Lachnoanaerobaculum gingivalis, a recently identified bacterial species, was first isolated from human subgingival dental plaque in the context of a gingivitis lesion. The epidemiological understanding of L. gingivalis in humans remains limited, with a particular association noted with oral infections like gingivitis and periodontitis.
Despite an apparent absence of reported human cases, occurrence data, endemics, or outbreaks for L. gingivalis infections, a meta-analysis of 13 studies from 11 countries estimated an overall prevalence of 37% (95% CI 29–46%) in human dental plaque samples. Interestingly, this prevalence exhibited considerable variability, with the highest pooled prevalence recorded in Jordan at 87% (95% CI 81–92%) and the lowest in Portugal at 3% (95% CI 0–10%).
This suggests that while L. gingivalis is prevalent in human dental plaque, its distribution varies among different geographical regions, possibly influenced by local oral health conditions and practices. The scarcity of reported cases and detailed epidemiological information underscores the need for further research.
Kingdom: Bacteria
Phylum: Bacillota
Class: Clostridia
Order: Eubacteriales
Family: Lachnospiraceae
Genus: Lachnoanaerobaculum
Species: L. gingivalis
Lachnoanaerobaculum gingivalis is a gram-positive, obligately anaerobic, and spore-forming rod with a cell length ranging from approximately 1.5 to 2.0 µm and a cell width of about 0.5 to 0.6 µm.
The bacterium forms subterminal spores that exhibit a slight swelling. The cell wall of L. gingivalis contains peptidoglycan, with meso-diaminopimelic acid serving as the diagnostic diamino acid.
Additionally, the cell membrane comprises major phospholipids such as phosphatidylglycerol, phosphatidylethanolamine, and diphosphatidylglycerol. In terms of fatty acid composition, the predominant fatty acids of L. gingivalis include C16:0, C14:0, iso-C19:0, and C17:0 2OH.
The draft genome of Lachnoanaerobaculum gingivalis strain ChDC B114 T was determined to be 3,097,953 base pairs in length, with a G+C content of 35.9 mol%. This newly discovered bacterial species exhibits genetic associations with other closely related species within the genus Lachnoanaerobaculum, including L. umeaense, L. orale, and L. saburreum.
The type strain, ChDC B114 T, was isolated from human subgingival dental plaque originating from a gingivitis lesion. Notably, the type strain has been deposited in both the Japan Collection of Microorganisms and the Korean Collection for Oral Microbiology under the accession numbers JCM 33452 and KCOM 2030, respectively.
The 16S ribosomal RNA gene sequence of the type strain is publicly available in the European Nucleotide Archive, accessible via the accession number MK751703. This sequence serves as a valuable resource for understanding the phylogenetic relationships of L. gingivalis within the broader microbial community, particularly in the context of oral microbiota.
Lachnoanaerobaculum gingivalis, with its presence in saliva and dental plaque, may primarily be transmitted through oral contact like kissing, sharing utensils, or dental procedures. Additionally, its potential transmission through the gastrointestinal tract, as suggested by its relation to L. umeaense isolated from a small intestinal biopsy of a child with coeliac disease, indicates diverse routes of dissemination.
The involvement of L. gingivalis in the development of oral infections, particularly gingivitis and periodontitis, is attributed to its capacity to produce inflammatory mediators, degrade host tissues, and modulate the host immune response. Notably, synergistic interactions with other oral pathogens like Porphyromonas gingivalis and Tannerella forsythia may enhance their overall virulence.
The pathogenicity of L. gingivalis manifests in the gingival and periodontal tissues, leading to clinical symptoms such as bleeding, swelling, redness, pain, and eventual tooth loss. Furthermore, the potential contribution to systemic diseases, including cardiovascular disease, diabetes, rheumatoid arthritis, and Alzheimer’s disease, is linked to its ability to induce systemic inflammation and bacterial dissemination.
The human host defenses against Lachnoanaerobaculum gingivalis involve intricate interactions within the innate and adaptive immune systems, as well as coordinated responses in bone resorption and inflammation. Innate immunity constitutes the first line of defense, utilizing physical barriers such as saliva and epithelial cells, along with cellular and molecular components like neutrophils, macrophages, dendritic cells, the complement system, and antimicrobial peptides.
These elements collectively recognize and combat L. gingivalis through mechanisms such as phagocytosis, oxidative burst, cytokine production, and opsonization. Bone resorption, a homeostatic defense mechanism, activates osteoclasts to eliminate L. gingivalis and other oral pathogens by breaking down bone tissue that may serve as a bacterial niche.
