Aggressive Periodontitis
Chronic Periodontitis
Periodontal Pocket
Periodontal Attachment Loss
Dental Scaling
Aggregatibacter actinomycetemcomitans
Periodontal Index
Gingival Crevicular Fluid
Root Planing
Gingival Hemorrhage
Pasteurellaceae
Receptors, LH
Alveolar Bone Loss
Dental Plaque
Selenomonas
Subgingival Curettage
Periodontium
Porphyromonas gingivalis
Prevotella intermedia
Periapical Periodontitis
Periodontal Debridement
Fibromatosis, Gingival
Bacteroides
Metronidazole
Amoxicillin
Case-Control Studies
Exotoxins
Statistics, Nonparametric
Interleukin-1beta
Periodontal Diseases
Treponema denticola
Public Health
Genetics, Medical
Health Policy
Research
Public Health Practice
Health Services Research
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)The exact cause of aggressive periodontitis is not fully understood, but it is believed to be linked to factors such as genetics, smoking, and poor oral hygiene. Treatment options include antibiotics, surgical therapy, and lifestyle changes such as improved oral hygiene and quitting smoking.
A more detailed definition of aggressive periodontitis is: "An acute or chronic form of periodontitis that is characterized by rapid attachment loss, bone destruction, exuberant inflammation, and pain, and often affects young adults who are otherwise healthy. The condition can lead to tooth loss if left untreated."
Causes and risk factors:
* Poor oral hygiene
* Smoking
* Genetics
* Hormonal changes
* Malnutrition
* Diabetes
* Obesity
Symptoms:
* Gum redness, swelling, and bleeding
* Pockets between the teeth and gums
* Bad breath
* Loose teeth or teeth that have moved out of their sockets
* Changes in the shape of the gum line
Diagnosis:
* Physical examination of the teeth and gums
* X-rays or other imaging tests to assess bone loss and other changes
* Blood tests to check for underlying conditions such as diabetes or cardiovascular disease
Treatment:
* Professional scaling and root planing (a deep cleaning of the teeth)
* Antibiotics to control infection
* Surgery to remove infected tissue or repair damaged bone
* Changes to oral hygiene habits, such as brushing and flossing more frequently
Prevention:
* Good oral hygiene practices such as brushing and flossing regularly
* Regular dental check-ups and cleanings
* Avoiding smoking and other harmful habits
* Maintaining a healthy diet and getting enough exercise
Prognosis:
* With proper treatment and good oral hygiene, the condition can be managed and teeth can be saved.
* Without treatment, the condition can progress and lead to tooth loss.
Complications:
* Tooth loss
* Bone loss
* Infection of other parts of the body (sepsis)
* Heart disease
* Stroke
Note: This definition is a general overview of chronic periodontitis and is not intended to be a substitute for professional medical advice. If you suspect you have chronic periodontitis, it is important to consult with a dentist or other qualified healthcare professional for an accurate diagnosis and appropriate treatment.
It is common for people with poor oral hygiene habits, smokers or those with systemic diseases such as diabetes or heart disease to experience periodontal attachment loss. It can also be a consequence of aging, as the supporting bone and gum tissue around the teeth can degenerate over time.
There are several risk factors for periodontal attachment loss, including:
* Poor oral hygiene habits
* Smoking
* Systemic diseases such as diabetes or heart disease
* Genetic predisposition
* Poor diet
* Inadequate salivary flow
* Malocclusion (bad bite)
There are several treatment options available for periodontal attachment loss, including:
* Scaling and root planing (a deep cleaning of the teeth and beneath the gum line)
* Guided tissue regeneration (a surgical procedure to promote new bone growth)
* Bone grafting (a surgical procedure to repair or replace damaged bone)
* Dental implants (artificial tooth roots that are placed in the jawbone to support a dental crown or bridge)
It is important to note that periodontal attachment loss can be prevented with proper oral hygiene habits, regular dental check-ups and prompt treatment of any oral health issues.
