seen in either of the other 2 drug groups or the control population. The prevalence of gingival overgrowth induced by amlodipine or diltiazem was not statistically significant when compared to the control group. The severity of overgrowth within the nifedipine group was found to be related to the amount of gingival inflammation and also to the gender of the subject, with males being 3 times as likely to develop overgrowth than females. Conclusions: The prevalence of clinically significant overgrowth related to chronic medication with calcium channel blockers is low, i.e., 6.3% for nifedipine. Males are 3 times as likely as females to develop clinically significant overgrowth. The presence of gingival inflammation is an important cofactor for the expression of this effect. J Periodontol 1999; 70: 63‐67.
Mandel ID: Chemotherapeutic agents for controlling plaque and gingivitis. Abstract There has been a vigorous search for many years for chemical agents that could supplement or even supplant patient‐dependent mechanical … Mandel ID: Chemotherapeutic agents for controlling plaque and gingivitis. Abstract There has been a vigorous search for many years for chemical agents that could supplement or even supplant patient‐dependent mechanical plaque control and thus reduce or prevent oral disease. 5 categories of agents or approaches have been considered: (1) broad spectrum antiseptics, (2) antibiotics aimed at specific bacteria. (3) single or combinations of enzymes that could modify plaque structure or activity, (4) non‐enzymatic dispersing or modifying agents and (5) agents that could affect bacterial attachment. The success of these approaches can be evaluated clinically by the use of standard scoring methods for measuring plaque and gingivitis and their safety established by soft tissue and microbiologic examination. Antiseptic agents have received the bulk of the attention over the years. At present, only 2 antiseptics, the bis‐biguanide, chlorhexidine gluconate (Peridox) and a combination of phenol related essential oils (Listerine). have developed sufficient supporting data in 6–month (or longer) studies to gain the approval of the Council On Dental Therapeutics of the American Dental Association. On the basis of short‐term studies, cetylpyridinium chloride, zinc and copper salts, sanguinarine and octenidine warrant continued study as does stannous fluoride at an appropriate concentration. On the basis of current research, a new generation of more specific antibacterial agents that interfere with attachment to pellicle can be developed. It is hard to predict, however, that they will affect gingivitis, at least until there is more information on what specific organisms should be targétéd.
Abstract Apical subgingival plaque samples were taken from 19 subjects exhibiting active destructive periodontal disease. The predominant cultivable Gram negative species from 50 active sites were compared to 69 inactive … Abstract Apical subgingival plaque samples were taken from 19 subjects exhibiting active destructive periodontal disease. The predominant cultivable Gram negative species from 50 active sites were compared to 69 inactive sites of comparable pocket depth and attachment level loss. Active disease sites were chosen which showed a significant loss of attachment within a two‐month interval. Proportions of Gram negative rods were higher in active periodontal disease sites than in inactive sites. Species which were found to be significantly elevated only in active sites were Bacteroides intermedius , “fusiform” Bacteroides, Actinobacillus actinomycetemcomitans , and Wolinella recta. Fuso‐hacterium nucleattum, Capnocytophaga gingivalis , and Eikenella corrodens , were found in significantly increased proportions in active sites of some subjects and inactive sites of others.
We report the primary structure and cDNA cloning of human fibroblast collagenase inhibitor, a glycoprotein that appears to play a central role in modulating the activity of a number of … We report the primary structure and cDNA cloning of human fibroblast collagenase inhibitor, a glycoprotein that appears to play a central role in modulating the activity of a number of metalloendoproteases of connective tissue origin including collagenase, gelatinase, and proteoglycanase. Secreted human fibroblast collagenase inhibitor was purified and subjected to automated Edman degradation. The secreted protein consists of 184 amino acid residues; it contains two sites of N-linked oligosaccharide linkage and six disulfide bonds. Synthetic oligonucleotide probes based on selected amino acid sequences of the inhibitor were used to screen a lambda gt10 cDNA library from a human fibroblast line. Two overlapping cDNA clones were characterized to determine the complete coding and noncoding sequences of the specific mRNA. The amino acid sequence deduced from the nucleotide sequence agrees with that determined by protein sequencing. One clone appears to contain the complete 5' end and, in addition, the cDNA sequence predicts a 23-amino acid leader peptide. The other clone represents the 3' end of the mature message and includes a short poly(A)+ tract. This 3' sequence is remarkably similar to a reported cDNA encoding part of the protein derived from mouse fibroblast poly(A)+ RNA. However, this inhibitor has no substantial homology with previously sequenced protease inhibitors.
Human gingival fibroblasts were used to study the in vitro attachment of cells to the root surface of periodontally-involved teeth. The portion of the root exposed to the disease process … Human gingival fibroblasts were used to study the in vitro attachment of cells to the root surface of periodontally-involved teeth. The portion of the root exposed to the disease process had little or no cell attachment; on the remainder of the root, the cells attached normally. Prior extraction of the roots with phenol-water or the mechanical removal of diseased cementum allowed the cells to attach normally. All things being equal, the extrapolation of these data to an in vivo situation dictates that a clinical success would depend upon complete removal of toxic materials from diseased cementum or the removal of the cementum itself.
