Aggregatibacter actinomycetemcomitans
Pasteurellaceae
Aggressive Periodontitis
Aggregatibacter segnis
Aggregatibacter aphrophilus
Exotoxins
Aggregatibacter
Chronic Periodontitis
Campylobacter rectus
Periodontal Pocket
Periodontal Diseases
Gingival Hemorrhage
Treponema denticola
Periodontitis
Dental Plaque
Prevotella intermedia
Fusobacterium nucleatum
Porphyromonas gingivalis
Dental Devices, Home Care
Actinobacillus
Cardiobacterium
Biofilms
Peri-Implantitis
Periodontium
Alveolar Bone Loss
Streptococcus gordonii
Haemophilus somnus
Periodontal Index
Adhesins, Bacterial
Bacterial Toxins
Haemophilus
Periodontal Attachment Loss
Gingival Crevicular Fluid
Mouth
Bacterial Adhesion
Gene Expression Regulation, Bacterial
Nicotinamide Phosphoribosyltransferase
Bacteroides
Virulence Factors
Gram-Negative Bacteria
Molecular Sequence Data
Epithelial Cells
Bacteria
Polymerase Chain Reaction
Phenotypic variation in Actinobacillus actinomycetemcomitans during laboratory growth: implications for virulence. (1/6)
This study examined alteration of specific virulence traits associated with phenotypic changes seen when a low-passage disease-associated and well maintained parent strain of Actinobacillus actinomycetemcomitans was compared to a laboratory-grown spontaneous variant/mutant. Clinical isolates of A. actinomycetemcomitans recovered from periodontitis patients typically grow as rough, adherent colonies on primary culture but undergo transformation to smooth, non-adherent colonies following repeated passage in vitro. The relationship of these phenotypic changes to the virulence of the organism or to the processes that underlie this transformation are not understood. A fresh clinical isolate, designated strain CU1000, was obtained from the first molar site of a patient with classical signs of localized juvenile periodontitis and used as the parent strain to study virulence-related phenotypes. Following several passages of CU1000 on selective agar, a spontaneous variant that demonstrated smooth, opaque, non-adherent colonies was isolated and designated strain CU1060. This study compared the properties of these two strains with respect to colony morphology, autoaggregation, surface appendages, adherence to saliva-coated hydroxyapatite (SHA), LPS chemotype and activity, induction of fibroblast proteinase activity and antigenic properties. CU1000 demonstrated rough, raised, star-positive colonies which upon electron microscopic examination revealed the presence of large, flexible, bundled fibrils. In addition, CU1000 showed adherence to SHA, several unique protein antigens and elevated endotoxin and fibroblast proteinase activity. CU1060, on the other hand, showed minimal adherence to SHA and fewer reactive proteins compared to the fresh clinical isolates. This strain formed smooth, opaque colonies on agar, showed minimal fibril formation and limited endotoxin and fibroblast-proteinase-inducing activity. These findings demonstrate that clinical isolates of A. actinomycetemcomitans undergo significant virulence-reducing phenotypic alterations during in vitro passage and support the need to study this organism in its clinical form. (+info)Structural and genetic analyses of O polysaccharide from Actinobacillus actinomycetemcomitans serotype f. (2/6)
The oral bacterium Actinobacillus actinomycetemcomitans is implicated as a causative agent of localized juvenile periodontitis (LJP). A. actinomycetemcomitans is classified into five serotypes (a to e) corresponding to five structurally and antigenically distinct O polysaccharide (O-PS) components of their respective lipopolysaccharide molecules. Serotype b has been reported to be the dominant serotype isolated from LJP patients. We determined the lipopolysaccharide O-PS structure from A. actinomycetemcomitans CU1000, a strain isolated from a 13-year-old African-American female with LJP which had previously been classified as serotype b. The O-PS of strain CU1000 consisted of a trisaccharide repeating unit composed of L-rhamnose and 2-acetamido-2-deoxy-D-galactose (molar ratio, 2:1) with the structure -->2)-alpha-L-Rhap-(1-3)-2-O-(beta-D-GalpNAc)-alpha-L-Rhap-(1-->* O-PS from strain CU1000 was structurally and antigenically distinct from the O-PS molecules of the five known A. actinomycetemcomitans serotypes. Strain CU1000 was mutagenized with transposon IS903phikan, and three mutants that were deficient in O-PS synthesis were isolated. All three transposon insertions mapped to a single 1-kb region on the chromosome. The DNA sequence of a 13.1-kb region surrounding these transposon insertions contained a cluster of 14 open reading frames that was homologous to gene clusters responsible for the