Porphyromonas gingivalis is a common oral bacterium found in the human oral cavity. It is one of the widespread pathogens linked with periodontal disease, a chronic inflammatory condition affecting the gums and aiding structures of the teeth. As an obligate anaerobe, P. gingivalis colonizes dental plaque as a secondary colonizer, frequently attaching to primary colonizers like P. intermedia and Streptococcus gordonii.
According to the World Health Organisation, periodontal disease affects 10 to 15% of adult populations globally. P. gingivalis was found in the oral cavities of healthy people at a rate ranging from 10% to 66%. These opportunistic bacteria have infected 40-100% of adult periodontitis patients.
Based on their potential to develop abscesses in a model of mice, P. gingivalis variants have been classified as invasive or non-invasive. In vivo and in vitro assays have proved that the invasive variant of P. gingivalis has more pathogenic activity than the non-invasive strain.
Emerging evidence suggests that Porphyromonas gingivalis and the associated periodontal disease may have implications beyond oral health. The bacterium has been implicated in developing and progressing various systemic conditions, including cardiovascular diseases, respiratory infections, rheumatoid arthritis, adverse pregnancy outcomes, and even Alzheimer’s disease.
P. gingivalis is a primary etiological agent in the progression & pathogenesis of periodontal disease inflammatory events. This periodontopathic pathogen was discovered in 85% of the subgingival plaque collections from chronic periodontitis patients.
Recent epidemiological studies in the United States indicate that periodontal disease impacts one-half of the population over 30 and is the top-notch cause of adult cavities. According to the American Academy of Periodontology’s (AAP) periodontal disease classification system, periodontal diseases are divided into two major categories: gingival diseases and periodontitis, depending on whether the periodontal attachment has been destroyed.
Kingdom: Bacteria
Phylum: Bacteroidetes
Class: Bacteroidia
Order: Bacteroidales
Family: Porphyromonadaceae
Genus: Porphyromonas
Species: Porphyromonas gingivalis
Porphyromonas gingivalis belongs to the gram-negative, anaerobic, non-motile bacterial species that can exist as single cells, shorter chains, or pairs.
The bacterium is encapsulated with a polysaccharide capsule, and the cell wall contains peptidoglycan. P. gingivalis expresses fimbriae and pili on its outer surface. These hair-like appendages facilitate adhesion to host cells and surfaces, allowing the bacterium to colonize the oral cavity and form biofilms.
The primary antigenic variation in Porphyromonas gingivalis is attributed to two prominent outer membrane protein families: the FimA and Mfa1 fimbriae. These fimbrial proteins are involved in adhesion and colonization of the bacterium in the oral cavity.
The FimA protein is classified into six major types (I-V and Ib), while the Mfa1 protein is classified into two types (A and B). Each antigenic type is characterized by differences in the amino acid sequence and immunological properties of these fimbrial proteins.
Additionally, Porphyromonas gingivalis possesses other surface-associated proteins and polysaccharides contributing to antigenic variation and immune evasion. These include the RgpA and RgpB proteases, the Kgp protease, and lipopolysaccharides (LPS).
Porphyromonas gingivalis colonizes the oral cavity and forms biofilms on tooth surfaces and subgingival (below the gum line) areas. It can adhere to and invade oral epithelial cells, establishing a reservoir of infection.
The capacity of P. gingivalis to inhibit neutrophil migration over intact epithelial barriers may severely limit the host’s ability to address the bacterial challenge. And it contributes to the pathogenesis of the periodontal disease.
P. gingivalis use bacteroidetes targeted type IX secretion system (T9SS) to secrete virulence components. The complex recognizes T9SS effector proteins through their ubiquitous C-terminal domains (CTDs). PorN, a periplasmic polypeptide produced by P. gingivalis, forms enormous ring-shaped structures in conjunction with the PorK membrane’s outer lipoprotein. PorN additionally bridges the PorM monomer of the PorLM energy module and the effector’s CTD.
