Aggressive Periodontitis: Inflammation and loss of PERIODONTIUM that is characterized by rapid attachment loss and bone destruction in the presence of little local factors such as DENTAL PLAQUE and DENTAL CALCULUS. This highly destructive form of periodontitis often occurs in young people and was called early-onset periodontitis, but this disease also appears in old people.Periodontitis: Inflammation and loss of connective tissues supporting or surrounding the teeth. This may involve any part of the PERIODONTIUM. Periodontitis is currently classified by disease progression (CHRONIC PERIODONTITIS; AGGRESSIVE PERIODONTITIS) instead of age of onset. (From 1999 International Workshop for a Classification of Periodontal Diseases and Conditions, American Academy of Periodontology)Chronic Periodontitis: Chronic inflammation and loss of PERIODONTIUM that is associated with the amount of DENTAL PLAQUE or DENTAL CALCULUS present. Chronic periodontitis occurs mostly in adults and was called adult periodontitis, but this disease can appear in young people.Periodontal Pocket: An abnormal extension of a gingival sulcus accompanied by the apical migration of the epithelial attachment and bone resorption.Periodontal Attachment Loss: Loss or destruction of periodontal tissue caused by periodontitis or other destructive periodontal diseases or by injury during instrumentation. Attachment refers to the periodontal ligament which attaches to the alveolar bone. It has been hypothesized that treatment of the underlying periodontal disease and the seeding of periodontal ligament cells enable the creating of new attachment.Dental Scaling: Removal of dental plaque and dental calculus from the surface of a tooth, from the surface of a tooth apical to the gingival margin accumulated in periodontal pockets, or from the surface coronal to the gingival margin.Aggregatibacter actinomycetemcomitans: A species of Gram-negative, facultatively anaerobic spherical or rod-shaped bacteria indigenous to dental surfaces. It is associated with PERIODONTITIS; BACTERIAL ENDOCARDITIS; and ACTINOMYCOSIS.Periodontal Index: A numerical rating scale for classifying the periodontal status of a person or population with a single figure which takes into consideration prevalence as well as severity of the condition. It is based upon probe measurement of periodontal pockets and on gingival tissue status.Gingival Crevicular Fluid: A fluid occurring in minute amounts in the gingival crevice, believed by some authorities to be an inflammatory exudate and by others to cleanse material from the crevice, containing sticky plasma proteins which improve adhesions of the epithelial attachment, have antimicrobial properties, and exert antibody activity. (From Jablonski, Illustrated Dictionary of Dentistry, 1982)Dental Plaque Index: An index which scores the degree of dental plaque accumulation.Root Planing: A procedure for smoothing of the roughened root surface or cementum of a tooth after subgingival curettage or scaling, as part of periodontal therapy.Gingival Hemorrhage: The flowing of blood from the marginal gingival area, particularly the sulcus, seen in such conditions as GINGIVITIS, marginal PERIODONTITIS, injury, and ASCORBIC ACID DEFICIENCY.Pasteurellaceae: A family of coccoid to rod-shaped nonsporeforming, gram-negative, nonmotile, facultatively anaerobic bacteria that includes the genera ACTINOBACILLUS; HAEMOPHILUS; MANNHEIMIA; and PASTEURELLA.Gingiva: Oral tissue surrounding and attached to TEETH.Occlusal Adjustment: Selective grinding of occlusal surfaces of the teeth in an effort to eliminate premature contacts and occlusal interferences; to establish optimal masticatory effectiveness, stable occlusal relationships, direction of main occlusal forces, and efficient multidirectional patterns, to improve functional relations and to induce physiologic stimulation of the masticatory system; to eliminate occlusal trauma; to eliminate abnormal muscle tension; to aid in the stabilization of orthodontic results; to treat periodontal and temporomandibular joint problems; and in restorative procedures. (From Jablonski, Dictionary of Dentistry, 1992)Alveolar Bone Loss: Resorption or wasting of the tooth-supporting bone (ALVEOLAR PROCESS) in the MAXILLA or MANDIBLE.Dental Plaque: A film that attaches to teeth, often causing DENTAL CARIES and GINGIVITIS. It is composed of MUCINS, secreted from salivary glands, and microorganisms.Gingivitis: Inflammation of gum tissue (GINGIVA) without loss of connective tissue.Selenomonas: Curved bacteria, usually crescent-shaped rods, with ends often tapered, occurring singly, in pairs, or short chains. They are non-encapsulated, non-sporing, motile, and ferment glucose. Selenomonas are found mainly in the human buccal cavity, the rumen of herbivores, and the cecum of pigs and several rodents. (From Bergey's Manual of Determinative Bacteriology, 9th ed)Subgingival Curettage: Removal of degenerated and necrotic epithelium and underlying connective tissue of a periodontal pocket in an effort to convert a chronic ulcerated wound to an acute surgical wound, thereby insuring wound healing and attachment or epithelial adhesion, and shrinkage of the marginal gingiva. The term is sometimes used in connection with smoothing of a root surface or ROOT PLANING. (Jablonski; Illustrated Dictionary of Dentistry, 1982)Periodontium: The structures surrounding and supporting the tooth. Periodontium includes the gum (GINGIVA), the alveolar bone (ALVEOLAR PROCESS), the DENTAL CEMENTUM, and the PERIODONTAL LIGAMENT.Porphyromonas gingivalis: A species of gram-negative, anaerobic, rod-shaped bacteria originally classified within the BACTEROIDES genus. This bacterium produces a cell-bound, oxygen-sensitive collagenase and is isolated from the human mouth.Prevotella intermedia: A species of gram-negative, anaerobic, rod-shaped bacteria originally classified within the BACTEROIDES genus. This bacterium is a common commensal in the gingival crevice and is often isolated from cases of gingivitis and other