Abstract We previously reported that low‐dose doxycycline (DOXY) therapy reduces host‐derived collagenase activity in gingival tissue of adult periodontitis (AP) patients. However, it was not clear whether this in vivo … Abstract We previously reported that low‐dose doxycycline (DOXY) therapy reduces host‐derived collagenase activity in gingival tissue of adult periodontitis (AP) patients. However, it was not clear whether this in vivo effect was direct or indirect. In the present study, inflamed human gingival tissue, obtained from AP patients during periodontal surgery, was extracted and the extracts partially purified by (NH4) 2 SO 4 precipitation. The extracts were then analyzed for collagenase activity using SDS‐PAGE/fluorography/laser densitometry, and for gelatinase activity using type I gelatin zymography as well as a new quantitative assay using biotinylated type I gelatin as substrate. DOXY was added to the incubation mixture at a final concentration of 0–1000 μM. The concentration of DOXY required to inhibit 50% of the gingival tissue collagenase (IC 50 ) was found to be 16–18 μM in the presence or absence of 1.2 mM APMA (an optimal organomercurial activator of latent procollagenases); this IC 50 for DOXY was similar to that exhibited for collagenase or matrix metalloproteinase (MMP)‐8 from polymorphonuclear leukocytes (PMNs) and from gingival crevicular fluid (GCF) of AP patients. Of interest, Porphyromonas gingivalis collagenase was also inhibited by similar DOXY levels (IC 50 = 15 μM), however the collagenase activity observed in the gingival tissue extracts was found to be of mammalian not bacterial origin based on the production of the specific α A (3/4) and α B (1/4) collagen degradation fragments. In contrast, the inhibition of collagenase purified from culture media of human gingival fibroblasts (MMP‐1) required much greater DOXY levels (IC 50 =280 μM). The predominant molecular forms of gelatinolytic activity present in the AP patients gingival tissue extracts were found to closely correspond to the 92 kD PMN‐type gelatinase (MMP‐9) although small quantities of 72 kD fibroblast‐type gelatinase (MMP‐2), and some other low molecular weight gelatinases, were also detected. The IC 50 of DOXY versus gingival tissue gelatinolytic activity was estimated at 30–50 μM measured using either type I gelatin zymography or the biotinylated type I gelatin assay. We conclude that MMPs in inflamed gingival tissue of AP patients, like those in GCF, originate primarily from infiltrating PMNs rather than resident gingival cells (fibroblasts and epithelial cells) or monocyte/macrophages, and that their pathologically‐elevated tissue‐degrading activities can be directly inhibited by pharmacologic levels of doxycycline.
<i>Porphyromonas gingivalis</i> produces arginine-specific cysteine proteinase (Arg-gingipain, RGP) and lysine-specific cysteine proteinase (Lys-gingipain, KGP) in the extracellular and cell-associated forms. Two separate genes (<i>rgpA</i> and <i>rgpB</i>) and a single gene … <i>Porphyromonas gingivalis</i> produces arginine-specific cysteine proteinase (Arg-gingipain, RGP) and lysine-specific cysteine proteinase (Lys-gingipain, KGP) in the extracellular and cell-associated forms. Two separate genes (<i>rgpA</i> and <i>rgpB</i>) and a single gene (<i>kgp</i>) have been found to encode RGP and KGP, respectively. We constructed <i>rgpA rgpB kgp</i> triple mutants by homologous recombination with cloned <i>rgp</i> and <i>kgp</i> DNA interrupted by drug resistance gene markers. The triple mutants showed no RGP or KGP activity in either cell extracts or culture supernatants. The culture supernatants of the triple mutants grown in a rich medium had no proteolytic activity toward bovine serum albumin or gelatin derived from human type I collagen. Moreover, the mutants did not grow in a defined medium containing bovine serum albumin as the sole carbon/energy source. These results indicate that the proteolytic activity of <i>P. gingivalis</i> toward bovine serum albumin and gelatin derived from human type I collagen appears to be attributable to RGP and KGP. The hemagglutinin gene <i>hagA</i> of <i>P. gingivalis</i> possesses the adhesin domain regions responsible for hemagglutination and hemoglobin binding that are also located in the C-terminal regions of <i>rgpA</i> and <i>kgp</i>. A<i>rgpA kgp hagA</i> triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for <i>P. gingivalis</i> cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.
In previous papers we have reported longitudinal re- sults of periodontal treatment based on mean values for all treated teeth,1,2 and analysis based on mean values from the half mouths … In previous papers we have reported longitudinal re- sults of periodontal treatment based on mean values for all treated teeth,1,2 and analysis based on mean values from the half mouths of patients.3These methods of analysis, however, did not reveal specifically what happened over time to pockets of various depth and attach- ment levels.