Gingipains contribute to the destruction of periodontal tissues. They can degrade extracellular matrix components, including collagen and elastin, which are crucial for maintaining tissue integrity. By breaking down these structural proteins, gingipains facilitate tissue damage and promote the spread of infection.
Gingipains can cleave subclass 1 and 3 IgG antibodies, important adaptive immune response components. By degrading these antibodies, P. gingivalis can evade the recognition and neutralizing effects of specific antibodies, reducing the effectiveness of the host immune response. Rgp oversees inducing the inflammatory response in the host through the p38 MAPK transducer channel. This reaction is probably involved in the breakdown of tissue, bone and the inflammatory aspect of periodontitis.
Gingipains can activate host proteases, such as matrix metalloproteinases (MMPs), in tissue remodeling. By activating MMPs, gingipains contribute to the breakdown of connective tissues and the progression of periodontal disease.
Polymorphonuclear leukocytes (PMNs): PMNs are highly efficient phagocytes that engulf and internalize pathogens, including Porphyromonas gingivalis. They recognize and bind to the bacterium through specific receptors on their cell surface. PMNs contain granules filled with antimicrobial proteins and enzymes. These granules fuse with the phagosome upon activation, releasing their contents to further eliminate P. gingivalis. The granule components include lysozyme, elastase, myeloperoxidase, and lactoferrin, collectively contributing to bactericidal activity.
In response to P. gingivalis infection, PMNs can undergo NETosis (Formation of Neutrophil Extracellular Traps), which releases web-like structures composed of DNA, histones, and antimicrobial proteins. These structures, known as neutrophil extracellular traps (NETs), can trap and kill the bacterium, preventing its spread and promoting its clearance.
Gingival Inflammation: Porphyromonas gingivalis infection can lead to inflammation of the gums (gingivitis). It is characterized by the gum tissues’ redness, swelling, and tenderness. Gingivitis caused by gingivalis is typically chronic and can progress to more severe forms of periodontal disease if left untreated.
Periodontal Pocket Formation: As the infection progresses, gingivalis can invade the deeper periodontal tissues, forming periodontal pockets. These are spaces or gaps between the gum tissue and the tooth root. Periodontal pockets can harbor the bacterium and contribute to further tissue damage and bone loss.
Gum Recession: Porphyromonas gingivalis infection can cause the gums to recede, gradually exposing more of the tooth root. Gum recession can lead to tooth sensitivity, increased vulnerability to decay, and aesthetic concerns.
Microbiological culture:Â A clinical sample, such as dental plaque or gingival crevicular fluid, is collected using sterile instruments or swabs from the affected site. Blood agar supplemented with selective agents, such as hemin and menadione, is commonly used for culturing P. gingivalis, the colonies of P. gingivalis appear small, dark, and translucent or pigmented. They often exhibit a characteristic “black-pigmented” appearance due to the production of iron sulfide.
Molecular Detection of Porphyromonas gingivalis
Isothermal Amplification: Isothermal amplification techniques, such as loop-mediated isothermal amplification (LAMP) or recombinase polymerase amplification (RPA), enable the amplification of specific DNA sequences from Porphyromonas gingivalis at a constant temperature. These methods utilize a set of primers that target unique regions of the bacterium’s DNA. The amplification process accumulates a large amount of DNA, making it detectable even at low initial concentrations. Isothermal amplification techniques do not require complex thermal cycling, making them fast and suitable for point-of-care testing.
Lateral Flow Strip: The amplified DNA from the isothermal amplification reaction can be detected using lateral flow strip (LFS) technology. LFS is a simple, portable, and rapid diagnostic format commonly used in point-of-care testing. The amplified DNA is hybridized with specific capture probes attached to the test strip in this method. The hybridized DNA then migrates along the strip, and when it reaches the detection zone, it interacts with immobilized signal probes. This interaction produces a visible signal, such as a color change or a line appearance, indicating the presence of Porphyromonas gingivalis.