Here are some common causes of gingival hemorrhage:
1. Poor oral hygiene: When you don't brush and floss regularly, plaque and tartar can build up along the gum line, leading to inflammation and bleeding.
2. Gingivitis: This is an early stage of gum disease that can cause swollen, red gums that bleed easily.
3. Periodontitis: This is a more advanced stage of gum disease that can cause the gums to pull away from the teeth and create pockets where bacteria can grow, leading to bleeding.
4. Injury to the gums: If you accidentally bite your lip or tongue, or if you have a sharp object pierce your gum, it can cause bleeding.
5. Medications: Certain medications such as aspirin, warfarin, and prednisone can thin the blood and increase the risk of gingival hemorrhage.
6. Hormonal changes: Changes in hormone levels during pregnancy, menstruation, or menopause can increase the risk of gingival hemorrhage.
7. Vitamin deficiencies: Deficiencies in vitamins such as vitamin C and K can impair the body's ability to clot blood and increase the risk of bleeding gums.
8. Systemic diseases: Certain systemic diseases such as diabetes, rheumatoid arthritis, and liver disease can increase the risk of gingival hemorrhage.
If you experience gingival hemorrhage, your dentist may perform a thorough examination to determine the underlying cause. Treatment options will depend on the severity of the condition, but may include professional cleaning, antibiotics, or surgery. It is important to maintain good oral hygiene practices and visit your dentist regularly to prevent and manage gingival hemorrhage.
The alveolar bone is a specialized type of bone that forms the socket in which the tooth roots are embedded. It provides support and stability to the teeth and helps maintain the proper position of the teeth in their sockets. When the alveolar bone is lost, the teeth may become loose or even fall out completely.
Alveolar bone loss can be detected through various diagnostic methods such as dental X-rays, CT scans, or MRI scans. Treatment options for alveolar bone loss depend on the underlying cause and may include antibiotics, bone grafting, or tooth extraction.
In the context of dentistry, alveolar bone loss is a common complication of periodontal disease, which is a chronic inflammatory condition that affects the supporting structures of the teeth, including the gums and bone. The bacteria that cause periodontal disease can lead to the destruction of the alveolar bone, resulting in tooth loss.
In addition to periodontal disease, other factors that can contribute to alveolar bone loss include:
* Trauma or injury to the teeth or jaw
* Poorly fitting dentures or other prosthetic devices
* Infections or abscesses in the mouth
* Certain systemic diseases such as osteoporosis or cancer
Overall, alveolar bone loss is a significant issue in dentistry and can have a major impact on the health and function of the teeth and jaw. It is essential to seek professional dental care if symptoms of alveolar bone loss are present to prevent further damage and restore oral health.
Plaque is a key risk factor for dental caries (tooth decay) and periodontal disease, which can lead to tooth loss if left untreated. In addition, research suggests that there may be a link between oral bacteria and certain systemic diseases, such as heart disease and diabetes. Therefore, maintaining good oral hygiene practices, such as regular brushing and flossing, is essential to prevent the accumulation of plaque and promote overall health.
Gingivitis can be treated with good oral hygiene practices, such as brushing and flossing regularly, and by visiting a dentist for regular check-ups and professional cleanings. If left untreated, gingivitis can progress to periodontitis, a more severe form of gum disease that can lead to permanent damage and tooth loss.
Some common symptoms of gingivitis include:
* Red and swollen gums
* Bleeding during brushing or flossing
* Bad breath
* Tenderness or pain in the gums
* A decrease in the amount of saliva
Treatment for gingivitis typically involves a combination of good oral hygiene practices and professional dental care. This may include:
* Regular brushing and flossing to remove plaque and bacteria from the teeth
* Professional cleanings ( scaling and root planing) to remove plaque and tartar from the teeth
* Antibiotics to treat any underlying infections
* Changes to diet and lifestyle to reduce the risk of further irritation to the gums.