synthesis of A. actinomycetemcomitans serotype b, c, and e O-PS antigens. The CU1000 gene cluster contained two genes that were not present in serotype-specific O-PS antigen clusters of the other five known A. actinomycetemcomitans serotypes. These data indicate that strain CU1000 should be assigned to a new A. actinomycetemcomitans serotype, designated serotype f. A PCR assay using serotype-specific PCR primers showed that 3 out of 20 LJP patients surveyed (15%) harbored A. actinomycetemcomitans strains carrying the serotype f gene cluster. The finding of an A. actinomycetemcomitans serotype showing serological cross-reactivity with anti-serotype b-specific antiserum suggests that a reevaluation of strains previously classified as serotype b may be warranted. (+info)Tight-adherence genes of Actinobacillus actinomycetemcomitans are required for virulence in a rat model. (3/6)
Actinobacillus actinomycetemcomitans is a Gram-negative coccobacillus that has been associated with localized aggressive periodontitis and infections of the heart, brain, and urinary tract. Wild-type clinical isolates have the remarkable ability to adhere tenaciously and nonspecifically to solid surfaces such as glass, plastic, and hydroxyapatite. Adherence by A. actinomycetemcomitans is mediated by the tight-adherence (tad) gene locus, which consists of 14 genes (flp-1-flp-2-tadV-rcpCAB-tadZABCDEFG). All but 2 of the genes have been shown to be required for the secretion and assembly of long, bundled Flp1 fibrils. To test whether the tad locus is required for colonization and disease, we developed a rat model for periodontal disease. To mimic the natural route of infection, Sprague-Dawley rats were inoculated orally by adding bacteria directly to their food for 8 days. After inoculation with wild-type or mutant strains defective in adherence (flp-1 and tadA), the rats were assessed for colonization of the oral cavity and pathogenesis. Wild-type A. actinomycetemcomitans was able to colonize and persist for at least 12 weeks in the oral cavity, elicit a humoral immune response, and cause significant bone loss in rats. In contrast, rats fed flp-1 or tadA mutant strains showed no bone loss and their immune responses were indistinguishable from those of the uninoculated controls. These results demonstrate the critical importance of the tad locus in the colonization and pathogenesis of A. actinomycetemcomitans. (+info)Novel surface structures are associated with the adhesion of Actinobacillus actinomycetemcomitans to collagen. (4/6)
Actinobacillus actinomycetemcomitans is a gram-negative, facultative, anaerobic bacterium that colonizes the human oral cavity and the upper respiratory tract. This bacterium is strongly associated with localized aggressive periodontitis and adult periodontitis and is the causative agent for other serious systemic infections. Recently, we have identified a protein, EmaA (extracellular matrix protein adhesin A), that mediates the adhesion of A. actinomycetemcomitans to collagen. The conserved sequence and predicted secondary structure suggest that EmaA is an orthologue of the Yersinia enterocolitica adhesin YadA. Electron microscopy examinations of A. actinomycetemcomitans have identified antenna-like protrusions associated with the surface of the bacterium. These structures are absent on emaA mutant strains and can be restored by transformation of the mutant strain with emaA in trans. The loss of these structures is associated with a decrease in the binding of this bacterium to collagen. The antenna-like structures are composed of a long rod that terminates in an ellipsoidal head region. The analysis of these structures using image processing techniques has provided an initial estimate of the overall dimensions, which suggests that the appendages are oligomeric structures formed by either three or four subunits. Together, the data suggest that emaA is required for the expression of novel appendages on the surface of A. actinomycetemcomitans that mediate the adhesion of the bacterium to collagen. (+info)HACEK infective endocarditis: characteristics and outcomes from a large, multi-national cohort. (5/6)
(+info)Epithelial cell invasion by Actinobacillus actinomycetemcomitans strains from restriction fragment-length polymorphism groups associated with juvenile periodontitis or carrier status. (6/6)