Regular and proper oral hygiene is essential for preventing Porphyromonas gingivalis It is usually brushing your teeth at least twice daily with fluoride toothpaste, flossing daily to remove plaque and debris between teeth, and using antimicrobial mouthwash to reduce bacterial load in the oral cavity.
Smoking is an increasing risk factor for periodontal disease and may exacerbate infection with gingivalis. Quitting smoking or avoiding tobacco products can significantly reduce the risk of periodontal disease development and promote better oral health.
Professional dental cleanings at the dentist are essential to eliminate plaque and tartar accumulation, which can harbor gingivalis and other dangerous germs. Dental cleanings aid in the maintenance of dental health and the prevention of periodontal disease.
Routine dental check-ups allow early detection of any signs of periodontal disease or gingivalis infection. Regular examinations help promptly identify and address oral health issues, preventing further complications.
Porphyromonas gingivalis infection of oral epithelium inhibits neutrophil transepithelial migration – PubMed (nih.gov)
Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line – PMC (nih.gov)
Porphyromonas gingivalis is a common oral bacterium found in the human oral cavity. It is one of the widespread pathogens linked with periodontal disease, a chronic inflammatory condition affecting the gums and aiding structures of the teeth. As an obligate anaerobe, P. gingivalis colonizes dental plaque as a secondary colonizer, frequently attaching to primary colonizers like P. intermedia and Streptococcus gordonii.
According to the World Health Organisation, periodontal disease affects 10 to 15% of adult populations globally. P. gingivalis was found in the oral cavities of healthy people at a rate ranging from 10% to 66%. These opportunistic bacteria have infected 40-100% of adult periodontitis patients.
Based on their potential to develop abscesses in a model of mice, P. gingivalis variants have been classified as invasive or non-invasive. In vivo and in vitro assays have proved that the invasive variant of P. gingivalis has more pathogenic activity than the non-invasive strain.
Emerging evidence suggests that Porphyromonas gingivalis and the associated periodontal disease may have implications beyond oral health. The bacterium has been implicated in developing and progressing various systemic conditions, including cardiovascular diseases, respiratory infections, rheumatoid arthritis, adverse pregnancy outcomes, and even Alzheimer’s disease.
P. gingivalis is a primary etiological agent in the progression & pathogenesis of periodontal disease inflammatory events. This periodontopathic pathogen was discovered in 85% of the subgingival plaque collections from chronic periodontitis patients.
Recent epidemiological studies in the United States indicate that periodontal disease impacts one-half of the population over 30 and is the top-notch cause of adult cavities. According to the American Academy of Periodontology’s (AAP) periodontal disease classification system, periodontal diseases are divided into two major categories: gingival diseases and periodontitis, depending on whether the periodontal attachment has been destroyed.
Kingdom: Bacteria
Phylum: Bacteroidetes
Class: Bacteroidia
Order: Bacteroidales
Family: Porphyromonadaceae
Genus: Porphyromonas
Species: Porphyromonas gingivalis
Porphyromonas gingivalis belongs to the gram-negative, anaerobic, non-motile bacterial species that can exist as single cells, shorter chains, or pairs.
The bacterium is encapsulated with a polysaccharide capsule, and the cell wall contains peptidoglycan. P. gingivalis expresses fimbriae and pili on its outer surface. These hair-like appendages facilitate adhesion to host cells and surfaces, allowing the bacterium to colonize the oral cavity and form biofilms.
The primary antigenic variation in Porphyromonas gingivalis is attributed to two prominent outer membrane protein families: the FimA and Mfa1 fimbriae. These fimbrial proteins are involved in adhesion and colonization of the bacterium in the oral cavity.
The FimA protein is classified into six major types (I-V and Ib), while the Mfa1 protein is classified into two types (A and B). Each antigenic type is characterized by differences in the amino acid sequence and immunological properties of these fimbrial proteins.