It's important to note that while gingivitis is a mild form of gum disease, it can still have serious consequences if left untreated. Regular dental check-ups and good oral hygiene practices are essential for preventing and treating gingivitis.
Symptoms of periapical periodontitis may include:
* Pain or tenderness in the affected tooth
* Swelling and redness in the gum tissue
* Bad breath or a bad taste in the mouth
* Discharge of pus from the affected tooth
Periapical periodontitis is typically diagnosed through a combination of clinical examination and diagnostic tests such as radiographs (x-rays) or dental scans. Treatment may involve antibiotics, a root canal, or extraction of the affected tooth, depending on the severity of the infection and the extent of damage to the pulp and surrounding tissues.
Definition:
Actinobacillus infections are bacterial infections caused by the Actinobacillus genus of bacteria. These bacteria can cause a range of illnesses, from mild to severe, and can affect various parts of the body, including the skin, respiratory tract, digestive system, and bloodstream.
Causes:
Actinobacillus infections are typically caused by exposure to contaminated food or water or through contact with an infected animal or person. The bacteria can enter the body through cuts or wounds or through the respiratory tract. People with weakened immune systems, such as those with HIV/AIDS or undergoing chemotherapy, are more susceptible to Actinobacillus infections.
Symptoms:
The symptoms of Actinobacillus infections can vary depending on the severity of the infection and the location of the infection. Common symptoms include fever, chills, muscle aches, joint pain, and swollen lymph nodes. In more severe cases, Actinobacillus infections can cause pneumonia, meningitis, or sepsis.
Diagnosis:
Diagnosis of Actinobacillus infections typically involves a combination of physical examination, medical history, and laboratory tests. Blood cultures, PCR tests, and imaging studies such as X-rays or CT scans may be ordered to confirm the diagnosis and determine the severity of the infection.
Treatment:
The treatment of Actinobacillus infections depends on the severity of the infection and the location of the infection. Mild cases may be treated with antibiotics such as penicillin or amoxicillin, while more severe cases may require hospitalization and intravenous antibiotics. In some cases, surgical drainage of abscesses or removal of infected tissue may be necessary.
Prevention:
Prevention of Actinobacillus infections is key to avoiding the potential complications of these bacterial infections. Practicing good hygiene, such as washing your hands frequently and thoroughly, can help prevent the spread of Actinobacillus infections. Avoiding close contact with people who are sick and covering wounds or cuts can also help prevent infection.
Prognosis:
The prognosis for Actinobacillus infections is generally good if treated promptly and effectively. However, in more severe cases or those with underlying medical conditions, the prognosis may be guarded. It is important to seek medical attention immediately if symptoms persist or worsen over time.
Complications:
Actinobacillus infections can lead to a variety of complications if left untreated or if treatment is delayed. These complications include:
* Abscesses: Actinobacillus infections can cause abscesses, which are pockets of pus that form in response to the infection. Abscesses can be painful and may require surgical drainage.
* Cellulitis: Actinobacillus infections can also cause cellulitis, a more widespread infection of the skin and underlying tissues.
* Sepsis: In severe cases, Actinobacillus infections can lead to sepsis, a life-threatening condition that occurs when the body's response to an infection becomes uncontrolled and causes widespread inflammation.
* Amputations: In some cases, Actinobacillus infections may be so severe that they require amputation of affected limbs or digits.
It is important to seek medical attention immediately if you suspect you have an Actinobacillus infection. With prompt and effective treatment, the prognosis for these infections is generally good. However, delays in treatment can lead to serious complications and long-term consequences.
Gingival fibromatosis is relatively rare and usually does not require treatment unless it becomes inflamed or infected. Treatment options may include antibiotics, surgical removal of the growth, or other methods to reduce inflammation and improve oral hygiene.