Background The purpose of this study was to assess the effect of the dose of nifedipine, a dihydropyridine calcium antagonist, on the increased risk of mortality seen in the randomized … Background The purpose of this study was to assess the effect of the dose of nifedipine, a dihydropyridine calcium antagonist, on the increased risk of mortality seen in the randomized secondary-prevention trials and to review the mechanisms by which this adverse effect might occur. Methods and Results We restricted the dose-response meta-analysis to the 16 randomized secondary-prevention trials of nifedipine for which mortality data were available. Recent trials of any calcium antagonist and formulation were also reviewed for information about the possible mechanisms of action that might increase mortality. Overall, the use of nifedipine was associated with a significant adverse effect on total mortality (risk ratio, 1.16, with a 95% CI of 1.01 to 1.33). This summary estimate fails to draw attention to an important dose-response relationship. For daily doses of 30 to 50, 60, and 80 mg, the risk ratios for total mortality were 1.06 (95% CI, 0.89 to 1.27), 1.18 (95% CI, 0.93 to 1.50), and 2.83 (95% CI, 1.35 to 5.93), respectively. In a formal test of dose response, the high doses of nifedipine were significantly associated with increased mortality ( P =.01). While the mechanism of this adverse effect is not known, there are several plausible explanations, including the established proischemic effect, negative inotropic effects, marked hypotension, recently reported prohemorrhagic effects attributed to antiplatelet and vasodilatory actions of calcium antagonists, and possibly proarrhythmic effects. Conclusions In patients with coronary disease, the use of short-acting nifedipine in moderate to high doses causes an increase in total mortality. Other calcium antagonists may have similar adverse effects, in particular those of the dihydropyridine type. Long-term safety data are lacking for most calcium antagonists.
The present article reviews, in detail, the current knowledge of the oral and dental aspects of chronic renal failure (CRF). Worldwide, increasing numbers of persons have CRF; thus, oral health … The present article reviews, in detail, the current knowledge of the oral and dental aspects of chronic renal failure (CRF). Worldwide, increasing numbers of persons have CRF; thus, oral health care staffs are increasingly likely to provide care for patients with such disease. Chronic renal failure can give rise to a wide spectrum of oral manifestations, affecting the hard or soft tissues of the mouth. The majority of affected individuals have disease that does not complicate oral health care; nevertheless, the dental management of such individuals does require that the clinician understand the multiple systems that can be affected. The clinician should also consider the adverse side-effects of drug therapy and appropriate prescribing, in view of compromised renal clearance.
Gingipains are trypsin‐like cysteine proteinases produced by Porphyromonas gingivalis , a major causative bacterium of adult periodontitis. HRgpA (95 kDa) and RgpB (50 kDa), products of 2 distinct but related … Gingipains are trypsin‐like cysteine proteinases produced by Porphyromonas gingivalis , a major causative bacterium of adult periodontitis. HRgpA (95 kDa) and RgpB (50 kDa), products of 2 distinct but related genes, rgpA and rgpB , respectively, are specific for Arg‐Xaa peptide bonds. Kgp, a product of the kgp gene, is specific for Lys‐Xaa bonds. HRgpA and Kgp are non‐covalent complexes containing separate catalytic and adhesion/hemagglutinin domains, while RgpB has only a catalytic domain with a primary structure essentially identical to that of the catalytic subunit of HRgp. HR gp A and R gp B induce vascular permeability enhancement through activation of the kallikrein/kinin pathway and activate the blood coagulation system, which, respectively, are potentially associated with gingival crevicular fluid production and progression of inflammation leading to alveolar bone loss in the periodontitis site. Kgp is the most potent fibrinogen/fibrin degrading enzyme of the 3 gingipains in human plasma and is involved in the bleeding tendency at the diseased gingiva. HRgpA activates coagulation factors and degrades fi‐brinogen/fibrin more efficiently than RgpB due to the adhesion/hemagglutinin domains, which have affinity for phospholipids and fibrinogen. Gingipains degrade macrophage CD14, thus inhibiting activation of the leukocytes through the lipopolysaccharide (LPS) receptor, and thereby facilitating sustained colonization of P. gingivalis . Gingipains play a role in bacterial housekeeping and infection, including amino acid uptake from host proteins and fimbriae maturation. Based on the important activities of gingipains in the bacterial infection and the pathogenesis of periodontitis, the bacterial proteinases can be targets for periodontal disease therapy. Immunization with RgpB, HRgpA, or a portion of HRgpA catalytic domain attenuated P. gingivalis induced disorders in mice. In addition, a trypsin‐like proteinase inhibitor retarded P. gingivalis growth specifically. Gingipains are potent virulence factors of P. gingivalis , and are likely to be associated with the development of periodontitis. It is, therefore, suggested that gingipain inhibition by vaccination and gingipain‐specific inhibitors is a useful therapy for adult periodontitis caused by P. gingivalis infection. J Periodontol 2003;74:111‐118.