The epithelial cell invasiveness of Actinobacillus actinomycetemcomitans strains of different restriction fragment-length polymorphism (RFLP) groups associated with disease conversion and asymptomatic carrier status in localized juvenile periodontitis was examined. Twenty clinical isolates were studied for their ability to invade KB monolayers, using the quantitative gentamicin killing assay. Five isolates were found to be invasive, five were not invasive; and the other 10 did not invade better than an invasion negative control Haemophilus aphrophilus strain ATCC 19415. Using probe-specific DNA fingerprinting. 11 strains were assigned to RFLP group II (disease-associated); 4 to RFLP type XIII (carrier status associated); and the other to groups III, IV, V and VII. Eight isolates, all RFLP group II, were leukotoxin producers as determined by PCR amplification of the lkt promoter region. No correlation was found between invasiveness and RFLP group. Leukotoxin production was more associated with noninvasive than invasive strains. (+info)Pasteurellaceae infections can affect both domesticated animals such as cattle, sheep, and swine, as well as wild animals like birds and rodents. In humans, these bacteria can cause opportunistic infections, particularly in people with weakened immune systems or underlying medical conditions.
Some of the most common Pasteurellaceae infections include:
1. Mannheimia haemolytica pneumonia: This is a severe type of pneumonia that affects cattle and other ruminants, and can be transmitted to humans through close contact with infected animals.
2. Pasteurella multocida infection: This bacterium can cause a range of infections, including skin infections, respiratory infections, and eye infections, in both animals and humans.
3. Haemophilus parasuis infection: This bacterium is known to cause pneumonia and other respiratory infections in swine, and can also affect humans, particularly those with compromised immune systems.
4. Actinobacillus pleuropneumoniae infection: This bacterium causes a type of pneumonia called pleuropneumonia, which is common in swine and can be transmitted to humans through close contact with infected animals.
Pasteurellaceae infections are typically treated with antibiotics, and the specific treatment depends on the type of bacteria causing the infection and the severity of the disease. In some cases, supportive care such as fluids, oxygen therapy, and pain management may also be necessary.
Prevention of Pasteurellaceae infections includes good hygiene practices, such as hand washing and proper cleaning and disinfection of animal facilities and equipment. Vaccination of animals against certain strains of Pasteurellaceae bacteria can also help prevent infections. In humans, avoiding close contact with infected animals and practicing good hygiene practices can help prevent transmission of the bacteria.
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.
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.
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.
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 main causes of periodontitis are poor oral hygiene, smoking, and certain medical conditions such as diabetes and heart disease. The symptoms of periodontitis include:
* Redness and swelling of the gums
* Bad breath
* Bleeding while brushing or flossing
* Pocket formation between the teeth and gums
* Loose teeth or changes in the bite
* Changes in the color or shape of the gums
If left untreated, periodontitis can lead to serious complications such as:
* Tooth loss
* Bone loss around the teeth
* Infection of the dental implant or prosthetic tooth
* Spread of bacteria to other parts of the body, leading to systemic diseases such as heart disease and diabetes.
Periodontitis can be treated by a dentist or periodontist with a combination of non-surgical and surgical procedures, including:
* Scaling and root planing (deep cleaning of the teeth and roots)
* Antibiotics to treat infection
* Bone grafting to restore lost bone tissue
* Gum grafting to cover exposed roots
* Dental implants or prosthetic teeth to replace missing teeth.
It is important to practice good oral hygiene, including brushing and flossing regularly, to prevent periodontitis. Early detection and treatment can help prevent the progression of the disease and save teeth from being lost.
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.
Peri-implantitis is characterized by symptoms such as bleeding, swelling, pain, and difficulty chewing. The condition is caused by a combination of factors, including poor oral hygiene, smoking, poorly fitted dentures, and an excessive amount of bacteria on the implant surface.
Treatment for peri-implantitis typically involves a thorough cleaning of the implant surface and surrounding tissues, as well as antibiotics to reduce inflammation. In severe cases, surgical intervention may be necessary to remove any infected tissue and restore the health of the implant and supporting bone.
