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.
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 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.
An abnormal extension of a gingival sulcus accompanied by the apical migration of the epithelial attachment and bone resorption.
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.
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.
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.
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.
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)
An index which scores the degree of dental plaque accumulation.
A procedure for smoothing of the roughened root surface or cementum of a tooth after subgingival curettage or scaling, as part of periodontal therapy.
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.
A family of coccoid to rod-shaped nonsporeforming, gram-negative, nonmotile, facultatively anaerobic bacteria that includes the genera ACTINOBACILLUS; HAEMOPHILUS; MANNHEIMIA; and PASTEURELLA.
Oral tissue surrounding and attached to TEETH.
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)
Resorption or wasting of the tooth-supporting bone (ALVEOLAR PROCESS) in the MAXILLA or MANDIBLE.
A film that attaches to teeth, often causing DENTAL CARIES and GINGIVITIS. It is composed of MUCINS, secreted from salivary glands, and microorganisms.
Inflammation of gum tissue (GINGIVA) without loss of connective tissue.
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)
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)
The structures surrounding and supporting the tooth. Periodontium includes the gum (GINGIVA), the alveolar bone (ALVEOLAR PROCESS), the DENTAL CEMENTUM, and the PERIODONTAL LIGAMENT.
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.
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.
Inflammation of the PERIAPICAL TISSUE. It includes general, unspecified, or acute nonsuppurative inflammation. Chronic nonsuppurative inflammation is PERIAPICAL GRANULOMA. Suppurative inflammation is PERIAPICAL ABSCESS.
Infections with bacteria of the genus ACTINOBACILLUS.
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).
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)
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.
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).
A broad-spectrum semisynthetic antibiotic similar to AMPICILLIN except that its resistance to gastric acid permits higher serum levels with oral administration.
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.
Infections with bacteria of the family BACTEROIDACEAE.
Toxins produced, especially by bacterial or fungal cells, and released into the culture medium or environment.
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)
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.
Pathological processes involving the PERIODONTIUM including the gum (GINGIVA), the alveolar bone (ALVEOLAR PROCESS), the DENTAL CEMENTUM, and the PERIODONTAL LIGAMENT.
A species of bacteria in the family SPIROCHAETACEAE, frequently isolated from periodontal pockets (PERIODONTAL POCKET).

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 is a severe form of periodontal disease that affects the tissues surrounding and supporting the teeth, including the gums, periodontal ligament, and alveolar bone. It is characterized by rapid destruction of the periodontal tissues and can result in significant tooth loss if left untreated.

Aggressive periodontitis typically affects younger individuals, often before the age of 30, and can progress rapidly, even in the absence of obvious dental plaque or calculus accumulation. It is often associated with a genetic predisposition and may cluster in families.

The disease is classified as localized or generalized based on the distribution of affected sites. Localized aggressive periodontitis typically affects no more than two teeth next to each other, while generalized aggressive periodontitis involves at least three or four teeth in different areas of the mouth.

In addition to genetic factors, other risk factors for aggressive periodontitis include smoking, diabetes, and hormonal changes. Treatment typically involves a combination of thorough dental cleanings, antibiotics, and sometimes surgical intervention to remove damaged tissue and promote healing. Regular maintenance care is essential to prevent recurrence and further progression of the disease.

Periodontitis is a severe form of gum disease that damages the soft tissue and destroys the bone supporting your teeth. If left untreated, it can lead to tooth loss. It is caused by the buildup of plaque, a sticky film of bacteria that constantly forms on our teeth. The body's immune system fights the bacterial infection, which causes an inflammatory response. If the inflammation continues for a long time, it can damage the tissues and bones that support the teeth.

The early stage of periodontitis is called gingivitis, which is characterized by red, swollen gums that bleed easily when brushed or flossed. When gingivitis is not treated, it can advance to periodontitis. In addition to plaque, other factors that increase the risk of developing periodontitis include smoking or using tobacco products, poor oral hygiene, diabetes, a weakened immune system, and genetic factors.

Regular dental checkups and good oral hygiene practices, such as brushing twice a day, flossing daily, and using an antimicrobial mouth rinse, can help prevent periodontitis. Treatment for periodontitis may include deep cleaning procedures, medications, or surgery in severe cases.

Chronic periodontitis is a type of gum disease that is characterized by the inflammation and infection of the tissues surrounding and supporting the teeth. It is a slow-progressing condition that can lead to the destruction of the periodontal ligament and alveolar bone, which can result in loose teeth or tooth loss if left untreated.

Chronic periodontitis is caused by the buildup of dental plaque and calculus (tartar) on the teeth, which harbor bacteria that release toxins that irritate and inflame the gums. Over time, this chronic inflammation can lead to the destruction of the periodontal tissues, including the gingiva, periodontal ligament, and alveolar bone.