The aim of this study was to assess the prevalence and extent of gingival recession, gingival bleeding, and dental calculus in United States adults, using data collected in the third … The aim of this study was to assess the prevalence and extent of gingival recession, gingival bleeding, and dental calculus in United States adults, using data collected in the third National Health and Nutrition Examination Survey (NHANES III).The study group consisted of 9,689 persons 30 to 90 years of age obtained by a stratified, multi-stage probability sampling method in 1988 to 1994. The weighted sample is representative of U.S. adults 30 years or older and represents approximately 105.8 million civilian, non-institutionalized Americans. Gingival recession, gingival bleeding, and dental calculus were assessed at the mesio-buccal and mid-buccal surfaces in 2 randomly selected quadrants, one maxillary and one mandibular. Data analysis accounted for the complex sampling design used.We estimate that 23.8 million persons have one or more tooth surfaces with > or = 3 mm gingival recession; 53.2 million have gingival bleeding; 97.1 million have calculus; and 58.3 million have subgingival calculus; and the corresponding percentages are 22.5%, 50.3%, 91.8%, and 55.1% of persons, respectively. The prevalence, extent, and severity of gingival recession increased with age, as did the prevalence of subgingival calculus and the extent of teeth with calculus and gingival bleeding. Males had significantly more gingival recession, gingival bleeding, subgingival calculus, and more teeth with total calculus than females. Of the 3 race/ethnic groups studied, non-Hispanic blacks had the highest prevalence and extent of gingival recession and dental calculus, whereas Mexican Americans had the highest prevalence and extent of gingival bleeding. Mexican Americans had similar prevalence and extent of gingival recession compared with non-Hispanic whites. Gingival recession was much more prevalent and also more severe at the buccal than the mesial surfaces of teeth. Gingival bleeding also was more prevalent at the buccal than mesial surfaces, whereas calculus was most often present at the mesial than buccal surfaces.Dental calculus, gingival bleeding, and gingival recession are common in the U.S. adult population. In addition to their unfavorable effect on esthetics and self-esteem, these conditions also are associated with destructive periodontal diseases and root caries. Appropriate measures to prevent or control these conditions are desirable, and this may also be effective in improving the oral health of the U.S. adult population.
Abstract Gingival overgrowth is a well‐documented unwanted effect, associated with phenytoin, cyclosporin. and the calcium channel blockers. The pathogenesis of drug‐induced gingival overgrowth is uncertain, and there appears to be … Abstract Gingival overgrowth is a well‐documented unwanted effect, associated with phenytoin, cyclosporin. and the calcium channel blockers. The pathogenesis of drug‐induced gingival overgrowth is uncertain, and there appears to be no unifying hypothesis that links together the 3 commonly implicated drugs. In this review, we consider a multifactorial model which expands on the interaction between drug and/or metabolite, with the gingival fibroblasts. Factors which impact upon this model include age. genetic predisposition, pharmacokinetic variables, plaque‐induced inflammatory and immunological changes and activation of growth factors. Of these, genetic factors which give rise to fibroblast heterogeneity, gingival inflammation, and pharmacokinetic variables appear to be significant in the expression of gingival overgrowth, A more thorough understanding of the pathogenesis of this unwanted effect will hopefully elucidate appropriate mechanisms for its control.
Abstract Background/Aims: Drug‐induced gingival overgrowth remains a significant problem for the periodontologist. Many patients medicated with the drugs implicated in this unwanted effect experience significant, recurrent gingival problems that require … Abstract Background/Aims: Drug‐induced gingival overgrowth remains a significant problem for the periodontologist. Many patients medicated with the drugs implicated in this unwanted effect experience significant, recurrent gingival problems that require repeated surgical excisions. In this review, we attempt to identify and quantify the various “risk factors” associated with both the development and expression of the drug‐induced gingival changes. Method: The risk factors appraised include age, sex, drug variables, concomitant medication, periodontal variables and genetic factors. Elucidation of such factors may help to identify “at risk patients” and then develop appropriate treatment strategies. Results: Of the factors identified, the only one that can be affected by the periodontologist is the patents' periodontal condition. However, drug variables and concomitant medication do impact upon the expression of gingival overgrowth. Conclusion: The identificatioin of risk factors associated with both the prevalence and severity of drug‐induced gingival overgrowth is important for all parties involved with this unwanted effect. Both periodontologist and patient have an important rôle to play in improving oral hygiene and gingival health. Likewise, there is always an opportinity to establish a close liaison between the patient's physician and the periodontologist to try and identify alternative drug regimens that can help reduce the impact of this unwanted effect.
Gingival diseases are a diverse family of complex and distinct pathological entities found within the gingiva that are the result of a variety of etiologies. There are several clinical characteristics … Gingival diseases are a diverse family of complex and distinct pathological entities found within the gingiva that are the result of a variety of etiologies. There are several clinical characteristics common to all gingival diseases and these features include clinical signs of inflammation, signs and symptoms that are confined to the gingiva, reversibility of the disease by removing the etiology, the presence of bacterial laden plaque to initiate and/or exacerbate the severity of the disease and a possible role as a precursor for attachment loss around teeth. Defining and classifying gingival diseases has not been an easy task. The tools and methods to identify gingival diseases have varied depending on the criteria used by epidemiologists, researchers, or the practicing clinician. The classification of gingival disease in this review relied upon experimental and/or epidemiological human studies that accurately and reliably assessed an underlying functional derangement that was localized to the gingiva and was reported in a peer-reviewed journal. The classification of gingival diseases that depends on dental plaque to initiate the disease process(es) has been categorized into two groups. The two categories of plaque-induced gingival diseases are those affected by local factors and those that are affected by local factors and modified by specific systemic factors found in the host. In this review, the clinical characteristics of gingival disease associated with plaque, endogenous hormone fluctuations, drugs, systemic diseases, and malnutrition were investigated.