Preventative measures for peri-implantitis include good oral hygiene practices such as regular brushing and flossing, avoiding smoking and excessive alcohol consumption, and ensuring proper fit and maintenance of dentures and other prosthetic devices. Early detection and treatment of the condition can help prevent more severe complications and ensure the long-term success of the implant.
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.
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.
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.
Aggregatibacter
Aggregatibacter segnis
Aggregatibacter aphrophilus
Aggregatibacter actinomycetemcomitans
Aggregatibacter iron-regulated sRNA
Index of oral health and dental articles
Capnophile
Actinobacillus
Epoxygenase
N-glycosyltransferase
Dental plaque
List of long species names
HrrF RNA
Aggressive periodontitis
Parish Sedghizadeh
Coccobacillus
Actinomyces
Bacterial cellular morphologies
Pasteurellaceae
HACEK organisms
DNA adenine methylase
Periodontal disease
Jørgen Slots
Dispersin B
PrrF RNA
Tryptic soy-serum-bacitracin-vancomycin
Conserved signature indels
List of bacterial vaginosis microbiota
Maresin
Cytolethal distending toxin
Aggregatibacter actinomycetemcomitans typing
Aggregatibacter actinomycetemcomitans | The Antimicrobial Index Knowledgebase - TOKU-E
The association between Aggregatibacter actinomycetemcomitans JP2 clone and periodontitis: A systematic review and meta...
Isotype: RIgG2b, RIgM, Positive Tested Species Reactivity: Aggregatibacter-actinomycetemcomitans-serotype-d
Prevalence of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia on different population...
The Journal of Contemporary Dental Practice
Effectiveness of Corrective Exercise Program and Kinesio Taping in Management of Patellofemoral Pain Syndrome
HOMD :: Genome Info
Genetic modifications : unintentional effects (...) - Inf'OGM
Bawang (Garlic/Allium sativum) : Philippine Herbal Therapy / Alternative Medicine in the Philippines
Frontiers | Toll Like Receptors as Sensors of the Tumor Microbial Dysbiosis: Implications in Cancer Progression
Salivary proteome of aphthous stomatitis reveals the participation of vitamin metabolism, nutrients, and bacteria | medRxiv
DeCS
MESH TREE NUMBER CHANGES - 2014 MeSH. July 29, 2013
Was there a plague in Portugal? - PMIXI
Health Research Library | Urinary Tract Health and Antibacterial Benefits: In-Vitro | Cranberry Institute
What's Hiding in the Gums of Dogs and Humans?
Pesquisa | Portal Regional da BVS
EffectiveDB
Combination of 10% EDTA, Photosan, and a blue light hand-held photopolymerizer to inactivate leading oral bacteria in dentistry...
Biofilm growth and IL-8 & TNF-α-inducing properties of Candida albicans in the presence of oral gram-positive and gram-negative...
In-vitro evaluation of antibacterial potential of cyanoacrylate tissue adhesives for intraoral wound closure
Andi Hamim Zaidan - Research output
- Universitas Airlangga
The gnd gene encoding a novel 6-phosphogluconate dehydrogenase and its adjacent region of Actinobacillus actinomycetemcomitans...
Periodontal Index | Colorado PROFILES
Pre GI: CDS description
Interaction of oral bacteria with gingival epithelial cell multilayers<...