The signs and symptoms of chronic periodontitis include:

* Red, swollen, or tender gums
* Bleeding gums during brushing or flossing
* Persistent bad breath (halitosis)
* Receding gums (exposure of the tooth root)
* Loose teeth or changes in bite alignment
* Deep periodontal pockets (spaces between the teeth and gums)

Risk factors for chronic periodontitis include poor oral hygiene, smoking, diabetes, genetics, and certain medications. Treatment typically involves a thorough dental cleaning to remove plaque and calculus, followed by additional procedures such as scaling and root planing or surgery to eliminate infection and promote healing of the periodontal tissues. Good oral hygiene practices, regular dental checkups, and quitting smoking are essential for preventing chronic periodontitis and maintaining good oral health.

A periodontal pocket is a pathological space or gap that develops between the tooth and the surrounding gum tissue (gingiva) as a result of periodontal disease. This condition is also known as a "periodontal depth" or "probing depth." It is measured in millimeters using a dental probe, and it indicates the level of attachment loss of the gingival tissue to the tooth.

In a healthy periodontium, the sulcus (the normal space between the tooth and gum) measures 1-3 mm in depth. However, when there is inflammation due to bacterial accumulation, the gums may become red, swollen, and bleed easily. As the disease progresses, the sulcus deepens, forming a periodontal pocket, which can extend deeper than 3 mm.

Periodontal pockets provide an environment that is conducive to the growth of harmful bacteria, leading to further tissue destruction and bone loss around the tooth. If left untreated, periodontal disease can result in loose teeth and eventually tooth loss. Regular dental check-ups and professional cleanings are essential for maintaining healthy gums and preventing periodontal pockets from developing or worsening.

Periodontal attachment loss (PAL) is a clinical measurement in dentistry that refers to the amount of connective tissue attachment between the tooth and its surrounding supportive structures (including the gingiva, periodontal ligament, and alveolar bone) that has been lost due to periodontal disease. It is typically expressed in millimeters and represents the distance from the cementoenamel junction (CEJ), which is the point where the tooth's crown meets the root, to the bottom of the periodontal pocket.

Periodontal pockets are formed when the gums detach from the tooth due to inflammation and infection caused by bacterial biofilms accumulating on the teeth. As the disease progresses, more and more of the supporting structures are destroyed, leading to increased pocket depths and attachment loss. This can eventually result in loose teeth and even tooth loss if left untreated.

Therefore, periodontal attachment loss is an important indicator of the severity and progression of periodontal disease, and its measurement helps dental professionals assess the effectiveness of treatment interventions and monitor disease status over time.

Dental scaling is a professional dental cleaning procedure that involves the removal of plaque, tartar (calculus), and stains from the tooth surfaces. This is typically performed by a dentist or dental hygienist using specialized instruments called scalers and curettes. The procedure helps to prevent gum disease and tooth decay by removing bacterial deposits that can cause inflammation and infection of the gums. Dental scaling may be recommended as part of a routine dental check-up or if there are signs of periodontal disease, such as red, swollen, or bleeding gums. In some cases, local anesthesia may be used to numb the area and make the procedure more comfortable for the patient.

'Aggregatibacter actinomycetemcomitans' is a gram-negative, rod-shaped bacterium that belongs to the family Pasteurellaceae. It is facultatively anaerobic, meaning it can grow in both the presence and absence of oxygen. This bacterium is commonly found as part of the oral microbiota in humans and is associated with periodontal diseases such as localized aggressive periodontitis. Additionally, it has been implicated in various extraoral infections, including endocarditis, meningitis, and septicemia, particularly in individuals with underlying medical conditions. The bacterium's virulence factors include leukotoxin, cytolethal distending toxin, and adhesins, which contribute to its pathogenicity.

The Periodontal Index (PI) is not a current or widely used medical/dental term. However, in the past, it was used to describe a method for assessing and measuring the severity of periodontal disease, also known as gum disease.

Developed by Henry H. Klein and colleagues in 1978, the Periodontal Index was a scoring system that evaluated four parameters: gingival inflammation, gingival bleeding, calculus (tartar) presence, and periodontal pocket depths. The scores for each parameter ranged from 0 to 3, with higher scores indicating worse periodontal health. The overall PI score was the sum of the individual parameter scores, ranging from 0 to 12.

However, due to its limited ability to predict future disease progression and the introduction of more comprehensive assessment methods like the Community Periodontal Index (CPI) and the Basic Periodontal Examination (BPE), the use of the Periodontal Index has become less common in dental practice and research.

Gingival crevicular fluid (GCF) is defined as the serum transudate or inflammatory exudate that flows from the gingival sulcus or periodontal pocket. It is a physiological fluid found in the narrow space between the tooth and the surrounding gum tissue, which deepens during periodontal disease. The analysis of GCF has been used as a non-invasive method to assess the status of periodontal health and disease since it contains various markers of inflammation, host response, and bacterial products.