purulent lesions related to the mouth.Periapical Periodontitis: Inflammation of the PERIAPICAL TISSUE. It includes general, unspecified, or acute nonsuppurative inflammation. Chronic nonsuppurative inflammation is PERIAPICAL GRANULOMA. Suppurative inflammation is PERIAPICAL ABSCESS.Actinobacillus Infections: Infections with bacteria of the genus ACTINOBACILLUS.Periodontal Debridement: Removal or disruption of DENTAL DEPOSITS and plaque-retentive DENTAL CALCULUS from tooth surfaces and within the periodontal pocket space without deliberate removal of CEMENTUM as done in ROOT PLANING and often in DENTAL SCALING. The goal is to conserve dental cementum to help maintain or re-establish healthy periodontal environment and eliminate PERIODONTITIS by using light instrumentation strokes and nonsurgical techniques (e.g., ultrasonic, laser instruments).Fibromatosis, Gingival: Generalized or localized diffuse fibrous overgrowth of the gingival tissue, usually transmitted as an autosomal dominant trait, but some cases are idiopathic and others produced by drugs. The enlarged gingiva is pink, firm, and has a leather-like consistency with a minutely pebbled surface and in severe cases the teeth are almost completely covered and the enlargement projects into the oral vestibule. (Dorland, 28th ed)Bacteroides: A genus of gram-negative, anaerobic, rod-shaped bacteria. Its organisms are normal inhabitants of the oral, respiratory, intestinal, and urogenital cavities of humans, animals, and insects. Some species may be pathogenic.Metronidazole: A nitroimidazole used to treat AMEBIASIS; VAGINITIS; TRICHOMONAS INFECTIONS; GIARDIASIS; ANAEROBIC BACTERIA; and TREPONEMAL INFECTIONS. It has also been proposed as a radiation sensitizer for hypoxic cells. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985, p133), this substance may reasonably be anticipated to be a carcinogen (Merck, 11th ed).Amoxicillin: A broad-spectrum semisynthetic antibiotic similar to AMPICILLIN except that its resistance to gastric acid permits higher serum levels with oral administration.Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.Bacteroidaceae Infections: Infections with bacteria of the family BACTEROIDACEAE.Exotoxins: Toxins produced, especially by bacterial or fungal cells, and released into the culture medium or environment.Statistics, Nonparametric: A class of statistical methods applicable to a large set of probability distributions used to test for correlation, location, independence, etc. In most nonparametric statistical tests, the original scores or observations are replaced by another variable containing less information. An important class of nonparametric tests employs the ordinal properties of the data. Another class of tests uses information about whether an observation is above or below some fixed value such as the median, and a third class is based on the frequency of the occurrence of runs in the data. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1284; Corsini, Concise Encyclopedia of Psychology, 1987, p764-5)Interleukin-1beta: An interleukin-1 subtype that is synthesized as an inactive membrane-bound pro-protein. Proteolytic processing of the precursor form by CASPASE 1 results in release of the active form of interleukin-1beta from the membrane.Periodontal Diseases: Pathological processes involving the PERIODONTIUM including the gum (GINGIVA), the alveolar bone (ALVEOLAR PROCESS), the DENTAL CEMENTUM, and the PERIODONTAL LIGAMENT.Treponema denticola: A species of bacteria in the family SPIROCHAETACEAE, frequently isolated from periodontal pockets (PERIODONTAL POCKET).Polymorphism, Single Nucleotide: A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the MAJOR HISTOCOMPATIBILITY COMPLEX.Tooth Loss: The failure to retain teeth as a result of disease or injury.Bacterial Processes: The functions, behavior, and activities of bacteria.IgA Deficiency: A dysgammaglobulinemia characterized by a deficiency of IMMUNOGLOBULIN A.Dysgammaglobulinemia: An immunologic deficiency state characterized by selective deficiencies of one or more, but not all, classes of immunoglobulins.Streptococcus mutans: A polysaccharide-producing species of STREPTOCOCCUS isolated from human dental plaque.Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp.Saliva: The clear, viscous fluid secreted by the SALIVARY GLANDS and mucous glands of the mouth. It contains MUCINS, water, organic salts, and ptylin.Dental Research: The study of laws, theories, and hypotheses through a systematic examination of pertinent facts and their interpretation in the field of dentistry. (From Jablonski, Illustrated Dictionary of Dentistry, 1982, p674)Periodontics: A dental specialty concerned with the histology, physiology, and pathology of the tissues that support, attach, and surround the teeth, and of the treatment and prevention of disease affecting these tissues.Dental Implantation: The grafting or inserting of a prosthetic device of alloplastic material into the oral tissue beneath the mucosal or periosteal layer or within the bone. Its purpose is to provide support and retention to a partial or complete denture.Dental Implants: Biocompatible materials placed into (endosseous) or onto (subperiosteal) the jawbone to support a crown, bridge, or artificial tooth, or to stabilize a diseased tooth.Dental Implants, Single-Tooth: Devices, usually alloplastic, surgically inserted into or onto the jawbone, which support a single prosthetic tooth and serve either as abutments or as cosmetic replacements for missing teeth.Guided Tissue Regeneration, Periodontal: Techniques for enhancing and directing cell growth to repopulate specific parts of the PERIODONTIUM that have been damaged by PERIODONTAL DISEASES; TOOTH DISEASES; or TRAUMA, or to correct TOOTH ABNORMALITIES. Repopulation and repair is achieved by guiding the progenitor cells to reproduce in the desired location by blocking contact with surrounding tissue by use of membranes composed of synthetic or natural material that may include growth inducing factors as well.