Synonyms:
* Gingival fibroma
* Pyogenic granuloma
* Peripheral giant cell granuloma
* Fibromatous hyperplasia of the gingiva
Note: The term "fibromatosis" refers to the excessive growth of fibrous tissue, which can occur in various parts of the body. In the context of oral health, it specifically refers to the growth of fibrous tissue on the gums.
Some common types of Bacteroidaceae infections include:
1. Bacteroiditis: This is an infection caused by Bacteroides fragilis, which is a common resident of the human gut microbiome. Bacteroiditis can occur when the bacteria enter the bloodstream or other parts of the body, causing symptoms such as fever, chills, and swelling.
2. Parabacteroides infection: This type of infection is caused by the bacterium Parabacteroides distasonis, which is found in the gut microbiome. Parabacteroides infections can cause a range of symptoms, including diarrhea, abdominal pain, and fever.
3. Chryseobacterium infection: This type of infection is caused by the bacterium Chryseobacterium spp., which is found in the environment and can enter the body through wounds or other openings. Chryseobacterium infections can cause symptoms such as fever, chills, and swelling.
Bacteroidaceae infections can be diagnosed through a variety of tests, including blood cultures, urine cultures, and tissue biopsies. Treatment typically involves the use of antibiotics, and in some cases, surgical intervention may be necessary to remove infected tissue or repair damaged structures.
Preventive measures for Bacteroidaceae infections include good hygiene practices such as handwashing, proper wound care, and avoiding close contact with people who are sick. In some cases, antibiotic prophylaxis may be recommended to prevent infection in individuals who are at high risk of developing Bacteroidaceae infections, such as those with weakened immune systems or chronic medical conditions.
In conclusion, Bacteroidaceae is a family of bacteria that can cause a variety of infections in the body, ranging from mild to severe. Understanding the causes, symptoms, diagnosis, and treatment options for these infections can help healthcare providers provide effective care for individuals who are affected by Bacteroidaceae infections. Preventive measures such as good hygiene practices and antibiotic prophylaxis can also help reduce the risk of developing these infections.
There are several types of periodontal diseases, including:
1. Gingivitis: This is the mildest form of periodontal disease, characterized by redness, swelling, and bleeding of the gums. It is reversible with proper treatment and good oral hygiene.
2. Periodontitis: This is a more severe form of periodontal disease, characterized by the destruction of the periodontal ligament and the jawbone. It can cause teeth to become loose or fall out.
3. Advanced periodontitis: This is the most severe form of periodontal disease, characterized by extensive bone loss and severe gum damage.
4. Periodontal abscess: This is a pocket of pus that forms in the gum tissue as a result of the infection.
5. Peri-implantitis: This is a condition that affects the tissues surrounding dental implants, similar to periodontal disease.
The causes and risk factors for periodontal diseases include:
1. Poor oral hygiene
2. Smoking
3. Diabetes
4. Genetic predisposition
5. Hormonal changes during pregnancy or menopause
6. Poor diet
7. Stress
8. Certain medications
The symptoms of periodontal diseases can include:
1. Redness, swelling, and bleeding of the gums
2. Bad breath
3. Loose teeth or teeth that feel like they are shifting in their sockets
4. Pus between the teeth and gums
5. Changes in the way teeth fit together when biting down
Treatment for periodontal diseases typically involves a combination of professional cleaning, antibiotics, and changes to oral hygiene habits at home. In severe cases, surgery may be necessary to remove infected tissue and restore the health of the teeth and gums.