The dental plaque index (DPI) is a clinical measurement used in dentistry to assess the amount of dental plaque accumulation on a person's teeth. It was first introduced by Silness and Löe in 1964 as a method to standardize the assessment of oral hygiene and the effectiveness of oral hygiene interventions.

The DPI is based on a visual examination of the amount of plaque present on four surfaces of the teeth, including the buccal (cheek-facing) and lingual (tongue-facing) surfaces of both upper and lower first molars and upper and lower incisors. The examiner assigns a score from 0 to 3 for each surface, with higher scores indicating greater plaque accumulation:

* Score 0: No plaque detected, even after probing the area with a dental explorer.
* Score 1: Plaque detected by visual examination and/or probing but is not visible when the area is gently dried with air.
* Score 2: Moderate accumulation of soft deposits that are visible upon visual examination before air drying, but which can be removed by scraping with a dental explorer.
* Score 3: Abundant soft matter, visible upon visual examination before air drying and not easily removable with a dental explorer.

The DPI is calculated as the average score of all surfaces examined, providing an overall measure of plaque accumulation in the mouth. It can be used to monitor changes in oral hygiene over time or to evaluate the effectiveness of different oral hygiene interventions. However, it should be noted that the DPI has limitations and may not accurately reflect the presence of bacterial biofilms or the risk of dental caries and gum disease.

Root planing is a dental procedure that involves the cleaning and smoothing of the root surfaces of teeth. It is typically performed as a part of periodontal therapy to treat and manage gum disease. The goal of root planing is to remove tartar, calculus, and bacterial toxins from the roots of teeth, which helps to promote the reattachment of the gums to the teeth and prevent further progression of periodontal disease. This procedure is usually performed under local anesthesia and may require multiple appointments depending on the severity of the case.

Gingival hemorrhage is the medical term for bleeding of the gingiva, or gums. It refers to the condition where the gums bleed, often as a result of trauma or injury, but also can be caused by various systemic conditions such as disorders of coagulation, leukemia, or scurvy.

Gingival hemorrhage is commonly seen in individuals with poor oral hygiene and periodontal disease, which can cause inflammation and damage to the gums. This can lead to increased susceptibility to bleeding, even during routine activities such as brushing or flossing. It's important to address any underlying causes of gingival hemorrhage to prevent further complications.

Pasteurellaceae is a family of Gram-negative, facultatively anaerobic or aerobic, non-spore forming bacteria that are commonly found as normal flora in the upper respiratory tract, gastrointestinal tract, and genitourinary tract of animals and humans. Some members of this family can cause a variety of diseases in animals and humans, including pneumonia, meningitis, septicemia, and localized infections such as abscesses and cellulitis.

Some notable genera within Pasteurellaceae include:

* Pasteurella: includes several species that can cause respiratory tract infections, septicemia, and soft tissue infections in animals and humans. The most common species is Pasteurella multocida, which is a major pathogen in animals and can also cause human infections associated with animal bites or scratches.
* Haemophilus: includes several species that are normal flora of the human respiratory tract and can cause respiratory tract infections, including bronchitis, pneumonia, and meningitis. The most well-known species is Haemophilus influenzae, which can cause severe invasive diseases such as meningitis and sepsis, particularly in young children.
* Mannheimia: includes several species that are normal flora of the upper respiratory tract of ruminants (such as cattle and sheep) and can cause pneumonia and other respiratory tract infections in these animals. The most common species is Mannheimia haemolytica, which is a major pathogen in cattle and can also cause human infections associated with animal contact.
* Actinobacillus: includes several species that are normal flora of the upper respiratory tract and gastrointestinal tract of animals and can cause respiratory tract infections, septicemia, and localized infections in these animals. The most common species is Actinobacillus pleuropneumoniae, which causes a severe form of pneumonia in pigs.

Overall, Pasteurellaceae family members are important pathogens in both veterinary and human medicine, and their infections can range from mild to severe and life-threatening.

Gingiva is the medical term for the soft tissue that surrounds the teeth and forms the margin of the dental groove, also known as the gum. It extends from the mucogingival junction to the base of the cervical third of the tooth root. The gingiva plays a crucial role in protecting and supporting the teeth and maintaining oral health by providing a barrier against microbial invasion and mechanical injury.

Occlusal adjustment is a dental procedure that involves modifying the shape and alignment of the biting surfaces of teeth to improve their fit and relationship with the opposing teeth. The goal of occlusal adjustment is to create a balanced and harmonious bite, which can help alleviate symptoms such as tooth wear, sensitivity, pain, or temporomandibular joint disorders (TMJD).