Humoral immune responses in periodontal disease may have mucosal and systemic immune features. (1/126)
The humoral immune response, especially IgG and IgA, is considered to be protective in the pathogenesis of periodontal disease, but the precise mechanisms are still unknown. Immunoglobulins arriving at the periodontal lesion are from both systemic and local tissue sources. In order to understand better the local immunoglobulin production, we examined biopsy tissue from periodontitis lesions for the expression of IgM, IgG, IgA, IgE and in addition the IgG and IgA subclasses and J-chain by in situ hybridization. Tissues examined were superficial inflamed gingiva and the deeper granulation tissue from periodontal sites. These data confirm that IgM, and IgG and IgA subclass proteins and J-chain can be locally produced in the periodontitis tissues. IgG1 mRNA-expressing cells were predominant in the granulation tissues and in the gingiva, constituting approx. 65% of the total IgG-expressing plasma cells. There was a significantly increased proportion of IgA-expressing plasma cells in the gingiva compared with the granulation tissue (P < 0.01). Most of the IgA-expressing plasma cells were IgA1, but a greater proportion expressed IgA2 mRNA and J-chain mRNA in the gingival tissues (30.5% and 7.5%, respectively) than in the periodontal granulation tissues (19% and 0-4%, respectively). The J-chain or dimeric IgA2-expressing plasma cells were located adjacent to the epithelial cells, suggesting that this tissue demonstrates features consistent with a mucosal immune response. Furthermore, we were able to detect the secretory component in gingival and junctional epithelial cells, demonstrating that the periodontal epithelium shares features with mucosal epithelium. In contrast, deeper tissues had more plasma cells that expressed IgM, and less expressing IgA, a response which appears more akin to the systemic immune response. In conclusion, this study suggests that immune mechanisms involved in the pathogenesis of periodontitis may involve features of both the mucosal and systemic immune systems, dependent on tissue location. (+info)Neutrophil dysfunctions, IL-8, and soluble L-selectin plasma levels in rapidly progressive versus adult and localized juvenile periodontitis: variations according to disease severity and microbial flora. (2/126)
We used flow cytometry to analyze the expression of adhesion molecules and the oxidative burst of whole-blood polymorphonuclear neutrophils (PMN) from 26 patients with periodontitis. Three different clinical entities were studied: adult periodontitis (AP), localized juvenile periodontitis (LJP), and rapidly progressive periodontitis (RPP). Unstimulated PMN from the patients showed reduced Lewis x, sialyl-Lewis x, and L-selectin expression relative to those from healthy control subjects. These alterations were present whatever the severity of periodontal disease. However, PMN from RPP patients showed increased basal H2O2 production and decreased L-selectin shedding. These latter impairments, which correlated with increased IL-8 plasma levels, could contribute to initial vascular damage. In addition, decreased IL-8 priming of H2O2 production by PMN from RPP patients could account for a lower bactericidal capacity of PMN, leading to the large number of bacteria in the subgingival region of RPP patients. Soluble L-selectin plasma levels were also decreased in the RPP group, indicating more severe or diffuse endothelial damage. These abnormalities were not found in the patients with less destructive forms of periodontitis (AP and LJP). Porphyromonas gingivalis, a bacterial pathogen known to increase IL-8 production by PMN, was found in the periodontal pockets of RPP patients only. These results show links among PMN abnormalities, the clinical form of periodontitis, and the gingival bacterial flora. (+info)Localisation of a gene for prepubertal periodontitis to chromosome 11q14 and identification of a cathepsin C gene mutation. (3/126)
Prepubertal periodontitis (PPP) is a rare and rapidly progressive disease of young children that results in destruction of the periodontal support of the primary dentition. The condition may occur as part of a recognised syndrome or may occur as an isolated finding. Both autosomal dominant and recessive forms of Mendelian transmission have been reported for PPP. We report a consanguineous Jordanian family with four members affected by PPP in two nuclear sibships. The parents of the affected subjects are first cousins. We have localised a gene of major effect for PPP in this kindred (Zmax=3.55 for D11S901 at theta=0.00) to a 14 cM genetic interval on chromosome 11q14 flanked by D11S916 and D11S1367. This PPP candidate interval overlaps the region of chromosome 11q14 that contains the cathepsin C gene responsible for Papillon-Lefevre and Haim-Munk syndromes. Sequence analysis of the cathepsin C gene from PPP affected subjects from this Jordanian family indicated that all were homozygous for a missense mutation (1040A-->G) that changes a tyrosine to a cysteine. All four parents were heterozygous carriers of this Tyr347Cys cathepsin C mutation. None of the family members who were heterozygous carriers for this mutation showed any clinical findings of PPP. None of the 50 controls tested were found to have this Tyr347Cys mutation. This is the first reported gene mutation for non-syndromic periodontitis and shows that non-syndromic PPP is an allelic variant of the type IV palmoplantar ectodermal dysplasias. (+info)Regulation of immunoglobulin G2 production by prostaglandin E(2) and platelet-activating factor. (4/126)