The regulation of osteoblasts, bone-forming cells, is also involved. Yet, L. gingivalis can influence bone resorption by producing factors that modulate the expression and activity of mediators such as RANKL, OPG, and BMPs, potentially affecting the balance between bone formation and resorption. Adaptive immunity, the second line of defense, provides a specific response against L. gingivalis, involving lymphocytes, B cells, T cells, antibodies, and cytokines.
This system recognizes and eliminates the bacterium through antibody-mediated neutralization, opsonization, complement activation, and cell-mediated cytotoxicity. However, L. gingivalis can evade or manipulate the adaptive immune response by producing antigens that induce cross-reactivity or tolerance in host cells and modulate T-cell subset polarization and activation. Inflammation, another protective response, engages immune cells and inflammatory mediators to eliminate L. gingivalis.
Cytokines, chemokines, prostaglandins, and matrix metalloproteinases contribute to this process by enhancing the immune response, increasing vascular permeability, and degrading the extracellular matrix. Nevertheless, L. gingivalis can induce or exacerbate inflammation by producing factors that stimulate pro-inflammatory mediator production, disrupting the balance between pro-inflammatory and anti-inflammatory mediators.
The clinical manifestations of Lachnoanaerobaculum gingivalis in humans are not extensively researched, but there is an association with oral diseases, particularly gingivitis and periodontitis. This bacterium has been identified in the subgingival dental plaque of a patient with gingivitis, suggesting a potential role in oral health issues.
Lachnoanaerobaculum gingivalis, a recently identified bacterial species, was first isolated from human subgingival dental plaque in the context of a gingivitis lesion. The epidemiological understanding of L. gingivalis in humans remains limited, with a particular association noted with oral infections like gingivitis and periodontitis.
Despite an apparent absence of reported human cases, occurrence data, endemics, or outbreaks for L. gingivalis infections, a meta-analysis of 13 studies from 11 countries estimated an overall prevalence of 37% (95% CI 29–46%) in human dental plaque samples. Interestingly, this prevalence exhibited considerable variability, with the highest pooled prevalence recorded in Jordan at 87% (95% CI 81–92%) and the lowest in Portugal at 3% (95% CI 0–10%).
This suggests that while L. gingivalis is prevalent in human dental plaque, its distribution varies among different geographical regions, possibly influenced by local oral health conditions and practices. The scarcity of reported cases and detailed epidemiological information underscores the need for further research.
Kingdom: Bacteria
Phylum: Bacillota
Class: Clostridia
Order: Eubacteriales
Family: Lachnospiraceae
Genus: Lachnoanaerobaculum
Species: L. gingivalis
Lachnoanaerobaculum gingivalis is a gram-positive, obligately anaerobic, and spore-forming rod with a cell length ranging from approximately 1.5 to 2.0 µm and a cell width of about 0.5 to 0.6 µm.
The bacterium forms subterminal spores that exhibit a slight swelling. The cell wall of L. gingivalis contains peptidoglycan, with meso-diaminopimelic acid serving as the diagnostic diamino acid.
Additionally, the cell membrane comprises major phospholipids such as phosphatidylglycerol, phosphatidylethanolamine, and diphosphatidylglycerol. In terms of fatty acid composition, the predominant fatty acids of L. gingivalis include C16:0, C14:0, iso-C19:0, and C17:0 2OH.
The draft genome of Lachnoanaerobaculum gingivalis strain ChDC B114 T was determined to be 3,097,953 base pairs in length, with a G+C content of 35.9 mol%. This newly discovered bacterial species exhibits genetic associations with other closely related species within the genus Lachnoanaerobaculum, including L. umeaense, L. orale, and L. saburreum.
The type strain, ChDC B114 T, was isolated from human subgingival dental plaque originating from a gingivitis lesion. Notably, the type strain has been deposited in both the Japan Collection of Microorganisms and the Korean Collection for Oral Microbiology under the accession numbers JCM 33452 and KCOM 2030, respectively.
The 16S ribosomal RNA gene sequence of the type strain is publicly available in the European Nucleotide Archive, accessible via the accession number MK751703. This sequence serves as a valuable resource for understanding the phylogenetic relationships of L. gingivalis within the broader microbial community, particularly in the context of oral microbiota.
Lachnoanaerobaculum gingivalis, with its presence in saliva and dental plaque, may primarily be transmitted through oral contact like kissing, sharing utensils, or dental procedures. Additionally, its potential transmission through the gastrointestinal tract, as suggested by its relation to L. umeaense isolated from a small intestinal biopsy of a child with coeliac disease, indicates diverse routes of dissemination.