During an occlusal adjustment procedure, the dentist uses specialized instruments like articulating paper or dental burs to identify and eliminate interferences in the bite. These interferences can be caused by high spots, rough edges, or misaligned teeth that prevent the upper and lower teeth from meeting evenly when the jaw is closed. By removing these interferences, the dentist aims to create a more stable and comfortable bite, reducing stress on the jaw joints and muscles.

It's important to note that occlusal adjustment should only be performed by a trained dental professional, as improper modifications can lead to further dental issues or discomfort.

Alveolar bone loss refers to the breakdown and resorption of the alveolar process of the jawbone, which is the part of the jaw that contains the sockets of the teeth. This type of bone loss is often caused by periodontal disease, a chronic inflammation of the gums and surrounding tissues that can lead to the destruction of the structures that support the teeth.

In advanced stages of periodontal disease, the alveolar bone can become severely damaged or destroyed, leading to tooth loss. Alveolar bone loss can also occur as a result of other conditions, such as osteoporosis, trauma, or tumors. Dental X-rays and other imaging techniques are often used to diagnose and monitor alveolar bone loss. Treatment may include deep cleaning of the teeth and gums, medications, surgery, or tooth extraction in severe cases.

Dental plaque is a biofilm or mass of bacteria that accumulates on the surface of the teeth, restorative materials, and prosthetic devices such as dentures. It is initiated when bacterial colonizers attach to the smooth surfaces of teeth through van der Waals forces and specific molecular adhesion mechanisms.

The microorganisms within the dental plaque produce extracellular polysaccharides that help to stabilize and strengthen the biofilm, making it resistant to removal by simple brushing or rinsing. Over time, if not regularly removed through oral hygiene practices such as brushing and flossing, dental plaque can mineralize and harden into tartar or calculus.

The bacteria in dental plaque can cause tooth decay (dental caries) by metabolizing sugars and producing acid that demineralizes the tooth enamel. Additionally, certain types of bacteria in dental plaque can cause periodontal disease, an inflammation of the gums that can lead to tissue damage and bone loss around the teeth. Regular professional dental cleanings and good oral hygiene practices are essential for preventing the buildup of dental plaque and maintaining good oral health.

Gingivitis is a mild form of gum disease (periodontal disease) that causes irritation, redness, swelling and bleeding of the gingiva, or gums. It's important to note that it is reversible with good oral hygiene and professional dental treatment. If left untreated, however, gingivitis can progress to a more severe form of gum disease known as periodontitis, which can result in tissue damage and eventual tooth loss.

Gingivitis is most commonly caused by the buildup of plaque, a sticky film of bacteria that constantly forms on our teeth. When not removed regularly through brushing and flossing, this plaque can harden into tartar, which is more difficult to remove and contributes to gum inflammation. Other factors like hormonal changes, poor nutrition, certain medications, smoking or a weakened immune system may also increase the risk of developing gingivitis.

Selenomonas is a genus of gram-negative, anaerobic bacteria that are commonly found in the oral cavity and gastrointestinal tract of humans and animals. These bacteria have a unique characteristic of having curved or spiral-shaped morphology and a polar flagellum for motility. They are named after their ability to reduce selenite to elemental selenium, which gives them a characteristic red color.

Selenomonas species are often associated with dental caries and periodontal disease due to their production of acid and other virulence factors that can contribute to tissue destruction. However, they also play important roles in the breakdown of complex carbohydrates and the production of volatile sulfur compounds in the gut.

It's worth noting that while Selenomonas species are generally considered to be commensal organisms, they have been implicated in various opportunistic infections, particularly in immunocompromised individuals or those with underlying medical conditions.

Subgingival curettage is a dental procedure that involves the removal of infected tissue from the area below the gum line (subgingival) down to the bottom of the periodontal pocket. This procedure is typically performed by a dentist or dental hygienist during a deep cleaning or scaling and root planing procedure to treat periodontal disease. The goal of subgingival curettage is to remove damaged, infected, or necrotic tissue from the periodontal pocket, which can help promote healing and reduce the depth of the pocket. This procedure may also be used as a diagnostic tool to assess the extent of periodontal damage and guide treatment planning.

The periodontium is a complex structure in the oral cavity that surrounds and supports the teeth. It consists of four main components:
1. Gingiva (gums): The pink, soft tissue that covers the crown of the tooth and extends down to the neck of the tooth, where it meets the cementum.
2. Cementum: A specialized, calcified tissue that covers the root of the tooth and provides a surface for the periodontal ligament fibers to attach.
3. Periodontal ligament (PDL): A highly vascular and cell-rich connective tissue that attaches the cementum of the tooth root to the alveolar bone, allowing for tooth mobility and absorption of forces during chewing.
4. Alveolar bone: The portion of the jawbone that contains the sockets (alveoli) for the teeth. It is a spongy bone with a rich blood supply that responds to mechanical stresses from biting and chewing, undergoing remodeling throughout life.