Preventing periodontal diseases includes:
1. Brushing teeth at least twice a day with a fluoride toothpaste
2. Flossing once a day to remove plaque from between the teeth
3. Using an antibacterial mouthwash
4. Eating a balanced diet and avoiding sugary or acidic foods
5. Quitting smoking
6. Maintaining regular dental check-ups and cleanings.
Aggressive periodontitis
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Genetic and immunological features of aggressive periodontitis
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Forms of periodontitis5
- In particular, the incidence of aggressive and difficult to treat forms of periodontitis is well-documented in patients with DM. (nih.gov)
- Classification Forms of Periodontitis AAP World Workshop in Clinical Periodontics, 1989 Adult periodontitis Early-onset periodontitis (may be prepubertal, juvenile, or rapidly progressive) Periodontitis associated with systemic disease 1 This system of classification is used as a means to properly diagnose and treat individuals with periodontal problems. (hovawartclub.hu)
- The overall classification system aimed to differentiate the more common forms of periodontitis, i.e. 11 595 The Periodontal Disease Classification System of the AAP - An Update pemphigoid), allergic reactions (e.g., restorative materials, toothpastes, gum Secondly, a new identification and classification system of periodontitis has been defined. (hovawartclub.hu)
- We studied a genetic locus on chromosome 9p21.3 that had previously been identified to be associated with myocardial infarction, in a group of 151 patients suffering from the most aggressive, early-onset forms of periodontitis, and a group of 1097 CHD patients who had already had a heart attack. (healthnewstrack.com)
- There are many forms of periodontitis. (daytonabeachdentalimplants.com)
Chronic and aggressive periodontitis2
- According to the 1999 classification, chronic and aggressive periodontitis were considered to represent different disease entities. (hovawartclub.hu)
- Serum nitric oxide concentration in generalized chronic and aggressive periodontitis in the Mexican population is not related to the severity of the disease. (nih.gov)
Gingivitis and periodontitis2
- Journal of the Canadian Dental Association December 2000, Vol. Classification included only gingivitis and periodontitis. (hovawartclub.hu)
- Periodontal (gum) diseases, including gingivitis and periodontitis, are serious infections that, left untreated, can lead to tooth loss. (daytonabeachdentalimplants.com)
Patients10
- Oral rehabilitation was undertaken in 15 patients treated for generalized aggressive periodontitis (GAgP), 12 patients treated for generalized chronic periodontitis (GCP), and 12 periodontally healthy patients. (nih.gov)
- Immune-inflammatory processes that seem to be modified in aggressive periodontitis patients may be transmitted vertically, explaining familial aggregation associated with this disease. (bvsalud.org)
- Expression of growth mediators in the gingival crevicular fluid of patients with aggressive periodontitis undergoing periodontal surgery. (bvsalud.org)
- To describe changes in growth factor mediators in the gingival crevicular fluid (GCF) of patients with aggressive periodontitis (AgP) undergoing regenerative (GTR) and access flap (AF) surgery . (bvsalud.org)
- Assessment and Comparison of Ghrelin and Chemerin Levels in Gingival Crevicular Fluid and Serum as Predictive Biomarkers in Aggressive Periodontitis Patients: A Study Protocol', European Journal of Molecular & Clinical Medicine , 7(2), pp. 2027-2033. (ejmcm.com)
- Researchers believe a larger, nationwide study is merited, and also advise dental professionals to seek education about preventing aggression from patients, and de-escalating when a patient does become aggressive. (dentalproductsreport.com)
- Do patients with aggressive periodontitis have evidence of diabetes? (dundee.ac.uk)
- The scientists went on to verify the association in further groups of 1100 CHD patients and 180 periodontitis patients. (healthnewstrack.com)
- Now we know for sure that there is a strong genetic link, patients with periodontitis should try to reduce their risk factors and take preventive measures at an early stage", he said. (healthnewstrack.com)
- Genetics may play role - Some patients may be predisposed to a more aggressive type of periodontitis. (daytonabeachdentalimplants.com)