Aphrophilus3
- A solitary abscess involving the tectum, specifically by Aggregatibacter aphrophilus , is an extremely rare condition with no known reported cases to date. (surgicalneurologyint.com)
- 2 ] We present a case of an isolated solitary Aggregatibacter aphrophilus brainstem abscess initially misdiagnosed as a glioma. (surgicalneurologyint.com)
- HN - 2014 MH - Aggregatibacter aphrophilus UI - D064207 MN - B3.440.450.600.224.750 MN - B3.660.250.550.170.750 MS - A species of Gram-negative, facultatively anaerobic spherical or rod-shaped bacteria indigenous to oral cavity and pharynx. (nih.gov)
Porphyromonas4
- The present cross-sectional study aimed to verify the prevalence of three periodontal pathogens, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, on different groups, with and without teeth. (bvsalud.org)
- In the direct assessment of genomic-based microbiome in oral samples, carriage of the oral pathogens Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans was associated with increased risk of pancreatic cancer. (bmj.com)
- After chemical characterization of a selected phenolic-rich cranberry extract, its values for minimum inhibitory concentration and minimum bactericidal concentration were calculated for the six bacteria forming the biofilm (Streptococcus oralis, Actinomyces naeslundii, Veillonella parvula, Fusobacterium nucleatum, Porphyromonas gingivalis, and Aggregatibacter actinomycetemcomitans). (cranberryinstitute.org)
- PCR was used to determine presence of the periodontopathic bacteria Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), Treponema denticola (Td), Prevotella intermedia (Pi) and Fusobacterium nucleatum (Fn). (bvsalud.org)
Bacteria3
- This study determined effects of co-infection with oral bacteria, including Streptococcus sanguinis, Fusobacterium nucleatum or Aggregatibacter actinomycetemcomitans, in herpes simplex virus type 1 (HSV-1)-infected oral epithelial cells. (nycu.edu.tw)
- The adhesion of four species of oral bacteria ( Streptococcus mutans , Streptococcus oralis , Aggregatibacter actinomycetemcomitas , and Veilonella parvula ) was studied on surfaces with or without the artificial saliva coating. (nih.gov)
- AN - infection: coordinate IM with PASTEURELLACEAE INFECTIONS (IM) HN - 2014 MH - Aggregatibacter segnis UI - D064208 MN - B3.440.450.600.224.875 MN - B3.660.250.550.170.875 MS - A species of Gram-negative, facultatively anaerobic pleomorphic rod-shaped often filamentous bacteria in the genus of AGGREGATIBACTER found in the oral cavity. (nih.gov)
Actinomycetemcomitans leukotoxin6
- 4. Aggregatibacter actinomycetemcomitans leukotoxin induces cytosol acidification in LFA-1 expressing immune cells. (nih.gov)
- 6. Aggregatibacter actinomycetemcomitans Leukotoxin (LtxA) Requires Death Receptor Fas, in Addition to LFA-1, To Trigger Cell Death in T Lymphocytes. (nih.gov)
- 9. Aggregatibacter actinomycetemcomitans leukotoxin causes activation of lymphocyte function-associated antigen 1. (nih.gov)
- 15. Gangliosides block Aggregatibacter Actinomycetemcomitans leukotoxin (LtxA)-mediated hemolysis. (nih.gov)
- 17. Aggregatibacter actinomycetemcomitans leukotoxin: from threat to therapy. (nih.gov)
- 18. Aggregatibacter actinomycetemcomitans leukotoxin utilizes a cholesterol recognition/amino acid consensus site for membrane association. (nih.gov)
Periodontal1
- Three different studies about Aggregatibacter actinomycetemcomitans and its association with periodontal diseases were reviewed. (okstate.edu)
Streptococcus1
- METHODS AND RESULTS: Cellular uptake of Photosan was detected by fluorescence spectroscopy for Streptococcus mutans and Enterococcus faecalis but not for Aggregatibacter actinomycetemcomitans. (uni-regensburg.de)
Prevalence1
- To appraise the literature on the prevalence of the JP2 clone of Aggregatibacter actinomycetemcomitans (A.a.) and on its association with presence and progression of periodontitis in different populations . (bvsalud.org)
Periodontitis2
- 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)
- The association between Aggregatibacter actinomycetemcomitans JP2 clone and periodontitis: A systematic review and meta-analysis. (bvsalud.org)
Therapy1
- This study has approached this problem by developing doxycycline-loaded liposome doped with curcumin (NL-Cur+Dox) for combination antibacterial therapy against Aggregatibacter actinomycetemcomitans. (bvsalud.org)
Pathogen2
- 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)
- The aim of this study was to demonstrate that the periodontal pathogen Aggregatibacter actinomycetemcomitans (AA) can be killed by irradiation with blue light derived from a LED light -curing unit due to its endogenous photosensitizers . (bvsalud.org)
Presence1
- Genetic factors have recently been associated with presence of Aggregatibacter actinomycetemcomitans subgingivally in populations living in industrialized countries. (nih.gov)