Periodontal diseases, such as gingivitis and periodontitis, affect the health and integrity of the periodontium, leading to inflammation, bleeding, pocket formation, bone loss, and ultimately tooth loss if left untreated.

"Porphyromonas gingivalis" is a gram-negative, anaerobic, rod-shaped bacterium that is commonly found in the oral cavity and is associated with periodontal disease. It is a major pathogen in chronic periodontitis, which is a severe form of gum disease that can lead to destruction of the tissues supporting the teeth, including the gums, periodontal ligament, and alveolar bone.

The bacterium produces several virulence factors, such as proteases and endotoxins, which contribute to its pathogenicity. It has been shown to evade the host's immune response and cause tissue destruction through various mechanisms, including inducing the production of pro-inflammatory cytokines and matrix metalloproteinases.

P. gingivalis has also been linked to several systemic diseases, such as atherosclerosis, rheumatoid arthritis, and Alzheimer's disease, although the exact mechanisms of these associations are not fully understood. Effective oral hygiene practices, including regular brushing, flossing, and professional dental cleanings, can help prevent the overgrowth of P. gingivalis and reduce the risk of periodontal disease.

Prevotella intermedia is a gram-negative, anaerobic, rod-shaped bacterium that is commonly found in the oral cavity, upper respiratory tract, and gastrointestinal tract. It is a normal resident of the human microbiota but can also be an opportunistic pathogen, causing various types of infections such as periodontitis, endocarditis, and brain abscesses. P. intermedia has been associated with several diseases, including respiratory tract infections, bacteremia, and joint infections. It is often found in mixed infections with other anaerobic bacteria. Proper identification of this organism is important for the selection of appropriate antimicrobial therapy.

Periapical periodontitis is a medical condition that affects the tissues surrounding the root tip (apex) of a tooth. It is typically caused by bacterial infection that originates from the dental pulp, which is the soft tissue inside the tooth that contains nerves and blood vessels. When the dental pulp becomes inflamed or infected due to decay or injury, it can lead to periapical periodontitis if left untreated.

The infection spreads from the pulp through the root canal and forms an abscess at the tip of the tooth root. This results in inflammation and destruction of the surrounding bone and periodontal tissues, leading to symptoms such as pain, swelling, tenderness, and sensitivity to hot or cold temperatures.

Periapical periodontitis is usually treated with root canal therapy, which involves removing the infected pulp tissue, cleaning and disinfecting the root canal, and filling and sealing the space to prevent reinfection. In some cases, antibiotics may also be prescribed to help clear up any residual infection. If left untreated, periapical periodontitis can lead to more serious complications such as tooth loss or spread of infection to other parts of the body.

Actinobacillus infections are caused by bacteria belonging to the genus Actinobacillus, which are gram-negative, facultatively anaerobic, and non-motile rods. These bacteria can cause a variety of infections in humans and animals, including respiratory tract infections, wound infections, and septicemia.

The most common species that causes infection in humans is Actinobacillus actinomycetemcomitans, which is associated with periodontal disease, endocarditis, and soft tissue infections. Other species such as A. suis, A. lignieresii, and A. equuli can cause infections in animals and occasionally in humans, particularly those who have close contact with animals.

Symptoms of Actinobacillus infections depend on the site of infection and may include fever, chills, swelling, redness, pain, and purulent discharge. Diagnosis is typically made through culture and identification of the bacteria from clinical samples such as blood, wound secretions, or respiratory specimens. Treatment usually involves antibiotics that are effective against gram-negative bacteria, such as aminoglycosides, fluoroquinolones, or third-generation cephalosporins. In severe cases, surgical intervention may be necessary to drain abscesses or remove infected tissue.

Periodontal debridement is a dental procedure that involves the removal of plaque, calculus (tartar), and diseased tissue from the periodontal pocket around the teeth. The aim of this procedure is to smooth the root surface and create an environment that allows for the reattachment of healthy gum tissue to the tooth. This helps to prevent the progression of periodontal disease and promotes oral health. It is typically performed by a dental hygienist or dentist using specialized instruments, and may require local anesthesia to ensure patient comfort.

Gingival fibromatosis is a benign (non-cancerous) condition characterized by the excessive growth of gum (gingival) tissue. The overgrowth can affect one or both the maxilla (upper jaw) and mandible (lower jaw) and can lead to various dental and oral health issues, such as difficulty in chewing, speaking, and maintaining proper oral hygiene.

The etiology of gingival fibromatosis can be divided into two categories: hereditary and acquired. Hereditary gingival fibromatosis is often associated with genetic mutations, while acquired gingival fibromatosis can result from factors like chronic inflammation due to poor oral hygiene, certain medications (such as phenytoin, cyclosporine, or nifedipine), and systemic conditions (like leukemia).