We carried out a placebo-controlled, double-blind, randomized study of the hemostatic effect of tranexamic acid mouthwash after oral surgery in 39 patients receiving anticoagulant agents because of the presence of … We carried out a placebo-controlled, double-blind, randomized study of the hemostatic effect of tranexamic acid mouthwash after oral surgery in 39 patients receiving anticoagulant agents because of the presence of cardiac valvular stenosis, a prosthetic cardiac valve, or a vascular prosthesis. Surgery was performed with no change in the level of anticoagulant therapy, and treatment with the anticoagulant agent was continued after surgery. Before it was sutured, the operative field was irrigated in 19 patients with 10 ml of a 4.8 percent aqueous solution of tranexamic acid (an inhibitor of fibrinolysis) and in 20 patients with a placebo solution. For seven days thereafter, patients were instructed to rinse their mouths with 10 ml of the assigned solution for two minutes four times a day. There were no significant differences between the two treatment groups in base-line variables, including the level of anticoagulation at the time of surgery. Eight patients in the placebo group had a total of 10 postoperative bleeding episodes, whereas only 1 patient in the tranexamic acid group had a bleeding episode (P = 0.01). There were no systemic side effects. We conclude that local antifibrinolytic therapy is effective in preventing bleeding after oral surgery in patients who are being treated with anticoagulants.
A series of 20 cases of megacolon with spasm of the rectosigmoid in children is reported. Ovar Swenson was on staff at Boston Children's Hospital and had been treating many … A series of 20 cases of megacolon with spasm of the rectosigmoid in children is reported. Ovar Swenson was on staff at Boston Children's Hospital and had been treating many children with Hirschsprung's disease as well as performing colonic manometric studies on a number. He describes one key case, a six-year-old boy where he used a diverting colostomy, which 'cured' the child and was unable to show any sign of peristalsis in the distal limb. Barium studies invariably showed the distal segmental contractions right down to the anus. Barium studies invariably showed distal segmental contractions right down to the anus.
Abstract Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival … Abstract Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non‐periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored. Two broad categories of gingival diseases include non‐dental plaque biofilm–induced gingival diseases and dental plaque‐induced gingivitis. Non‐dental plaque biofilm‐induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque‐induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque‐induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non‐periodontitis patient or in a currently stable “periodontitis patient” i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced). A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1), and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis. Precision dental medicine defines a patient‐centered approach to care, and therefore, creates differences in the way in which a “case” of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations.
Abstract Objective This review proposes revisions to the current classification system for gingival diseases and provides a rationale for how it differs from the 1999 classification system. Importance Gingival inflammation … Abstract Objective This review proposes revisions to the current classification system for gingival diseases and provides a rationale for how it differs from the 1999 classification system. Importance Gingival inflammation in response to bacterial plaque accumulation (microbial biofilms) is considered the key risk factor for the onset of periodontitis. Thus, control of gingival inflammation is essential for the primary prevention of periodontitis. Findings The clinical characteristics common to dental plaque–induced inflammatory gingival conditions include: a) clinical signs and symptoms of inflammation that are confined to the gingiva: b) reversibility of the inflammation by removing or disrupting the biofilm; c) the presence of a high bacterial plaque burden to initiate the inflammation; d) systemic modifying factors (e.g., hormones, systemic disorders, drugs) which can alter the severity of the plaque‐induced inflammation and; e) stable (i.e., non‐changing) attachment levels on a periodontium which may or may not have experienced a loss of attachment or alveolar bone. The simplified taxonomy of gingival conditions includes: 1) introduction of the term “incipient gingivitis;” 2) a description of the extent and severity of gingival inflammation; 3) a description of the extent and severity of gingival enlargement and; 4) a reduction of categories in the dental plaque–induced gingival disease taxonomy. Conclusions Dental plaque–induced gingival inflammation is modified by various systemic and oral factors. The appropriate intervention is crucial for the prevention of periodontitis.
Abstract Objective Clinical gingival inflammation is a well‐defined site‐specific condition for which several measurement systems have been proposed and validated, and epidemiological studies consistently indicate its high prevalence globally. However, … Abstract Objective Clinical gingival inflammation is a well‐defined site‐specific condition for which several measurement systems have been proposed and validated, and epidemiological studies consistently indicate its high prevalence globally. However, it is clear that defining and grading a gingival inflammatory condition at a site level (i.e. a “gingivitis site”) is completely different from defining and grading a “gingivitis case” (GC) (i.e. a patient affected by gingivitis), and that a “gingivitis site” does not necessarily mean a “GC”. The purpose of the present review is to summarize the evidence on clinical, biochemical, microbiologic, genetic markers as well as symptoms associated with plaque‐induced gingivitis and to propose a set of criteria to define GC. Importance A universally accepted case definition for gingivitis would provide the necessary information to enable oral health professionals to assess the effectiveness of their prevention strategies and treatment regimens; help set priorities for therapeutic actions/programs by health care providers; and undertake surveillance. Findings Based on available methods to assess gingival inflammation, GC could be simply, objectively and accurately identified and graded using bleeding on probing score (BOP%) Conclusions A patient with intact periodontium would be diagnosed as a GC according to a BOP score ≥ 10%, further classified as localized (BOP score ≥ 10% and ≤30%) or generalized (BOP score &gt; 30%). The proposed classification may also apply to patients with a reduced periodontium, where a GC would characterize a patient with attachment loss and BOP score ≥ 10%, but without BOP in any site probing ≥4 mm in depth.
