
“The gut-oral axis connects your dog’s dental health to their digestive system through a continuous microbial exchange, with dogs swallowing up to 1.5 litres of bacteria-laden saliva daily. While we cannot prevent all plaque formation, we can profoundly influence the microbial balance at both ends of this axis, determining whether oral bacteria support digestive harmony or drive systemic inflammation.”
Summary
Periodontal disease directly disrupts a dog’s gut microbiome: every day dogs swallow approximately 0.75 to 1.5 litres of saliva, continuously seeding their gastrointestinal tract with oral bacteria and their metabolic products, making the mouth the gut’s primary microbial gateway and periodontitis a systemic condition with measurable consequences for gut health, liver function, and kidney disease risk.⁷˒⁸˒¹¹ This bidirectional system connects the oral and intestinal microbiomes, meaning that oral dysbiosis can trigger gut inflammation and, conversely, gut health influences which bacteria successfully colonise the mouth.⁷˒⁸˒¹¹
The canine oral microbiome harbours over 350 distinct bacterial species across multiple ecological niches, including supragingival plaque, subgingival pockets, soft tissues, and saliva.¹˒² When periodontal disease develops, pathogenic bacteria such as Porphyromonas gulae, the canine equivalent of the human keystone periodontal pathogen, proliferate and create cascading effects throughout the body.⁵˒⁶˒²⁵
At Bonza, the gut-oral axis is one of the eight gut-organ axes central to the “One Gut. Whole Dog.” philosophy, with the Biotics Triad in Bioactive Bites supporting the gut microbiome that reciprocally influences oral bacterial communities, and Superfoods & Ancient Grains providing the prebiotic fibre diversity that feeds the beneficial gut populations shown to reduce systemic inflammatory burden at both ends of this axis.
Key Takeaways
- High prevalence: Periodontal disease affects 80-90% of dogs by age three and up to 96% of dogs aged 12-14 years, making it the most common clinical condition in veterinary practice.[4,5]
- Diverse oral microbiome: The canine mouth harbours over 350 bacterial species across distinct niches, with 80% of taxa being unique to dogs and different from human oral bacteria.[1,2]
- Systemic disease connections: Research demonstrates significant associations between periodontal disease severity and histopathological changes in heart, liver, and kidney tissue.[7,8,9]
- Key pathogen identified: Porphyromonas gulae has emerged as the primary canine periodontal pathogen, with virulence characteristics similar to the human pathogen P. gingivalis.[5,6,25]
- Bidirectional communication: The gut-oral axis operates through multiple pathways including bacterial translocation via swallowing (0.75-1.5L saliva daily), inflammatory mediator signalling, and metabolite exchange.
- Breed susceptibility: Small and toy breeds (Yorkshire Terriers, Chihuahuas, Toy Poodles) show significantly higher rates and earlier onset of periodontal disease compared to larger breeds.[4,6]
- Nutritional intervention potential: Prebiotics, probiotics, postbiotics, omega-3 fatty acids, and functional ingredients like Ascophyllum nodosum seaweed can modulate both oral and gut microbiomes.[14,15,16,21]
- Treatment reduces risk: Research indicates that treatment of periodontal disease was associated with a 23% reduction in the risk of chronic kidney disease.[9]
Table of Contents
Introduction: Beyond the Toothbrush
The Canine Oral Microbiome: An Ecosystem Under Siege
- Diversity and Composition
- Ecological Niches Within the Mouth
- The Shift from Health to Disease
Periodontal Disease: A Systemic Condition
- Prevalence and Risk Factors
- Key Periodontal Pathogens
- Organ System Connections
The Gut-Oral Axis: Bidirectional Communication
- Oral-to-Gut Pathway
- Gut-to-Oral Pathway
- Inflammatory Signalling
- Metabolite Exchange
Nutritional Strategies for Gut-Oral Axis Support
- Prebiotics and Fibre
- Probiotics and Postbiotics
- Marine Bioactives
- Anti-inflammatory Nutrients
Practical Implementation for Dog Owners
Supporting Your Dog’s Gut-Oral Axis: The Bonza Approach
Introduction: Beyond the Toothbrush
When we think about our dog’s dental health, the image that typically comes to mind is one of brushing, dental chews, and perhaps the occasional professional cleaning. While these mechanical interventions certainly play a role in oral hygiene, they represent only a fraction of the story. The emerging science of the gut-oral axis reveals that your dog’s dental health is intimately connected to their digestive system – and that supporting one necessarily involves supporting the other.
The oral cavity serves as the gateway to the gastrointestinal tract, and this anatomical connection creates a continuous microbial superhighway. Every time your dog swallows, oral bacteria, their metabolites, and inflammatory signals travel to the gut. Conversely, the health of the intestinal microbiome influences which bacteria can successfully colonise the mouth and how the oral immune system responds to microbial challenges.[1,14]
This bidirectional relationship explains why periodontal disease has been associated with conditions seemingly unrelated to the mouth, including chronic kidney disease, liver pathology, and cardiovascular abnormalities.[7,8,9,10,11] It also opens exciting possibilities for nutritional interventions that can influence oral health through the gut and vice versa – a therapeutic approach that traditional dental care alone cannot achieve.
In this comprehensive guide, we explore the intricate connections between your dog’s mouth and gut, examine the scientific evidence linking oral health to systemic wellness, and provide practical nutritional strategies for supporting the gut-oral axis naturally.