The management of gingival fibromatosis typically involves surgical removal of the excess tissue. However, recurrence is common due to the condition's tendency for regrowth. Regular follow-ups with a dental professional are essential to monitor any potential regrowth and maintain good oral hygiene.

Bacteroides are a genus of gram-negative, anaerobic, rod-shaped bacteria that are normally present in the human gastrointestinal tract. They are part of the normal gut microbiota and play an important role in breaking down complex carbohydrates and other substances in the gut. However, some species of Bacteroides can cause opportunistic infections, particularly in individuals with weakened immune systems or when they spread to other parts of the body. They are resistant to many commonly used antibiotics, making infections caused by these bacteria difficult to treat.

Metronidazole is an antibiotic and antiprotozoal medication. It is primarily used to treat infections caused by anaerobic bacteria and certain parasites. Metronidazole works by interfering with the DNA of these organisms, which inhibits their ability to grow and multiply.

It is available in various forms, including tablets, capsules, creams, and gels, and is often used to treat conditions such as bacterial vaginosis, pelvic inflammatory disease, amebiasis, giardiasis, and pseudomembranous colitis.

Like all antibiotics, metronidazole should be taken only under the direction of a healthcare provider, as misuse can lead to antibiotic resistance and other complications.

Amoxicillin is a type of antibiotic known as a penicillin. It works by interfering with the ability of bacteria to form cell walls, which is necessary for their growth and survival. By disrupting this process, amoxicillin can kill bacteria and help to clear up infections.

Amoxicillin is used to treat a variety of bacterial infections, including respiratory tract infections, ear infections, skin infections, and urinary tract infections. It is available as a tablet, capsule, chewable tablet, or liquid suspension, and is typically taken two to three times a day.

Like all antibiotics, amoxicillin should be used only under the direction of a healthcare provider, and it is important to take the full course of treatment as prescribed, even if symptoms improve before the medication is finished. Misuse of antibiotics can lead to the development of drug-resistant bacteria, which can make infections more difficult to treat in the future.

A case-control study is an observational research design used to identify risk factors or causes of a disease or health outcome. In this type of study, individuals with the disease or condition (cases) are compared with similar individuals who do not have the disease or condition (controls). The exposure history or other characteristics of interest are then compared between the two groups to determine if there is an association between the exposure and the disease.

Case-control studies are often used when it is not feasible or ethical to conduct a randomized controlled trial, as they can provide valuable insights into potential causes of diseases or health outcomes in a relatively short period of time and at a lower cost than other study designs. However, because case-control studies rely on retrospective data collection, they are subject to biases such as recall bias and selection bias, which can affect the validity of the results. Therefore, it is important to carefully design and conduct case-control studies to minimize these potential sources of bias.

Bacteroidaceae is a family of gram-negative, anaerobic bacteria that are commonly found in the human gastrointestinal tract. Infections caused by Bacteroidaceae are relatively rare, but can occur in cases of severe trauma, surgery, or compromised immune systems. These infections may include bacteremia (bacteria in the blood), abscesses, and wound infections. Treatment typically involves the use of antibiotics that are effective against anaerobic bacteria. It is important to note that proper identification of the specific species causing the infection is necessary for appropriate treatment, as different species within Bacteroidaceae may have different susceptibilities to various antibiotics.

Exotoxins are a type of toxin that are produced and released by certain bacteria into their external environment, including the surrounding tissues or host's bloodstream. These toxins can cause damage to cells and tissues, and contribute to the symptoms and complications associated with bacterial infections.

Exotoxins are typically proteins, and they can have a variety of effects on host cells, depending on their specific structure and function. Some exotoxins act by disrupting the cell membrane, leading to cell lysis or death. Others interfere with intracellular signaling pathways, alter gene expression, or modify host immune responses.

Examples of bacterial infections that are associated with the production of exotoxins include:

* Botulism, caused by Clostridium botulinum
* Diphtheria, caused by Corynebacterium diphtheriae
* Tetanus, caused by Clostridium tetani
* Pertussis (whooping cough), caused by Bordetella pertussis
* Food poisoning, caused by Staphylococcus aureus or Bacillus cereus

Exotoxins can be highly potent and dangerous, and some have been developed as biological weapons. However, many exotoxins are also used in medicine for therapeutic purposes, such as botulinum toxin (Botox) for the treatment of wrinkles or dystonia.

Nonparametric statistics is a branch of statistics that does not rely on assumptions about the distribution of variables in the population from which the sample is drawn. In contrast to parametric methods, nonparametric techniques make fewer assumptions about the data and are therefore more flexible in their application. Nonparametric tests are often used when the data do not meet the assumptions required for parametric tests, such as normality or equal variances.