Additionally, Porphyromonas gingivalis possesses other surface-associated proteins and polysaccharides contributing to antigenic variation and immune evasion. These include the RgpA and RgpB proteases, the Kgp protease, and lipopolysaccharides (LPS).
Porphyromonas gingivalis colonizes the oral cavity and forms biofilms on tooth surfaces and subgingival (below the gum line) areas. It can adhere to and invade oral epithelial cells, establishing a reservoir of infection.
The capacity of P. gingivalis to inhibit neutrophil migration over intact epithelial barriers may severely limit the host’s ability to address the bacterial challenge. And it contributes to the pathogenesis of the periodontal disease.
P. gingivalis use bacteroidetes targeted type IX secretion system (T9SS) to secrete virulence components. The complex recognizes T9SS effector proteins through their ubiquitous C-terminal domains (CTDs). PorN, a periplasmic polypeptide produced by P. gingivalis, forms enormous ring-shaped structures in conjunction with the PorK membrane’s outer lipoprotein. PorN additionally bridges the PorM monomer of the PorLM energy module and the effector’s CTD.
Gingipains contribute to the destruction of periodontal tissues. They can degrade extracellular matrix components, including collagen and elastin, which are crucial for maintaining tissue integrity. By breaking down these structural proteins, gingipains facilitate tissue damage and promote the spread of infection.
Gingipains can cleave subclass 1 and 3 IgG antibodies, important adaptive immune response components. By degrading these antibodies, P. gingivalis can evade the recognition and neutralizing effects of specific antibodies, reducing the effectiveness of the host immune response. Rgp oversees inducing the inflammatory response in the host through the p38 MAPK transducer channel. This reaction is probably involved in the breakdown of tissue, bone and the inflammatory aspect of periodontitis.
Gingipains can activate host proteases, such as matrix metalloproteinases (MMPs), in tissue remodeling. By activating MMPs, gingipains contribute to the breakdown of connective tissues and the progression of periodontal disease.
Polymorphonuclear leukocytes (PMNs): PMNs are highly efficient phagocytes that engulf and internalize pathogens, including Porphyromonas gingivalis. They recognize and bind to the bacterium through specific receptors on their cell surface. PMNs contain granules filled with antimicrobial proteins and enzymes. These granules fuse with the phagosome upon activation, releasing their contents to further eliminate P. gingivalis. The granule components include lysozyme, elastase, myeloperoxidase, and lactoferrin, collectively contributing to bactericidal activity.
In response to P. gingivalis infection, PMNs can undergo NETosis (Formation of Neutrophil Extracellular Traps), which releases web-like structures composed of DNA, histones, and antimicrobial proteins. These structures, known as neutrophil extracellular traps (NETs), can trap and kill the bacterium, preventing its spread and promoting its clearance.
Gingival Inflammation: Porphyromonas gingivalis infection can lead to inflammation of the gums (gingivitis). It is characterized by the gum tissues’ redness, swelling, and tenderness. Gingivitis caused by gingivalis is typically chronic and can progress to more severe forms of periodontal disease if left untreated.
Periodontal Pocket Formation: As the infection progresses, gingivalis can invade the deeper periodontal tissues, forming periodontal pockets. These are spaces or gaps between the gum tissue and the tooth root. Periodontal pockets can harbor the bacterium and contribute to further tissue damage and bone loss.
Gum Recession: Porphyromonas gingivalis infection can cause the gums to recede, gradually exposing more of the tooth root. Gum recession can lead to tooth sensitivity, increased vulnerability to decay, and aesthetic concerns.
Microbiological culture:Â A clinical sample, such as dental plaque or gingival crevicular fluid, is collected using sterile instruments or swabs from the affected site. Blood agar supplemented with selective agents, such as hemin and menadione, is commonly used for culturing P. gingivalis, the colonies of P. gingivalis appear small, dark, and translucent or pigmented. They often exhibit a characteristic “black-pigmented” appearance due to the production of iron sulfide.