Abstract Objective This review proposes revisions to the current classification system for gingival diseases and provides a rationale for how it differs from the 1999 classification system. Importance Gingival inflammation … Abstract Objective This review proposes revisions to the current classification system for gingival diseases and provides a rationale for how it differs from the 1999 classification system. Importance Gingival inflammation in response to bacterial plaque accumulation (microbial biofilms) is considered the key risk factor for the onset of periodontitis. Thus, control of gingival inflammation is essential for the primary prevention of periodontitis. Findings The clinical characteristics common to dental plaque–induced inflammatory gingival conditions include: a) clinical signs and symptoms of inflammation that are confined to the gingiva: b) reversibility of the inflammation by removing or disrupting the biofilm; c) the presence of a high bacterial plaque burden to initiate the inflammation; d) systemic modifying factors (e.g., hormones, systemic disorders, drugs) which can alter the severity of the plaque‐induced inflammation and; e) stable (i.e., non‐changing) attachment levels on a periodontium which may or may not have experienced a loss of attachment or alveolar bone. The simplified taxonomy of gingival conditions includes: 1) introduction of the term “incipient gingivitis;” 2) a description of the extent and severity of gingival inflammation; 3) a description of the extent and severity of gingival enlargement and; 4) a reduction of categories in the dental plaque–induced gingival disease taxonomy. Conclusions Dental plaque–induced gingival inflammation is modified by various systemic and oral factors. The appropriate intervention is crucial for the prevention of periodontitis.
Abstract Objective Clinical gingival inflammation is a well‐defined site‐specific condition for which several measurement systems have been proposed and validated, and epidemiological studies consistently indicate its high prevalence globally. However, … Abstract Objective Clinical gingival inflammation is a well‐defined site‐specific condition for which several measurement systems have been proposed and validated, and epidemiological studies consistently indicate its high prevalence globally. However, it is clear that defining and grading a gingival inflammatory condition at a site level (i.e. a “gingivitis site”) is completely different from defining and grading a “gingivitis case” (GC) (i.e. a patient affected by gingivitis), and that a “gingivitis site” does not necessarily mean a “GC”. The purpose of the present review is to summarize the evidence on clinical, biochemical, microbiologic, genetic markers as well as symptoms associated with plaque‐induced gingivitis and to propose a set of criteria to define GC. Importance A universally accepted case definition for gingivitis would provide the necessary information to enable oral health professionals to assess the effectiveness of their prevention strategies and treatment regimens; help set priorities for therapeutic actions/programs by health care providers; and undertake surveillance. Findings Based on available methods to assess gingival inflammation, GC could be simply, objectively and accurately identified and graded using bleeding on probing score (BOP%) Conclusions A patient with intact periodontium would be diagnosed as a GC according to a BOP score ≥ 10%, further classified as localized (BOP score ≥ 10% and ≤30%) or generalized (BOP score &gt; 30%). The proposed classification may also apply to patients with a reduced periodontium, where a GC would characterize a patient with attachment loss and BOP score ≥ 10%, but without BOP in any site probing ≥4 mm in depth.
Tightness engineering has evolved as an efficient strategy for the design of knotted, woven, and entangled molecules and materials with desired properties and functions since tightness is a primary parameter … Tightness engineering has evolved as an efficient strategy for the design of knotted, woven, and entangled molecules and materials with desired properties and functions since tightness is a primary parameter that determines the property of a knotted strand. However, as an attractive topic that inspires mathematicians, physicists, chemists, and biologists, whether the smallest knot is exactly the tightest one remains unaddressed experimentally. To tackle this challenge, a series of organic trefoil knots with the backbone‐atom as short as 70 have been successfully synthesized by developing a new modular self‐assembly approach in this study. To our great surprise, with the help of gradient tandem mass spectrometry, the quantitative tightness evaluation suggested that the molecular trefoil knot with a backbone crossing ratio (BCR) of 24.0 is even tighter than the one with a BCR of 23.3 (i.e. the smallest organic trefoil knot with the shortest ropelength synthesized so far), thus demonstrating an unexpected yet interesting odd‐even effect to enhance the understanding of the tightness regulation of molecular knots.