Left untreated1
- Periodontitis can lead to bone loss and tooth loss if left untreated. (insureguardian.com)
Gums1
- We intend to push ahead with our work to try to understand more about the function of this RNA molecule and the pathway in which it operates in healthy gums and also in periodontitis. (healthnewstrack.com)
Infections2
- Abstract: The Gram negative pathogen, Aggregatibacter actinomycetemcomitans, is the etiologic agent of localized aggressive periodontitis (LAP) and other systemic infections, including infective endocarditis. (nih.gov)
- Our aim was to study the relationship between gum infections such as periodontitis as a risk factor for cerebral ischemic stroke and its correlation of periodontitis staging for stroke. (scidentj.com)
Systemic2
- Periodontitis was reclassified as chronic, aggressive (localized and generalized), necrotizing and as a manifestation of systemic disease. (hovawartclub.hu)
- 3. Classification of these conditions should be based on the primary systemic disease Classification of Diseases and Related Periodontitis Fine et al. (hovawartclub.hu)
Severe10
- Severe periodontitis was defined as having ≥2 inter-proximal sites with clinical attachment loss ≥6 mm (not on the same tooth) and ≥1 inter-proximal site with pocket depth ≥5 mm. (cambridge.org)
- Intake of vitamin D alone was not associated severe with periodontitis. (cambridge.org)
- However, studies on the relationship between severe periodontitis and serum 25-hydroxyvitamin D 25(OH)D are limited. (vitamindwiki.com)
- This study is designed to explore the relationship between 25(OH)D and severe periodontitis. (vitamindwiki.com)
- Severe periodontitis and serum 25(OH)D were the dependent and independent variables, respectively. (vitamindwiki.com)
- Univariate, multivariate, and subgroup analyses were performed to explore the relationship between severe periodontitis and serum 25(OH)D. (vitamindwiki.com)
- Among the 2928 participants, the average age of the population was 50 ± 13.71 years old, with 1425 (48.67%) males, 316 (10.79%) exhibited severe periodontitis. (vitamindwiki.com)
- Serum 25(OH)D showed a significantly negative association with severe periodontitis after adjusting all variables (OR 0.75, 95% CI 0.63-0.89). (vitamindwiki.com)
- In addition, severe periodontitis has a nonlinear relationship with serum 25(OH)D, whoes inflection point was 102 (nmol/L). On the left side of the inflection point (25(OH)D ≤ 102 nmol/L), the effect size was 0.98 and 95%CI was 0.98-0.99 (25(OH)D per 1 nmol/L increments). (vitamindwiki.com)
- Papillon lefevre syndrome (PLS) belongs to a heterogeneous group of skin diseases that are characterized by hyperkeratosis of palms and soles and presence of severe and early onset periodontitis. (who.int)
Genetic2
- Aggressive periodontitis intrigues clinicians and researchers due to its rapid progression and its evidences of genetic character. (bvsalud.org)
- The purpose of this study was to review the literature in order to comprehend the genetic and immunological features of aggressive periodontitis. (bvsalud.org)
Inflammation2
Onset4
- 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. (nih.gov)
- Replacement of "Early-Onset Periodontitis" with "Aggressive Periodontitis" (Table 2, Section III) There are forms of periodontal disease that clearly differ from chronic periodontitis. (hovawartclub.hu)
- A NEW CLASSIFICATION OF PERIODONTITIS The 1989 workshop recognized that periodontitis had several distinct clinical presentations, different ages of onset and rates of progression. (hovawartclub.hu)
- The 1999 classification, criticizing the concept and definition of an early onset periodontitis, has replaced it with aggressive periodontitis, has recognized the gingival diseases as a precursor of periodontitis (even though the). (hovawartclub.hu)
Serum1
- Group I includes 40 GCF samples from 40 subjects with aggressive and Group II includes 40 Serum samples from 40 subjects with aggressive periodontitis group. (ejmcm.com)
Tooth loss1
- Coronary heart disease is the leading cause of death worldwide, and periodontitis, which leads to the loss of connective tissue and the bone support of teeth, is the major cause of tooth loss in adults over 40 years. (healthnewstrack.com)
Destructive1