Molecular Detection of Porphyromonas gingivalis
Isothermal Amplification: Isothermal amplification techniques, such as loop-mediated isothermal amplification (LAMP) or recombinase polymerase amplification (RPA), enable the amplification of specific DNA sequences from Porphyromonas gingivalis at a constant temperature. These methods utilize a set of primers that target unique regions of the bacterium’s DNA. The amplification process accumulates a large amount of DNA, making it detectable even at low initial concentrations. Isothermal amplification techniques do not require complex thermal cycling, making them fast and suitable for point-of-care testing.
Lateral Flow Strip: The amplified DNA from the isothermal amplification reaction can be detected using lateral flow strip (LFS) technology. LFS is a simple, portable, and rapid diagnostic format commonly used in point-of-care testing. The amplified DNA is hybridized with specific capture probes attached to the test strip in this method. The hybridized DNA then migrates along the strip, and when it reaches the detection zone, it interacts with immobilized signal probes. This interaction produces a visible signal, such as a color change or a line appearance, indicating the presence of Porphyromonas gingivalis.
Regular and proper oral hygiene is essential for preventing Porphyromonas gingivalis It is usually brushing your teeth at least twice daily with fluoride toothpaste, flossing daily to remove plaque and debris between teeth, and using antimicrobial mouthwash to reduce bacterial load in the oral cavity.
Smoking is an increasing risk factor for periodontal disease and may exacerbate infection with gingivalis. Quitting smoking or avoiding tobacco products can significantly reduce the risk of periodontal disease development and promote better oral health.
Professional dental cleanings at the dentist are essential to eliminate plaque and tartar accumulation, which can harbor gingivalis and other dangerous germs. Dental cleanings aid in the maintenance of dental health and the prevention of periodontal disease.
Routine dental check-ups allow early detection of any signs of periodontal disease or gingivalis infection. Regular examinations help promptly identify and address oral health issues, preventing further complications.
Porphyromonas gingivalis infection of oral epithelium inhibits neutrophil transepithelial migration – PubMed (nih.gov)
Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line – PMC (nih.gov)
Porphyromonas gingivalis is a common oral bacterium found in the human oral cavity. It is one of the widespread pathogens linked with periodontal disease, a chronic inflammatory condition affecting the gums and aiding structures of the teeth. As an obligate anaerobe, P. gingivalis colonizes dental plaque as a secondary colonizer, frequently attaching to primary colonizers like P. intermedia and Streptococcus gordonii.
According to the World Health Organisation, periodontal disease affects 10 to 15% of adult populations globally. P. gingivalis was found in the oral cavities of healthy people at a rate ranging from 10% to 66%. These opportunistic bacteria have infected 40-100% of adult periodontitis patients.
Based on their potential to develop abscesses in a model of mice, P. gingivalis variants have been classified as invasive or non-invasive. In vivo and in vitro assays have proved that the invasive variant of P. gingivalis has more pathogenic activity than the non-invasive strain.
Emerging evidence suggests that Porphyromonas gingivalis and the associated periodontal disease may have implications beyond oral health. The bacterium has been implicated in developing and progressing various systemic conditions, including cardiovascular diseases, respiratory infections, rheumatoid arthritis, adverse pregnancy outcomes, and even Alzheimer’s disease.
P. gingivalis is a primary etiological agent in the progression & pathogenesis of periodontal disease inflammatory events. This periodontopathic pathogen was discovered in 85% of the subgingival plaque collections from chronic periodontitis patients.
Recent epidemiological studies in the United States indicate that periodontal disease impacts one-half of the population over 30 and is the top-notch cause of adult cavities. According to the American Academy of Periodontology’s (AAP) periodontal disease classification system, periodontal diseases are divided into two major categories: gingival diseases and periodontitis, depending on whether the periodontal attachment has been destroyed.