Mst Mostary Zannath | International Journal of Oral and Maxillofacial Surgery
H. El-Awour | International Journal of Oral and Maxillofacial Surgery

Ciclosporin

2025-06-21
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Blepharocheilodontic syndrome is a rare autosomal dominant disorder characterized by craniofacial anomalies. Bilateral cleft lip/palate, dental agenesis, and eyelid malformations are usually present in individuals with this condition; however, hypothyroidism … Blepharocheilodontic syndrome is a rare autosomal dominant disorder characterized by craniofacial anomalies. Bilateral cleft lip/palate, dental agenesis, and eyelid malformations are usually present in individuals with this condition; however, hypothyroidism or joyful agenesis and imperforate anus frame unusual phenotypic features. Objective: The aim of this systematic review was to create a current overview of blepharocheilodontic syndrome (BCD) through a case report. Methods: It was prepared according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines with the Prospective Prior International Registry of Systematic Reviews (PROSPERO). Updated scientific data were generally obtained from PubMed, Medline, Embase, Researchgate, Lilacs, Proquest, Google Scholar, Epistemonikos, Springer, ScienceDirect, Scielo, Ovid, Taylor&amp;Francis, Cochrane, Scientific Reports, UNA Discovery Service, Web of Science, Orphanet, ACPA, Dynamed, Dialnet, EBSPCO, and WebMD. The quality of evidence of the included articles was assessed using the Cochrane risk of bias tool. Results: A total of 296 articles were identified after the initial search and 129 duplicate articles were excluded after the first screening. Of the 167 papers screened by title and abstract, 22 met the parameters of the eligibility criteria. Conclusions: It is difficult to establish exact conclusions about CBD syndrome, the genetic origin and the dental and medical care guidelines are still under discussion and hardly detailed in the literature found, so the authors recommend caution in the results and the clinical-therapeutic follow-up of the published cases.
Introdução: O queratoquisto odontogênico (QO) é uma lesão cística de origem epitelial, frequentemente associada à síndrome de Gorlin. Apresenta crescimento agressivo e recorrência significativa após a enucleação convencional. A marsupialização … Introdução: O queratoquisto odontogênico (QO) é uma lesão cística de origem epitelial, frequentemente associada à síndrome de Gorlin. Apresenta crescimento agressivo e recorrência significativa após a enucleação convencional. A marsupialização tem sido utilizada como alternativa terapêutica para reduzir o tamanho do cisto antes da remoção definitiva. Este estudo apresenta um caso clínico de marsupialização de QO em região posterior de mandíbula. Este relato descreve o manejo clínico de um queratoquisto odontogênico por meio da técnica de marsupialização, avaliando os resultados em termos de redução volumétrica da lesão e preservação de estruturas anatômicas adjacentes. Metodologia: Esta revisão de literatura foi realizada com base em artigos científicos dispostos nas bases de dados MEDLINE via PubMed (Medical Literature Analysis and Retrieval System Online), LILACS (Literatura Latino-Americana e do Caribe em Ciências da Saúde) e Biblioteca Virtual em Saúde (BVS). Para a seleção dos estudos foram utilizados, como critérios de inclusão, artigos que estivessem dentro da abordagem temática, disponíveis na íntegra e de forma gratuita, nos idiomas inglês, português e espanhol. Como parâmetros de exclusão foram retirados artigos duplicados e que fugiam do tema central da pesquisa. Relato: Paciente do sexo masculino, 25 anos, compareceu ao Serviço de Saúde com aumento de volume indolor na região posterior de mandíbula. Foi solicitada a tomografia computadorizada, na qual revelou uma lesão hipodensa extensa. Optou-se pela marsupialização, criando uma comunicação entre o cisto e a cavidade oral, permitindo a drenagem contínua. O paciente foi monitorado por seis meses. Resultados: A marsupialização resultou em significativa redução do tamanho do cisto, permitindo posterior enucleação conservadora. Não houve comprometimento de estruturas nobres e o acompanhamento radiográfico demonstrou mínima recorrência após um ano. Conclusão: A marsupialização demonstrou ser uma abordagem eficaz para a redução volumétrica do QO, facilitando sua remoção definitiva e minimizando danos ósseos. Essa técnica pode ser considerada uma alternativa segura para o manejo de lesões extensas, reduzindo o risco de complicações pós-operatórias.
Recently, exercise physiology research has focused on optimizing athletic performance, emphasizing the importance of dietary supplementation and nutritional management. A notable strategy gaining prominence is mouth rinsing with solutions containing … Recently, exercise physiology research has focused on optimizing athletic performance, emphasizing the importance of dietary supplementation and nutritional management. A notable strategy gaining prominence is mouth rinsing with solutions containing carbohydrates, caffeine, and other substances, a simple approach that avoids gastrointestinal and psychological complications associated with liquid ingestion. While preliminary evidence suggests benefits such as increased endurance and reduced fatigue in elite athletes, there is a notable discrepancy between studies reporting efficacy, creating gaps in the literature. This integrative review sought to investigate the effects of mouth rinsing in athletes, spanning various sports modalities and providing practical insights for athletes, coaches, and healthcare professionals. The methodology included an extensive search in specific databases, resulting in 20 selected studies for discussion. The results highlighted that mouth rinsing with carbohydrates can enhance performance in endurance exercises, while mouth rinsing with caffeine showed positive effects, especially in high intensity and short-duration activities. The review emphasized the influence of different protocols, substances used, types of exercises, and assessment criteria on the heterogeneity of results. Despite variability, a thorough understanding of these interventions holds potential for personalized and effective strategies in enhancing athletic performance. The conclusion underscores the need for further research to fully elucidate the effects and mechanisms of these interventions, addressing future perspectives in this dynamic field.