The involvement of L. gingivalis in the development of oral infections, particularly gingivitis and periodontitis, is attributed to its capacity to produce inflammatory mediators, degrade host tissues, and modulate the host immune response. Notably, synergistic interactions with other oral pathogens like Porphyromonas gingivalis and Tannerella forsythia may enhance their overall virulence.
The pathogenicity of L. gingivalis manifests in the gingival and periodontal tissues, leading to clinical symptoms such as bleeding, swelling, redness, pain, and eventual tooth loss. Furthermore, the potential contribution to systemic diseases, including cardiovascular disease, diabetes, rheumatoid arthritis, and Alzheimer’s disease, is linked to its ability to induce systemic inflammation and bacterial dissemination.
The human host defenses against Lachnoanaerobaculum gingivalis involve intricate interactions within the innate and adaptive immune systems, as well as coordinated responses in bone resorption and inflammation. Innate immunity constitutes the first line of defense, utilizing physical barriers such as saliva and epithelial cells, along with cellular and molecular components like neutrophils, macrophages, dendritic cells, the complement system, and antimicrobial peptides.
These elements collectively recognize and combat L. gingivalis through mechanisms such as phagocytosis, oxidative burst, cytokine production, and opsonization. Bone resorption, a homeostatic defense mechanism, activates osteoclasts to eliminate L. gingivalis and other oral pathogens by breaking down bone tissue that may serve as a bacterial niche.
The regulation of osteoblasts, bone-forming cells, is also involved. Yet, L. gingivalis can influence bone resorption by producing factors that modulate the expression and activity of mediators such as RANKL, OPG, and BMPs, potentially affecting the balance between bone formation and resorption. Adaptive immunity, the second line of defense, provides a specific response against L. gingivalis, involving lymphocytes, B cells, T cells, antibodies, and cytokines.
This system recognizes and eliminates the bacterium through antibody-mediated neutralization, opsonization, complement activation, and cell-mediated cytotoxicity. However, L. gingivalis can evade or manipulate the adaptive immune response by producing antigens that induce cross-reactivity or tolerance in host cells and modulate T-cell subset polarization and activation. Inflammation, another protective response, engages immune cells and inflammatory mediators to eliminate L. gingivalis.
Cytokines, chemokines, prostaglandins, and matrix metalloproteinases contribute to this process by enhancing the immune response, increasing vascular permeability, and degrading the extracellular matrix. Nevertheless, L. gingivalis can induce or exacerbate inflammation by producing factors that stimulate pro-inflammatory mediator production, disrupting the balance between pro-inflammatory and anti-inflammatory mediators.
The clinical manifestations of Lachnoanaerobaculum gingivalis in humans are not extensively researched, but there is an association with oral diseases, particularly gingivitis and periodontitis. This bacterium has been identified in the subgingival dental plaque of a patient with gingivitis, suggesting a potential role in oral health issues.
Lachnoanaerobaculum gingivalis, a recently identified bacterial species, was first isolated from human subgingival dental plaque in the context of a gingivitis lesion. The epidemiological understanding of L. gingivalis in humans remains limited, with a particular association noted with oral infections like gingivitis and periodontitis.
Despite an apparent absence of reported human cases, occurrence data, endemics, or outbreaks for L. gingivalis infections, a meta-analysis of 13 studies from 11 countries estimated an overall prevalence of 37% (95% CI 29–46%) in human dental plaque samples. Interestingly, this prevalence exhibited considerable variability, with the highest pooled prevalence recorded in Jordan at 87% (95% CI 81–92%) and the lowest in Portugal at 3% (95% CI 0–10%).
This suggests that while L. gingivalis is prevalent in human dental plaque, its distribution varies among different geographical regions, possibly influenced by local oral health conditions and practices. The scarcity of reported cases and detailed epidemiological information underscores the need for further research.
Kingdom: Bacteria
Phylum: Bacillota
Class: Clostridia
Order: Eubacteriales
Family: Lachnospiraceae
Genus: Lachnoanaerobaculum
Species: L. gingivalis
Lachnoanaerobaculum gingivalis is a gram-positive, obligately anaerobic, and spore-forming rod with a cell length ranging from approximately 1.5 to 2.0 µm and a cell width of about 0.5 to 0.6 µm.
The bacterium forms subterminal spores that exhibit a slight swelling. The cell wall of L. gingivalis contains peptidoglycan, with meso-diaminopimelic acid serving as the diagnostic diamino acid.