Patients with localized juvenile periodontitis (LJP) have elevated levels of immunoglobulin G2 (IgG2) in their sera. This is also observed in vitro when peripheral blood leukocytes from LJP patients are stimulated with pokeweed mitogen. In previous studies, we showed that lymphocytes from subjects with no periodontitis (NP subjects) produced substantial amounts of IgG2 when they were cultured with monocytes from LJP patients (LJP monocytes). These observations indicate that monocytes or monocyte-derived mediators are positive regulators of the production of IgG2. The present study was initiated to determine if secreted factors from LJP monocytes were capable of enhancing IgG2 production and to determine if prostaglandin E2 (PGE(2)), which LJP monocytes produce at elevated levels, enhances IgG2 production. Experiments in a transwell system and with monocyte-conditioned media indicated that cell-cell contact was not necessary for LJP monocytes to augment the production of IgG2 by T and B cells from NP subjects. Moreover, the production of IgG2 was selectively induced by the addition of PGE(2) or platelet-activating factor (PAF), another lipid cytokine, which can elevate PGE(2) synthesis. Furthermore, IgG2 production was abrogated when cells were treated with indomethacin, a cyclooxygenase inhibitor that blocks the synthesis of PGE(2), or the PAF antagonists CV3988 and TEPC-15. The effects of indomethacin were completely reversed by PGE(2), indicating that this is the only prostanoid that is essential for the production of IgG2. Similarly, PGE(2) reversed the effects of a PAF antagonist, suggesting that the effects of PAF are mediated through the induction of PGE(2) synthesis. Together, these data indicate that PGE(2) and PAF are essential for the production of IgG2. (+info)Th1 and Th2 cytokine profile in patients with early onset periodontitis and their healthy siblings. (5/126)
Early onset periodontitis (EOP) is a chronic inflammatory periodontal disease with a strong genetic link affecting individuals aged 17 to 25. In the familial studies we tested the hypothesis about the role of Th1 and Th2 cytokines in the pathogenesis of EOP disease. The study involved 6 individuals with EOP disease and their 6 siblings with healthy periodontium. Actinobacillus actinomycetemcomitans (A. a), a bacterium typical for EOP, was detected in all people studied. Th1 and Th2 cytokine production was measured after in vitro stimulation. Peripheral blood mononuclear cells (PBMC) were isolated and cultivated for 24 h and 7 days with PWM, A. a. or Escherichia coli. The levels of IL-4, IFN-gamma, IgA, IgG and IgM were measured by ELISA methods. After in vitro stimulation of PBMC, a significantly higher production of IL-4 and significantly lower production of IFN-gamma were found in the group of patients compared with their healthy siblings. The increased level of IL-4 in patients was in good agreement with an increased level of IgM after stimulation of lymphocytes with E. coli. These results support Seymour's hypothesis according to which patients with progressive disease primarily activate Th2 lymphocytes while non-susceptible individuals activate Th1 lymphocytes. (+info)Beyond the specific plaque hypothesis: are highly leukotoxic strains of Actinobacillus actinomycetemcomitans a paradigm for periodontal pathogenesis? (6/126)
Actinobacillus actinomycetemcomitans is a facultative anaerobe implicated in a variety of periodontal diseases. Its presence is most closely associated with localized juvenile periodontitis (LIP), although the exact role of the organism in this and other periodontal diseases is not entirely clear. While A. actinomycetemcomitans produces several different putative virulence factors, the most widely studied is the leukotoxin. The leukotoxin selectively kills polymorphonuclear leukocytes and macrophages in vitro, constituting the host's first line of defense. Interestingly, even though all strains of A. actinomycetemcomitans have the genes encoding the leukotoxin, there is variability in leukotoxin expression. Differences in the structure of the promoter region of the leukotoxin gene operon were shown to correlate directly with levels of leukotoxin production. Highly leukotoxic forms appear to exhibit increased pathogenic potential, as evidenced by recent studies that have shown a significant association between the prevalence of such strains and the occurrence of LIP in several different populations. This represents the first demonstration of an association between a particular subset of a pathogenic species and a specific periodontal disease. Early identification of A. actinomycetemcomitans by microbial and genetic assays to evaluate leukotoxicity may enhance the efficacy of preventive and/or therapeutic techniques. Future investigations should continue to evaluate pathogenic variations of additional virulence factors expressed in vivo, not only of A. actinomycetemcomitans, but also of other periodontal bacteria and infectious disease pathogens. (+info)Defective Gi protein coupling in two formyl peptide receptor mutants associated with localized juvenile periodontitis. (7/126)