- It is a destructive form of periodontitis characterized by ALVEOLAR BONE LOSS of the MOLARS and INCISORS . (nih.gov)
Clinical3
- Surveys of aggressive periodontitis that use only clinical examinations, without radiographic examination to confirm the presence of a distinctive pattern of tissue loss, may overestimate the prevalence of this disease, particularly when a low threshold of attachment loss is used. (elsevierpure.com)
- Extensive clinical studies have indicated that the oral microbial flora is responsible for two major human diseases: dental caries and periodontitis ( Marsh, 1994 ). (frontiersin.org)
- Effect of surgical periodontal treatment associated to antimicrobial photodynamic therapy on chronic periodontitis: A randomized controlled clinical trial. (helbo.de)
Varies2
- In the presence of dental biofilm, host susceptibility to aggressive periodontitis varies among regions, countries and races. (bvsalud.org)
- The prevalence of aggressive periodontitis varies significantly between populations, and differences in race/ethnicities seem to be a key factor. (elsevierpure.com)
Dental2
- Inflamación y pérdida del PERIODONTIO que se caracteriza por rápidas destrucción ósea y pérdida del sistema de unión en presencia de factores locales como la PLACA DENTAL y CÁLCULO DENTAL. (bvsalud.org)
- The relationship between the dental disease periodontitis and coronary heart disease (CHD) has been known for several years. (healthnewstrack.com)
Populations4
- Epidemiologic studies of aggressive periodontitis have used different study designs and a range of examination methods and case definitions, and this greatly complicates the study of disease prevalence in populations. (elsevierpure.com)
- Studies consistently show that aggressive periodontitis is most prevalent in Africa and in populations of African descent and is least prevalent in Caucasians in Europe and North America. (elsevierpure.com)
- These findings show that aggressive periodontitis is a significant health problem in certain populations. (elsevierpure.com)
- Epidemiologic studies of aggressive periodontitis in high-risk populations are important and could provide vital data on the determinants of this disease, and this information is needed for the establishment of effective health-promotion measures. (elsevierpure.com)
20171
- Review Article A New Classification of Endodontic-Periodontal Lesions KhalidS.Al-Fouzan College of Dentistry, King Saud Bin Abdulaziz University, King Abdulaziz Medical City No. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases and Conditions, S162-S170. (hovawartclub.hu)
Juvenile1
- A localized aggressive periodontitis, formerly called localized juvenile periodontitis. (nih.gov)
Diabetes1
- Periodontitis is now recognized as one of the six major complications of diabetes. (nih.gov)
Teeth1
- 9. Aggressive periodontitis with supernumerary teeth: a retrospective study. (nih.gov)
Lead1
- Periodontitis can lead to the destruction of periodontium and adversely influence the overall health, wellbeing, and quality of life. (vitamindwiki.com)
Vitamin1
- To investigate whether intakes of Ca, vitamin D, casein and whey are associated with periodontitis and to investigate the possibility of interactions between them. (cambridge.org)
Treatment1
- The presentation of EG may be solitary, which rarely requires treatment, or multisystem, which requires aggressive therapy. (medscape.com)
Common1
- Periodontitis is very common, and around 90% of people aged over 60 suffer from it. (healthnewstrack.com)
Years1
- classification of periodontitis 6,7,8 which has been in use for the last 19 years. (hovawartclub.hu)
Early2
- Over much of the last century clinicians and researchers have grappled with the … 66, No. Abstract Objective Since the initial description of aggressive periodontitis (AgP) in the early 1900s, classification of this disease has been in flux. (hovawartclub.hu)
- In the meantime, because of its association with CHD, we think that periodontitis should be taken very seriously by dentists and diagnosed and treated as early as possible", said Dr. Schaefer. (healthnewstrack.com)
Condition1
- An unusual variation of the condition known as necrotizing periodontitis frequently affects persons with compromised immune systems. (insureguardian.com)
Risk1
- Periodontitis is an independent risk factor for cerebral ischemia and is a treatable and preventable disease. (scidentj.com)