Nonparametric statistical methods include tests such as the Wilcoxon rank-sum test (also known as the Mann-Whitney U test) for comparing two independent groups, the Wilcoxon signed-rank test for comparing two related groups, and the Kruskal-Wallis test for comparing more than two independent groups. These tests use the ranks of the data rather than the actual values to make comparisons, which allows them to be used with ordinal or continuous data that do not meet the assumptions of parametric tests.

Overall, nonparametric statistics provide a useful set of tools for analyzing data in situations where the assumptions of parametric methods are not met, and can help researchers draw valid conclusions from their data even when the data are not normally distributed or have other characteristics that violate the assumptions of parametric tests.

Interleukin-1 beta (IL-1β) is a member of the interleukin-1 cytokine family and is primarily produced by activated macrophages in response to inflammatory stimuli. It is a crucial mediator of the innate immune response and plays a key role in the regulation of various biological processes, including cell proliferation, differentiation, and apoptosis. IL-1β is involved in the pathogenesis of several inflammatory diseases, such as rheumatoid arthritis, inflammatory bowel disease, and atherosclerosis. It exerts its effects by binding to the interleukin-1 receptor, which triggers a signaling cascade that leads to the activation of various transcription factors and the expression of target genes.

According to the American Academy of Periodontology, periodontal diseases are chronic inflammatory conditions that affect the tissues surrounding and supporting the teeth. These tissues include the gums, periodontal ligament, and alveolar bone. The primary cause of periodontal disease is bacterial plaque, a sticky film that constantly forms on our teeth.

There are two major stages of periodontal disease:

1. Gingivitis: This is the milder form of periodontal disease, characterized by inflammation of the gums (gingiva) without loss of attachment to the teeth. The gums may appear red, swollen, and bleed easily during brushing or flossing. At this stage, the damage can be reversed with proper dental care and improved oral hygiene.
2. Periodontitis: If left untreated, gingivitis can progress to periodontitis, a more severe form of periodontal disease. In periodontitis, the inflammation extends beyond the gums and affects the deeper periodontal tissues, leading to loss of bone support around the teeth. Pockets filled with infection-causing bacteria form between the teeth and gums, causing further damage and potential tooth loss if not treated promptly.

Risk factors for developing periodontal disease include poor oral hygiene, smoking or using smokeless tobacco, genetic predisposition, diabetes, hormonal changes (such as pregnancy or menopause), certain medications, and systemic diseases like AIDS or cancer. Regular dental check-ups and good oral hygiene practices are crucial for preventing periodontal disease and maintaining overall oral health.

Treponema denticola is a gram-negative, spiral-shaped bacterium that belongs to the genus Treponema. It is commonly found in the oral cavity and is associated with periodontal diseases such as chronic periodontitis. T. denticola is one of the "red complex" bacteria, which also includes Porphyromonas gingivalis and Tannerella forsythia, that are strongly associated with periodontal disease. These bacteria form a complex biofilm in the subgingival area and contribute to the breakdown of the periodontal tissues, leading to pocket formation, bone loss, and ultimately tooth loss if left untreated.

T. denticola has several virulence factors, including lipopolysaccharides (LPS), proteases, fimbriae, and endotoxins, that allow it to evade the host's immune system and cause tissue damage. It can also modulate the host's immune response, leading to a chronic inflammatory state that contributes to the progression of periodontal disease.

In addition to its role in periodontal disease, T. denticola has been linked to several systemic diseases, including cardiovascular disease, diabetes, and rheumatoid arthritis. However, more research is needed to fully understand the relationship between T. denticola and these conditions.