The formyl peptide receptor (FPR) is a prototypical chemoattractant receptor expressed in neutrophils. It is well known that the FPR couples to G(i) proteins to activate phospholipase C, chemotaxis, and cytotoxic cell functions, but the in vivo role of the FPR in man has remained elusive. Recently, F110S and C126W mutations of the FPR have been associated with localized juvenile periodontitis. We studied FPR-F110S and FPR-C126W in comparison with wild-type FPR (FPR-WT) by coexpressing epitope-tagged versions of these receptors with the G protein Galpha(i2)beta(1)gamma(2) in Sf9 insect cells. FPRs were efficiently expressed in Sf9 membranes as assessed by immunoblotting using the beta(2)-adrenoreceptor as a standard. FPR-C126W differed from FPR-WT and FPR-F110S in migration on SDS-polyacrylamide gels and tunicamycin-sensitive glycosylation. FPR-WT efficiently reconstituted high-affinity agonist binding and agonist- and inverse agonist-regulated guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS) binding to Galpha(i2)beta(1)gamma(2). In contrast, FPR-F110S only weakly reconstituted agonist-stimulated GTPgammaS binding, and FPR-C126W was completely inefficient. Collectively, our data show almost complete and complete loss of G(i) protein coupling in FPR-F110S and FPR-C126W, respectively. The severe functional defects in FPR-F110S and FPR-C126W contrast with the discrete clinical symptoms associated with these mutations, indicating that loss of FPR function in host defense is, for the most part, readily compensated. (+info)Population structure and genetic diversity of Actinobacillus actinomycetemcomitans strains isolated from localized juvenile periodontitis patients. (8/126)
The phylogeny of 20 Actinobacillus actinomycetemcomitans strains isolated from patients with localized juvenile periodontitis (LJP) was investigated by using partial sequence analysis of 16S rRNA genes, arbitrarily primed PCR (AP-PCR), and four additional PCR assays that amplified polymorphic regions in the leukotoxin (lkt), cytolethal distending toxin (cdt), major fimbrial subunit (flp-1), and serotype-specific O polysaccharide gene clusters. Our analysis also included four strains isolated from healthy subjects and nine reference strains. We found that A. actinomycetemcomitans strains comprised three major phylogenetic lineages. One lineage consisted of serotype b strains, a second lineage consisted of serotype c strains, and a third lineage consisted of serotype a, d, e, and f strains. 16S rRNA sequences within each lineage were highly conserved (<1% base substitutions), whereas sequences between lineages were exceptionally divergent (1.9 to 5.0% substitutions). Two strains exhibited 16S rRNA sequences that were even more distantly related to those of the three major lineages (2.7 to 6.7% substitutions), indicating that additional minor lineages or variants exist. The distribution of 16S rRNA sequences and lkt, cdt, flp-1, and AP-PCR genotypes was consistent with a clonal population structure, with little evidence of assortative recombination between strains of different serotypes. Strains from all three major lineages were recovered from LJP patients, suggesting that phylogenetically diverse strains of A. actinomycetemcomitans carry pathogenic potential. (+info)Aggressive periodontitis[edit]. Involves inflammation of the gingiva and rapid and severe destruction of the periodontal ... Periodontitis:. Necrotizing Periodontal Diseases. Periodontitis. Periodontitis as a Manifestation of Systemic Disease. Other ... Aggressive Periodontitis. (slight: 1-2 mm CAL; moderate: 3-4 mm CAL; severe: , 5 mm CAL) A. Localised. B. Generalised (, 30% of ... Periodontitis as a manifestation of systemic disease[edit]. Periodontitis that is caused by systemic disease, there are ...
Aggressive periodontitis was found in 5.9% of the subjects (4.3% localized and 1.6% generalized). This was significantly ... Levin L, Baev V, Lev R, Stabholz A, Ashkenazi M (August 2006). "Aggressive periodontitis among young Israeli army personnel". J ... Albandar, JM; Muranga, MB; Rams, TE (2002). "Prevalence of aggressive periodontitis in school attendees in Uganda". Journal of ... Ereş, G; Saribay, A; Akkaya, M (2009). "Periodontal treatment needs and prevalence of localized aggressive periodontitis in a ...
"Microbiological Characterization in Children with Aggressive Periodontitis". Journal of Dental Research. 91 (10): 927-933. doi: ... There have been, however, a number of recent studies that identified the bacteria in healthy patients without periodontitis and ... "Impact of Periodontal Therapy on the Subgingival Microbiota of Severe Periodontitis: Comparison Between Good Responders and ... have also found that the bacterium is more commonly found in healthier patients when compared to patients with periodontitis. ...
Infection patterns in chronic and aggressive periodontitis. J Clin Perio 2005;32:1055-1061. ... Periodontal pathogens are bacteria that have been shown to significantly contribute to periodontitis. Although approximately ... of species that have been shown to be more closely related to the initial incidence and continued persistence of periodontitis ...
found in the mouth (e.g. Aggregatibacter actinomycetemcomitans). These are a cause of aggressive juvenile periodontitis. ...
... patients who have heavily broken down teeth or very mobile teeth due to diseases such as generalised aggressive periodontitis. ... "Fixed rehabilitation of patient with aggressive periodontitis using zygoma implants". Indian J Dent Res. 21. Kahnberg, Karl- ...
... in aggressive periodontitis, previously known as juvenile periodontitis. In 1982, Slots developed tryptic soy-serum-bacitracin- ... It was Slots' work, along with that of Newman, Socransky and others, that substantiated aggressive periodontitis as a bona fide ... Fryman A, Simonian K. Aggressive periodontitis: the historic quest for understanding. CDA Journal 2011;39(6):377-382. ... The predominant cultivable organisms in juveline periodontitis. Scand J Dent Res 1976;84(1):1-10 van Steenbergen, TJM. " ...