Kingdom: Bacteria
Phylum: Bacteroidetes
Class: Bacteroidia
Order: Bacteroidales
Family: Porphyromonadaceae
Genus: Porphyromonas
Species: Porphyromonas gingivalis
Porphyromonas gingivalis belongs to the gram-negative, anaerobic, non-motile bacterial species that can exist as single cells, shorter chains, or pairs.
The bacterium is encapsulated with a polysaccharide capsule, and the cell wall contains peptidoglycan. P. gingivalis expresses fimbriae and pili on its outer surface. These hair-like appendages facilitate adhesion to host cells and surfaces, allowing the bacterium to colonize the oral cavity and form biofilms.
The primary antigenic variation in Porphyromonas gingivalis is attributed to two prominent outer membrane protein families: the FimA and Mfa1 fimbriae. These fimbrial proteins are involved in adhesion and colonization of the bacterium in the oral cavity.
The FimA protein is classified into six major types (I-V and Ib), while the Mfa1 protein is classified into two types (A and B). Each antigenic type is characterized by differences in the amino acid sequence and immunological properties of these fimbrial proteins.
Additionally, Porphyromonas gingivalis possesses other surface-associated proteins and polysaccharides contributing to antigenic variation and immune evasion. These include the RgpA and RgpB proteases, the Kgp protease, and lipopolysaccharides (LPS).
Porphyromonas gingivalis colonizes the oral cavity and forms biofilms on tooth surfaces and subgingival (below the gum line) areas. It can adhere to and invade oral epithelial cells, establishing a reservoir of infection.
The capacity of P. gingivalis to inhibit neutrophil migration over intact epithelial barriers may severely limit the host’s ability to address the bacterial challenge. And it contributes to the pathogenesis of the periodontal disease.
P. gingivalis use bacteroidetes targeted type IX secretion system (T9SS) to secrete virulence components. The complex recognizes T9SS effector proteins through their ubiquitous C-terminal domains (CTDs). PorN, a periplasmic polypeptide produced by P. gingivalis, forms enormous ring-shaped structures in conjunction with the PorK membrane’s outer lipoprotein. PorN additionally bridges the PorM monomer of the PorLM energy module and the effector’s CTD.
Gingipains contribute to the destruction of periodontal tissues. They can degrade extracellular matrix components, including collagen and elastin, which are crucial for maintaining tissue integrity. By breaking down these structural proteins, gingipains facilitate tissue damage and promote the spread of infection.
Gingipains can cleave subclass 1 and 3 IgG antibodies, important adaptive immune response components. By degrading these antibodies, P. gingivalis can evade the recognition and neutralizing effects of specific antibodies, reducing the effectiveness of the host immune response. Rgp oversees inducing the inflammatory response in the host through the p38 MAPK transducer channel. This reaction is probably involved in the breakdown of tissue, bone and the inflammatory aspect of periodontitis.
Gingipains can activate host proteases, such as matrix metalloproteinases (MMPs), in tissue remodeling. By activating MMPs, gingipains contribute to the breakdown of connective tissues and the progression of periodontal disease.
Polymorphonuclear leukocytes (PMNs): PMNs are highly efficient phagocytes that engulf and internalize pathogens, including Porphyromonas gingivalis. They recognize and bind to the bacterium through specific receptors on their cell surface. PMNs contain granules filled with antimicrobial proteins and enzymes. These granules fuse with the phagosome upon activation, releasing their contents to further eliminate P. gingivalis. The granule components include lysozyme, elastase, myeloperoxidase, and lactoferrin, collectively contributing to bactericidal activity.
In response to P. gingivalis infection, PMNs can undergo NETosis (Formation of Neutrophil Extracellular Traps), which releases web-like structures composed of DNA, histones, and antimicrobial proteins. These structures, known as neutrophil extracellular traps (NETs), can trap and kill the bacterium, preventing its spread and promoting its clearance.
Gingival Inflammation: Porphyromonas gingivalis infection can lead to inflammation of the gums (gingivitis). It is characterized by the gum tissues’ redness, swelling, and tenderness. Gingivitis caused by gingivalis is typically chronic and can progress to more severe forms of periodontal disease if left untreated.