... runs in the patient's family. Familial aggregation of aggressive periodontitis is often discovered by ... Caries levels have seen to be lower in cases of aggressive periodontitis. Staging Cases of aggressive periodontitis have been ... Localized aggressive periodontitis (LAP) Generalized aggressive periodontitis (GAP) LAP is localised to first molar or incisor ... "Differential Diagnosis between Chronic versus Aggressive Periodontitis and Staging of Aggressive Periodontitis: A Cross- ...
"FAM5C contributes to aggressive periodontitis". PLOS ONE. 5 (4): e10053. Bibcode:2010PLoSO...510053C. doi:10.1371/journal.pone. ... "FAM5C contributes to aggressive periodontitis". PLOS ONE. 5 (4): e10053. Bibcode:2010PLoSO...510053C. doi:10.1371/journal.pone. ...
Another example is that the cause of aggressive periodontitis - resulting in rapid bone loss and teeth in need of extraction - ... "Aggressive periodontitis: The unsolved mystery" (PDF). Quintessence International. doi:10.3290/j.qi.a37387. (Articles with ...
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". Journal of Clinical Periodontology. 32 (10): 1055-61. doi:10.1111/ ... Well studied Periodontal pathogens are bacteria that have been shown to significantly contribute to periodontitis. Dental ... 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- ...
"Gene expression signatures in chronic and aggressive periodontitis: a pilot study". European Journal of Oral Sciences. 112 (3 ...
... 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 (Articles ... 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. ...
Differential Diagnosis between Chronic versus Aggressive Periodontitis and Staging of Aggressive Periodontitis: A Cross- ... Periodontitis initially begins as gingivitis and can progress onto chronic and subsequent aggressive periodontitis according to ... Chronic periodontitis is one of the seven categories of periodontitis as defined by the American Academy of Periodontology 1999 ... Not every case of gingivitis will progress onto chronic periodontitis, but all chronic periodontitis results from gingivitis. ...
Its role in aggressive periodontitis was first discovered by Danish-born periodontist Jørgen Slots, a professor of dentistry ... A systematic screen by RNA-seq and RT-PCR in HK1651 strain (a clinical isolate from an aggressive periodontitis patient), ... 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 ...
"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 ...
Nowzari is known for his advocacy against early in life periodontal disease (aggressive periodontitis). In an effort to bring ...
Aggressive periodontitis involves inflammation of the gingiva and rapid and severe destruction of the periodontal ligament, ... Moderate periodontitis Stage III: Severe periodontitis with potential for additional tooth loss Stage IV: Severe periodontitis ... "Serum Levels of Cytokines in Subjects with Generalized Chronic and Aggressive Periodontitis before and after Non-Surgical ... "Effect of patient age awareness on diagnostic agreement of chronic or aggressive periodontitis between clinicians; a pilot ...
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". ...
... gene cluster are not associated with aggressive periodontitis in a large Caucasian population". Genomics. 92 (5): 309-15. doi: ...
... administration of doxycycline versus metronidazole plus amoxicillin in the treatment of localized aggressive periodontitis: a ...
Patients often present with early-onset aggressive periodontitis associated with advanced alveolar bone loss and tooth mobility ... Dental practitioners who notice child patients who present with recurrent unexplained gingivitis and periodontitis along with ...
A Gram-negative, facultative anaerobe, nonmotile bacterium often found in association with localized aggressive periodontitis, ... Slots J (January 1976). "The predominant cultivable organisms in juvenile periodontitis". Scandinavian Journal of Dental ... and also suspected to be involved in chronic periodontitis. It was originally described as Bacterium actinomycetemcomitans (30 ...
The seven categories are as follows: Gingivitis Chronic periodontitis Aggressive periodontitis Periodontitis as a manifestation ... also increase susceptibility to periodontitis. Periodontitis may be associated with higher stress. Periodontitis occurs more ... Periodontitis Necrotizing periodontal diseases Necrotizing Gingivitis Necrotizing periodontitis Necrotizing stomatitis ... although this may be a symptom of progressing periodontitis in that person. Periodontitis has been linked to increased ...
... discovering the immunogenetic basis of aggressive periodontitis, reporting the viral cause of Kaposi's sarcoma (HHIV-8) in the ...
"Adult periodontitis" was reclassified "chronic periodontitis" and "early-onset periodontitis" to "aggressive periodontitis". ... "chronic periodontitis" and "aggressive periodontitis" Introduction of "Systemic Diseases" and Conditions Affecting the ... 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 ...
Periodontitis. Animal model: periodontitis in the rice rat (Oryzomys palustris). American Journal of Pathology 96(2):643-646. ... They are aggressive towards conspecifics and emit high-pitched squeaks while fighting. In dense vegetation, their perceptual ... The marsh rice rat is quite susceptible to periodontitis and has been used as a model system for the study of that disease. The ... Rice rats also eat eggs and young of the seaside sparrow (Ammodramus maritimus) and are aggressive towards the sparrow, ...
Periodontitis Perioral dermatitis Peripartum cardiomyopathy Peripheral blood vessel disorder Peripheral nervous disorder ... Parturiphobia Paruresis Parvovirus antenatal infection Pascuel-Castroviejo syndrome Pashayan syndrome Passive-aggressive ...
When P. nigrescens microflora colonize they trigger an over-aggressive response from the immune system and increase the ... "Association of periodontitis with increased colonization by Prevotella nigrescens". Journal of Investigative and Clinical ... and Porphyromonas gingivalis are associated with signs of carotid atherosclerosis in subjects with and without periodontitis". ...
Perri R, Nares S, Zhang S, Barros SP, Offenbacher S (January 2012). "MicroRNA modulation in obesity and periodontitis". Journal ... "Regulation of cancer aggressive features in melanoma cells by microRNAs". PLOS ONE. 6 (4): e18936. doi:10.1371/journal.pone. ...

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