SNPs in aggressive periodontitis patients". Genes and Immunity. 4 (1): 22-9. doi:10.1038/sj.gene.6363900. PMID 12595898. ...
Its role in aggressive periodontitis was first discovered by Danish-born periodontist Jørgen Slots, a professor of dentistry ... Although it has been found more frequently in localized aggressive periodontitis, prevalence in any population is rather high. ... 1985). The species has attracted attention because of its association with localized aggressive periodontitis. Recent studies ... non-motile bacterium that is often found in association with localized aggressive periodontitis, a severe infection of the ...
"Maresin 1 Biosynthesis and Proresolving Anti-infective Functions with Human-Localized Aggressive Periodontitis Leukocytes". ... that macrophages derived by culturing the monocytes isolated from the blood of patients with Localized aggressive periodontitis ...
2004). "Single nucleotide polymorphisms associated with aggressive periodontitis and severe chronic periodontitis in Japanese ...
In cases of aggressive periodontitis three major species of bacteria have been identified within the periodontal pocket. These ...
... of mRNAs for the various diacylglycerol kinase isoforms in neutrophils from patients with localized aggressive periodontitis". ...
"Adult periodontitis" was reclassified "chronic periodontitis" and "early-onset periodontitis" to "aggressive periodontitis". ... Aggressive periodontitis may occur in younger persons and there may a genetic aspect, with the trait sometimes running in ... Aggressive periodontitis is distinguished from the chronic form mainly by the faster rate of progression. Loss of attachment ... adult periodontitis, early-onset periodontitis, periodontitis associated with systemic disease, necrotizing ulcerative ...
... its association with localized aggressive periodontitis in young adolescents, and studies indicating that it can cause bone ...
The seven categories are as follows: Gingivitis Chronic periodontitis Aggressive periodontitis Periodontitis as a manifestation ... Periodontitis is caused by microorganisms that adhere to and grow on the tooth's surfaces, along with an over-aggressive immune ... According to some researchers periodontitis may be associated with higher stress. Periodontitis occurs more often in people ... although this may be a symptom of progressing periodontitis in that patient. Periodontitis has been linked to increased ...
Localized aggressive periodontitis (LAP) Generalized aggressive periodontitis (GAP) Aggressive periodontitis is much less ... Aggressive periodontitis runs in the patient's family. Familial aggregation of aggressive periodontitis is often discovered by ... Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis ... aggressive periodontitis was defined according to 3 primary features, in contrast to chronic periodontitis. These features are ...
Major drivers of this aggressive tissue destruction are matrix metalloproteinases (MMPs), cathepsins, and other osteoclast- ... "Patients with periodontitis were more likely to have poorly differentiated oral cavity SCC than those without periodontitis ( ... Chronic periodontitis is a common disease of the oral cavity consisting of chronic inflammation of the periodontal tissues that ... Title = Custom Tray Application of Peroxide Gel as an Adjunct to Scaling and Root Planing in the Treatment of Periodontitis: A ...
Periodontitis *Aggressive. *As a manifestation of systemic disease. *Chronic. *Perio-endo lesion ...
Periodontitis *Aggressive. *As a manifestation of systemic disease. *Chronic. *Perio-endo lesion ...
Periodontitis *Aggressive. *As a manifestation of systemic disease. *Chronic. *Perio-endo lesion ... or a sign of chronic periodontitis (gum disease).[9] Other less common causes are acid erosion (e.g. related to ...
Periodontitis *Aggressive. *As a manifestation of systemic disease. *Chronic. *Perio-endo lesion ...
Periodontitis *Aggressive. *As a manifestation of systemic disease. *Chronic. *Perio-endo lesion ...
Localized aggressive periodontitis. *Generalized aggressive periodontitis. *Periodontitis as a manifestation of systemic ... While some cases of gingivitis never progress to periodontitis,[3] periodontitis is always preceded by gingivitis.[4] ... A dental hygienist or dentist will also look for signs of periodontitis using X-rays or periodontal probing as well as other ... Gingivitis is reversible with good oral hygiene; however, without treatment, gingivitis can progress to periodontitis, in which ...
Periodontitis *Aggressive. *As a manifestation of systemic disease. *Chronic. *Perio-endo lesion ...
Localized aggressive periodontitis. *Generalized aggressive periodontitis. *Periodontitis as a manifestation of systemic ...
No direct association for P. intermedia and E. corrodens with aggressive periodontitis or periodontal health could be seen. A. ... These putative pathogens can be conclusively determined as the key-bacteria in patients with aggressive periodontitis. ... research was to analyze the prevalence of periodontitis-associated microorganisms in patients with aggressive periodontitis and ... subgingival plaque was sampled from four pockets and one healthy site of 45 aggressive periodontitis patients as well as from ...
Chronic Periodontitis. Denis Kinane, Jan Lindhe and Leonardo Trombelli. 21. Aggressive Periodontitis. Maurizio S. Tonetti and ... The Pathogenesis of Periodontitis. Gregory Seymour, Tord Berglundh and Leonardo Trombelli. 14. Modifying Factors. Evanthia ... Local Drug Delivery for the Treatment of Periodontitis. Maurizio S. Tonetti and Pierpaolo Cortellini. Part 13: Reconstructive ...