To investigate the oral microbiome and metabolome longitudinal changes associated with orthodontic treatment-induced gingival enlargement (OT-GE). Twenty-six subjects were divided into case and control groups based on the gingival overgrowth … To investigate the oral microbiome and metabolome longitudinal changes associated with orthodontic treatment-induced gingival enlargement (OT-GE). Twenty-six subjects were divided into case and control groups based on the gingival overgrowth index (GOi). The OT-GE group was divided into the no gingival enlargement (OT-GE0, n = 5) and persistent gingival enlargement (OT-GE1, n = 11). The control group included orthodontic treatment periodontal health (OT-GH, n = 5), and no orthodontic treatment periodontal health (NOT-GH, n = 5). Microbial composition and metabolites in saliva were investigated using cross-omics. Longitudinal analysis linked orthodontic treatment-induced gingival enlargement to distinct oral microbiome and metabolome shifts. The OT-GE group showed significantly higher bleeding on probing (BOP), plaque scores (p < 0.001), probing depth, GOi, and ligature wire differences (p < 0.05) versus controls. Microbial diversity and species richness were elevated in OT-GE (p < 0.05), though no differences emerged between OT-GE0 and OT-GE1) subgroup (p > 0.05). Cross-omics identified specific periodontal pathogens and metabolites linked to gingival enlargement. Disrupted amino acid biosynthesis pathways, particularly citrulline metabolism, correlated with functional gene dysregulation and microbial imbalance. Aberrant citrulline intake appeared to drive dysbiosis, potentially contributing to gingival overgrowth. OT-GE pathogenesis involves functional gene-regulated metabolite metabolism influencing periodontal pathogens.
To critically evaluate the recently published INfORM/IADR consensus paper containing ten key points for good clinical practice in the management of patients with temporomandibular disorders. After perusing the text of … To critically evaluate the recently published INfORM/IADR consensus paper containing ten key points for good clinical practice in the management of patients with temporomandibular disorders. After perusing the text of the document, followed by intensive discussion, the 10 key points were carefully analyzed and commented. Two key points could be replaced by other (clinically relevant) statements. In addition to terminologically and semantically imprecise formulations some verbal descriptions remain superficial and vague. While no distinction was made between acute and chronic TMDs, the INfORM/IADR author group differentiates between first-line and second-line therapeutic modalities without explaining the rationale for such a classification. Furthermore, no medication recommendations were made. We anticipate that the INfORM/IADR publication will have a beneficial impact on the care of TMD patients. However, in our opinion, a reflection on some of the contents of the 10-point document seems justified in order to reduce the risk of misinterpretation of some statements, which could lead to inappropriate diagnostic and therapeutic measures.
This study explores the physiology of TM7, a mysterious microbe, in preventing gum disease. A literature review of 42 articles examines TM7's interactions with other microbes, deeming the microbe's behavior … This study explores the physiology of TM7, a mysterious microbe, in preventing gum disease. A literature review of 42 articles examines TM7's interactions with other microbes, deeming the microbe's behavior could help modulate pathogenic bacteria in the oral cavity as a probiotic.
Gingival and periodontal diseases, such as gingivitis and periodontitis, were among the substantial threats to oral health that could cause serious health risks if not addressed in time. Timely and … Gingival and periodontal diseases, such as gingivitis and periodontitis, were among the substantial threats to oral health that could cause serious health risks if not addressed in time. Timely and accurately assessing the patient's condition was important in effectively controlling and preventing further injury to the oral cavity. This study aimed to review the literature on using convolutional neural networks (CNN) and other deep learning methods in diagnosing gingival diseases. Different studies reviewed in the literature analyzed images of teeth and gums through CNN models VGG16, Sequential, MobileNet, and InceptionV3, also classified using X-rays and Photographs of histopathological samples. The results of this study provided that these AI tools described were effective in classifying cases of gingivitis, periodontitis, dental caries, and tooth restorations at accuracies of between 75%-95%. Also, the article reviewed the basic elements of the CNNs architecture, such as convolutional layers, pooling layers, fully connected layers, activation mechanisms, and optimization methods. Such principles were fundamental in building better and more accurate gingival disease classification models. The findings of this research underscored the significant potential of leveraging AI and deep learning technologies to assist healthcare professionals in the early detection and effective management of gingival diseases. Implementing AI-powered diagnostic tools could revolutionize dental care by enabling more efficient, accurate, and accessible disease identification, ultimately leading to improved oral health outcomes for patients.
Patients with periodontitis are significantly more prone for undetected diabetes mellitus (DM). Gingival crevicular blood (GCB), which oozes during periodontal examination, can be utilized for screening DM patients. Therefore, it … Patients with periodontitis are significantly more prone for undetected diabetes mellitus (DM). Gingival crevicular blood (GCB), which oozes during periodontal examination, can be utilized for screening DM patients. Therefore, it is of interest to compare the efficacy of GCB with capillary finger prick blood (CFB). A strong positive correlation was observed in CFB and GCB with ‘r’ values of 0.93 suggestive of highly statistically significant (P&lt;0.0001).
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