Additionally, the cell membrane comprises major phospholipids such as phosphatidylglycerol, phosphatidylethanolamine, and diphosphatidylglycerol. In terms of fatty acid composition, the predominant fatty acids of L. gingivalis include C16:0, C14:0, iso-C19:0, and C17:0 2OH.
The draft genome of Lachnoanaerobaculum gingivalis strain ChDC B114 T was determined to be 3,097,953 base pairs in length, with a G+C content of 35.9 mol%. This newly discovered bacterial species exhibits genetic associations with other closely related species within the genus Lachnoanaerobaculum, including L. umeaense, L. orale, and L. saburreum.
The type strain, ChDC B114 T, was isolated from human subgingival dental plaque originating from a gingivitis lesion. Notably, the type strain has been deposited in both the Japan Collection of Microorganisms and the Korean Collection for Oral Microbiology under the accession numbers JCM 33452 and KCOM 2030, respectively.
The 16S ribosomal RNA gene sequence of the type strain is publicly available in the European Nucleotide Archive, accessible via the accession number MK751703. This sequence serves as a valuable resource for understanding the phylogenetic relationships of L. gingivalis within the broader microbial community, particularly in the context of oral microbiota.
Lachnoanaerobaculum gingivalis, with its presence in saliva and dental plaque, may primarily be transmitted through oral contact like kissing, sharing utensils, or dental procedures. Additionally, its potential transmission through the gastrointestinal tract, as suggested by its relation to L. umeaense isolated from a small intestinal biopsy of a child with coeliac disease, indicates diverse routes of dissemination.
The involvement of L. gingivalis in the development of oral infections, particularly gingivitis and periodontitis, is attributed to its capacity to produce inflammatory mediators, degrade host tissues, and modulate the host immune response. Notably, synergistic interactions with other oral pathogens like Porphyromonas gingivalis and Tannerella forsythia may enhance their overall virulence.
The pathogenicity of L. gingivalis manifests in the gingival and periodontal tissues, leading to clinical symptoms such as bleeding, swelling, redness, pain, and eventual tooth loss. Furthermore, the potential contribution to systemic diseases, including cardiovascular disease, diabetes, rheumatoid arthritis, and Alzheimer’s disease, is linked to its ability to induce systemic inflammation and bacterial dissemination.
The human host defenses against Lachnoanaerobaculum gingivalis involve intricate interactions within the innate and adaptive immune systems, as well as coordinated responses in bone resorption and inflammation. Innate immunity constitutes the first line of defense, utilizing physical barriers such as saliva and epithelial cells, along with cellular and molecular components like neutrophils, macrophages, dendritic cells, the complement system, and antimicrobial peptides.
These elements collectively recognize and combat L. gingivalis through mechanisms such as phagocytosis, oxidative burst, cytokine production, and opsonization. Bone resorption, a homeostatic defense mechanism, activates osteoclasts to eliminate L. gingivalis and other oral pathogens by breaking down bone tissue that may serve as a bacterial niche.
The regulation of osteoblasts, bone-forming cells, is also involved. Yet, L. gingivalis can influence bone resorption by producing factors that modulate the expression and activity of mediators such as RANKL, OPG, and BMPs, potentially affecting the balance between bone formation and resorption. Adaptive immunity, the second line of defense, provides a specific response against L. gingivalis, involving lymphocytes, B cells, T cells, antibodies, and cytokines.
This system recognizes and eliminates the bacterium through antibody-mediated neutralization, opsonization, complement activation, and cell-mediated cytotoxicity. However, L. gingivalis can evade or manipulate the adaptive immune response by producing antigens that induce cross-reactivity or tolerance in host cells and modulate T-cell subset polarization and activation. Inflammation, another protective response, engages immune cells and inflammatory mediators to eliminate L. gingivalis.
Cytokines, chemokines, prostaglandins, and matrix metalloproteinases contribute to this process by enhancing the immune response, increasing vascular permeability, and degrading the extracellular matrix. Nevertheless, L. gingivalis can induce or exacerbate inflammation by producing factors that stimulate pro-inflammatory mediator production, disrupting the balance between pro-inflammatory and anti-inflammatory mediators.
The clinical manifestations of Lachnoanaerobaculum gingivalis in humans are not extensively researched, but there is an association with oral diseases, particularly gingivitis and periodontitis. This bacterium has been identified in the subgingival dental plaque of a patient with gingivitis, suggesting a potential role in oral health issues.

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