One severe form of periodontitis is localized aggressive periodontitis (LAP), a condition to which individuals of African ... Periodontitis is mankinds most common chronic inflammatory disease. ... Periodontitis is mankinds most common chronic inflammatory disease. One severe form of periodontitis is localized aggressive ... periodontitis (LAP), a condition to which individuals of African origin demonstrate an increased susceptibility. The main ...
... from a deep periodontal pocket of an upper central incisor of a female African-American patient with aggressive periodontitis. ... is a major causative agent of localized juvenile periodontitis and other forms of chronic periodontitis (36). Moreover, A. ... Racial tropism of a highly toxic clone of A. actinomycetemcomitans associated with juvenile periodontitis. J. Clin. Microbiol. ... Actinobacillus actinomycetemcomitans is a member of the family Pasteurellaceae and a major causative agent of periodontitis. ...
Efficacy of amoxicillin and metronidazole combination for the management of generalized aggressive periodontitis. J Periodontol ... Patient medical condition, periodontitis and oral hygiene were the most important clinical factors in antibiotic prescribing, ... plus amoxicillin in the microbial profile and in the clinical parameters of subjects with generalized aggressive periodontitis ... periodontitis (86%), poor oral hygiene (77%), and to lesser extent smoking (48%) and the brand name of the dental implant ...
Localized aggressive periodontitis. *Generalized aggressive periodontitis. *Periodontitis as a manifestation of systemic ...
Aggressive periodontitis runs in the patients family.[15]. Familial aggregation of aggressive periodontitis is often ... Radiographic Features of Localised and Generalized Aggressive Periodontitis[edit]. Localised Aggressive Periodontitis[edit]. ... Radiographic Features of Localised and Generalized Aggressive Periodontitis *3.1 Localised Aggressive Periodontitis *3.1.1 ... Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis ...
... Mina D. Fahmy,1 Paul G. Luepke,1 ... "Retention of questionable and hopeless teeth in compliant patients treated for aggressive periodontitis," Journal of Clinical ... M. Simring and M. Goldberg, "The pulpal pocket approach: retrograde periodontitis," Journal of Periodontology, vol. 35, no. 1, ... G. Matuliene, B. E. Pjetursson, G. E. Salvi et al., "Influence of residual pockets on progression of periodontitis and tooth ...
Mechanisms and Treatment Response of Aggressive Periodontitis in Children. The safety and scientific validity of this study is ... Aggressive Periodontitis. Intervention ICMJE *Procedure: Diseased periodontal treatment Treatment includes scaling and root ... Diagnosed with localized aggressive periodontitis (LAP), defined by the presence of attachment loss ≥ 2mm and detected bone ... Mechanisms and Treatment Response of Aggressive Periodontitis in Children. Official Title ICMJE Mechanisms and Treatment ...
Periodontitis. Aggressive Periodontitis. Aggression. Periodontal Diseases. Mouth Diseases. Stomatognathic Diseases. Behavioral ... Efficacy of Three Antibiotic Protocols for Aggressive Periodontitis Treatment. The safety and scientific validity of this study ... Aggressive Periodontitis Drug: Scaling and Root Planing combined with moxifloxacin Phase 4 ... or amoxicillin plus metronidazole in one-stage scaling and root planing in treating generalized aggressive periodontitis. Forty ...
Subgingival microbiome in Chinese patients with generalized aggressive periodontitis compared to healthy controls.. Cui X1, Liu ... The aim of the study was to profile the subgingival microbiome of Chinese adults with generalized aggressive periodontitis ( ...
Objective: We have identified a group of African-American children with localized Aggressive Periodontitis (LAP) within one ... 748 Comprehensive Microbiological Characterization in Children with Localized Aggressive Periodontitis Friday, March 23, 2012: ...
... chronic periodontitis (odds ratio=2.2 (95% confidence interval: 1.16-4.35), P=0.02), and aggressive periodontitis (odds ratio= ... A 3 UTR transition within DEFB1 is associated with chronic and aggressive periodontitis. Journal. Genes and Immunity. Pages ( ... of the immune system toward microbial pathogens is considered as the key factor in the development of periodontitis. Defensins ... The association was consistent with the specific periodontitis forms: ...
... ... "GC Gene Polymorphisms and Vitamin D-Binding Protein Levels Are Related to the Risk of Generalized Aggressive Periodontitis," ...
Sleep Arousal Disorders ; Aggressive Periodontitis ; Experience ; Nigeria - Abuja Abstract: Objective: Aggressive periodontitis ... IV and Grade C chronic periodontitis (aggressive periodontitis) in this environment. Cases Description: We present the summary ... Aggressive periodontitis: experience in a Nigerian teaching hospital Authors: Elizabeth Bosede Dosumu, Author ; Oluwaseyi ... The diagnosis of aggressive periodontitis in this environment is delayed because of some influencing factors such as lack of ...
aggressive Periodontitis Aggressive Periodontitis during maintenance. Procedure: orthodontic treatment Patients with Aggressive ... aggressive periodontitis aggressive periodontitis patients during maintenance. Procedure: orthodontic treatment Patients with ... Periodontitis. Aggression. Aggressive Periodontitis. Periodontal Diseases. Mouth Diseases. Stomatognathic Diseases. Behavioral ... The Affect of Orthodontic Treatment on the Periodontal Status of Patients With Aggressive Periodontitis. The safety and ...