Periodontal Pocket Formation: As the infection progresses, gingivalis can invade the deeper periodontal tissues, forming periodontal pockets. These are spaces or gaps between the gum tissue and the tooth root. Periodontal pockets can harbor the bacterium and contribute to further tissue damage and bone loss.
Gum Recession: Porphyromonas gingivalis infection can cause the gums to recede, gradually exposing more of the tooth root. Gum recession can lead to tooth sensitivity, increased vulnerability to decay, and aesthetic concerns.
Microbiological culture:Â A clinical sample, such as dental plaque or gingival crevicular fluid, is collected using sterile instruments or swabs from the affected site. Blood agar supplemented with selective agents, such as hemin and menadione, is commonly used for culturing P. gingivalis, the colonies of P. gingivalis appear small, dark, and translucent or pigmented. They often exhibit a characteristic “black-pigmented” appearance due to the production of iron sulfide.
Molecular Detection of Porphyromonas gingivalis
Isothermal Amplification: Isothermal amplification techniques, such as loop-mediated isothermal amplification (LAMP) or recombinase polymerase amplification (RPA), enable the amplification of specific DNA sequences from Porphyromonas gingivalis at a constant temperature. These methods utilize a set of primers that target unique regions of the bacterium’s DNA. The amplification process accumulates a large amount of DNA, making it detectable even at low initial concentrations. Isothermal amplification techniques do not require complex thermal cycling, making them fast and suitable for point-of-care testing.
Lateral Flow Strip: The amplified DNA from the isothermal amplification reaction can be detected using lateral flow strip (LFS) technology. LFS is a simple, portable, and rapid diagnostic format commonly used in point-of-care testing. The amplified DNA is hybridized with specific capture probes attached to the test strip in this method. The hybridized DNA then migrates along the strip, and when it reaches the detection zone, it interacts with immobilized signal probes. This interaction produces a visible signal, such as a color change or a line appearance, indicating the presence of Porphyromonas gingivalis.
Regular and proper oral hygiene is essential for preventing Porphyromonas gingivalis It is usually brushing your teeth at least twice daily with fluoride toothpaste, flossing daily to remove plaque and debris between teeth, and using antimicrobial mouthwash to reduce bacterial load in the oral cavity.
Smoking is an increasing risk factor for periodontal disease and may exacerbate infection with gingivalis. Quitting smoking or avoiding tobacco products can significantly reduce the risk of periodontal disease development and promote better oral health.
Professional dental cleanings at the dentist are essential to eliminate plaque and tartar accumulation, which can harbor gingivalis and other dangerous germs. Dental cleanings aid in the maintenance of dental health and the prevention of periodontal disease.
Routine dental check-ups allow early detection of any signs of periodontal disease or gingivalis infection. Regular examinations help promptly identify and address oral health issues, preventing further complications.
Porphyromonas gingivalis infection of oral epithelium inhibits neutrophil transepithelial migration – PubMed (nih.gov)
Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line – PMC (nih.gov)
Loading...
Free CME credits
Both our subscription plans include Free CME/CPD AMA PRA Category 1 credits.
Digital Certificate PDF
On course completion, you will receive a full-sized presentation quality digital certificate.
medtigo Simulation
A dynamic medical simulation platform designed to train healthcare professionals and students to effectively run code situations through an immersive hands-on experience in a live, interactive 3D environment.
medtigo Points
medtigo points is our unique point redemption system created to award users for interacting on our site. These points can be redeemed for special discounts on the medtigo marketplace as well as towards the membership cost itself.
Community Forum post/reply = 5 points
*Redemption of points can occur only through the medtigo marketplace, courses, or simulation system. Money will not be credited to your bank account. 10 points = $1.
All Your Certificates in One Place
When you have your licenses, certificates and CMEs in one place, it's easier to track your career growth. You can easily share these with hospitals as well, using your medtigo app.