Crevicular fluid samples were collected from 11 patients with aggressive periodontitis (AgP), 11 with chronic periodontitis (CP ... HCMV and EBV in patients with chronic or aggressive periodontitis. Methods: ... may play a synergistic role with other infectious agents from the oral cavity associated with the development of periodontitis ... "
Aggressive Periodontitis. Anti-Infective Agents, Local. Periodontitis. Aggression. Periodontal Diseases. Mouth Diseases. ... Triclosan as Adjunctive Therapy in the Plaque Control in Children From Generalized Aggressive Periodontitis Families.. The ... Generalized aggressive periodontitis (GAP) is an inflammatory disease that causes the severe and rapid destruction of ... Triclosan as Adjunctive Therapy in the Plaque Control in Children From Generalized Aggressive Periodontitis Families. A ...
... didate genetic risk markers for periodontitis. Addi- tionally, periodontitis appears to contribute to the severity of some ... It has been classified into chronic (CP) or ag- gressive (AP) periodontitis according to disease onset, localization and ... and c-reactive protein levels in lebanese patients with aggressive periodontitis-HLA and CRP in aggressive periodontitis. Open ... and c-reactive protein levels in lebanese patients with aggressive periodontitis-HLA and CRP in aggressive periodontitis ...
Kamma, J J; Nakou, M; Gmür, R; Baehni, P C (2004). Microbiological profile of early onset/aggressive periodontitis patients. ... CONCLUSIONS: The microbial profile of the early onset/aggressive periodontitis population was complex. The agreement between ... CONCLUSIONS: The microbial profile of the early onset/aggressive periodontitis population was complex. The agreement between ... and to seek possible bacterial associations in the subgingival microbiota of early onset periodontitis/aggressive periodontitis ...
T/F: localized aggressive periodontitis seems to have a strong link to genetics ... if more than ______ teeth are affected by aggressive periodontitis, it is considered generalized ... which immunoglobulin seems to play a critical role in LOCALIZED aggressive periodontitis? ... when diagnosing aggressive perio, having no history of _______ disease or ________ infections is a critical sign ...
... chronic periodontitis, generalized aggressive periodontitis, Gum Disease, localized aggressive periodontitis, Periodontitis, ... This entry was posted in Gum Disease, Periodontics and tagged aggressive periodontitis, aggressive periodontitis treatment, ... with aggressive periodontitis commonly seen in the younger age group. Continue reading → ... Periodontitis (inflammation of the supporting tissues of the teeth or also known as the periodontium) can also occur in young ...
... ... A case of a 31-year-old female with aggressive periodontitis over 14 years is presented. From 1993 to 2000, no periodontal ...
Aggressive periodontitis, Chronic periodontitis, Genetic association, Plasmin, Plasminogen, Rs1247559, Rs4252120 Persistent URL ... A haplotype block downstream of plasminogen is associated with chronic and aggressive periodontitis. Publication. Publication. ... Aim: The intronic variant rs4252120 in the plasminogen gene (PLG) is known to be associated with aggressive periodontitis (AgP ... A haplotype block downstream of plasminogen is associated with chronic and aggressive periodontitis. Journal of Clinical ...
Saliva samples were collected from 10 patients with chronic periodontitis and 5 patients with aggressive periodontitis. The ... 80% in GAgP and 50% in GCP) was found to be more in aggressive periodontitis patients. Bacterial species like ,italic> ... Chronic periodontitis is characterised by moderate periodontal attachment loss which occurs over an extended period of time ... whereas rapid periodontal loss occurs in aggressive periodontitis. ...
- One severe form of periodontitis is localized aggressive periodontitis (LAP), a condition to which individuals of African origin demonstrate an increased susceptibility. (nih.gov)
- Periodontitis is mankind's most common chronic inflammatory disease. (nih.gov)
- Actinobacillus actinomycetemcomitans , a gram-negative, facultative, nonmotile coccobacillus, is a major causative agent of localized juvenile periodontitis and other forms of chronic periodontitis ( 36 ). (asm.org)
- The purpose of the current research was to analyze the prevalence of periodontitis-associated microorganisms in patients with aggressive periodontitis and periodontally healthy elders by using molecular-biologic detection methods like eubacterial PCR-amplification of 16S rDNA in combination with dot-blot hybridization. (hu-berlin.de)
- A multifactorial risk pattern of periodontitis has been recognized, where in addition to host and environmental factors, a pathogenic microbiota plays a primary role. (hu-berlin.de)
- These putative pathogens can be conclusively determined as the key-bacteria in patients with aggressive periodontitis. (hu-berlin.de)
- For the epidemiological study, subgingival plaque was sampled from four pockets and one healthy site of 45 aggressive periodontitis patients as well as from five sites of 21 elderly. (hu-berlin.de)
- The data revealed frequent colonization by T. forsythensis, P. gingivalis, F. nucleatum and C. rectus in patients with aggressive periodontitis, however individual variations were obvious. (hu-berlin.de)
- These species could be predominantly identified in periodontal pockets, but were significantly less common in the healthy sites of the periodontitis patients and in the elderly. (hu-berlin.de)
- A. actinomycetemcomitans could be detected in only a few patients, reducing its suspected importance in the etiology of aggressive periodontitis. (hu-berlin.de)
- No direct association for P. intermedia and E. corrodens with aggressive periodontitis or periodontal health could be seen. (hu-berlin.de)
- Actinobacillus actinomycetemcomitans is a member of the family Pasteurellaceae and a major causative agent of periodontitis. (asm.org)