The Canine Oral Microbiome: An Ecosystem Under Siege
Diversity and Composition
The canine oral cavity hosts a remarkably diverse microbial community. Landmark research from the Forsyth Institute and Waltham Petcare Science Institute identified 353 distinct bacterial taxa across 14 bacterial phyla, 23 classes, 37 orders, 66 families, and 148 genera.[1] Perhaps most striking is that approximately 80% of these taxa are unique to dogs and had not been previously characterised, highlighting the distinct nature of the canine oral ecosystem.
Importantly, only 16.4% of oral bacterial taxa are shared between dogs and humans based on 16S rRNA sequence similarity.[1] This fundamental difference means that assumptions based on human oral microbiology cannot be directly applied to dogs, and that products designed for human periodontal pathogens may be ineffective against canine-specific bacteria.[3]
The dominant phyla in healthy canine oral samples include Proteobacteria, Actinobacteria, Bacteroidetes, Firmicutes, and Fusobacteria.[2,23] The relative proportions of these groups shift dramatically during the transition from health to disease, with certain pathogenic species expanding while health-associated bacteria decline.
Ecological Niches Within the Mouth
Research from the Waltham Petcare Science Institute has demonstrated that distinct bacterial communities occupy different oral niches, each with unique characteristics.[2] Studies profiling supragingival plaque, buccal mucosa, tongue dorsum, and saliva from Labrador retrievers revealed three discrete oral niches: soft tissue surfaces (buccal and tongue dorsum mucosa), hard tissue surfaces (supragingival plaque), and saliva.
Supragingival plaque exhibited the highest bacterial diversity and the greatest number of significant differences in individual taxa compared to other niches.[2] Saliva showed the highest variability in microbial composition between individual dogs but the lowest overall bacterial diversity. These findings have important implications for sampling strategies in research and for understanding how oral bacteria interact with each other and the host.
The subgingival environment – below the gum line – represents a particularly critical niche. This oxygen-poor environment favours anaerobic bacteria, and as periodontal pockets deepen through disease progression, conditions increasingly favour pathogenic species that thrive without oxygen.[3,13]
The Shift from Health to Disease
A groundbreaking longitudinal study following 52 miniature Schnauzers over 60 weeks provided unprecedented insight into the bacterial changes accompanying periodontal disease development.[3] The research found that a group of aerobic Gram-negative species, including Bergeyella zoohelcum, Moraxella sp., Pasteurellaceae sp., and Neisseria shayeganii, decreased in proportion as teeth progressed to mild periodontitis.
This pattern – characterised by a reduction in health-associated taxa rather than simply an increase in pathogens – suggests that periodontitis development involves community-wide ecological shifts.[3] Several members of the Firmicutes phylum became more abundant as gingivitis severity increased, indicating that the transition from health to disease involves complex microbial dynamics rather than infection by a single pathogen.
Periodontal Disease: A Systemic Condition
Prevalence and Risk Factors
Periodontal disease represents the most common clinical condition diagnosed in dogs, with prevalence estimates ranging from 44% to over 90% depending on age and diagnostic criteria used.[4] Studies examining dogs presented at veterinary clinics have documented periodontitis in 82% of dogs aged 6-8 years and 96% of dogs aged 12-14 years.[5]
Small and toy breeds show significantly higher susceptibility to periodontal disease compared to larger breeds.[4,6] Yorkshire Terriers, Toy Poodles, Chihuahuas, and Miniature Schnauzers are particularly affected, likely due to a combination of factors including tooth crowding, genetic predisposition, and proportionally smaller jaw structures. In these breeds, periodontal disease often develops earlier and progresses more rapidly.
A recent study examining Porphyromonas gulae distribution in 665 small breed dogs found that dogs with at least one fimA genotype of the pathogen had significantly more severe periodontal disease compared to P. gulae-negative dogs.[6] The study demonstrated that periodontal disease severity and P. gulae colonisation both tended to increase with age across all breeds examined.
Key Periodontal Pathogens
Porphyromonas gulae has emerged as the bacterial species most often associated with periodontal disease in dogs.[5,25] First isolated in 2001 from the mouths of various animal hosts, this Gram-negative, black-pigmented anaerobe shares significant virulence characteristics with Porphyromonas gingivalis, the so-called “keystone pathogen” in human periodontitis.[5]
Research has demonstrated that P. gulae exhibits similar virulence mechanisms to P. gingivalis, including the production of gingipains (proteases), fimbriae for adhesion, lipopolysaccharide, and the ability to induce proinflammatory cytokine release from macrophages.[5,25] The P. gulae FimA protein, expressed on the bacterial cell surface, is classified into three genotypes (A, B, and C), with type C considered the most virulent and predominant in dogs with severe periodontitis.[6,12]
Other important periodontal pathogens include Tannerella forsythia, Fusobacterium nucleatum (a common pathogen in both dogs and humans), Campylobacter rectus, and various Treponema species.[3,13,25] These bacteria often work in concert, with some species facilitating colonisation by others and creating synergistic pathogenic effects.
Organ System Connections
The systemic implications of periodontal disease extend far beyond the oral cavity. A seminal study examining 45 dogs found significant associations between periodontal disease severity and histopathological changes in the kidney, myocardium (papillary muscle), and liver.[7] This groundbreaking research demonstrated that periodontal disease is not merely a local condition but one with whole-body consequences.
Post-mortem investigations of 44 mature toy and miniature Poodles quantified the relationship between periodontal disease burden and organ pathology.[8] Using ordinal logistic regression, researchers established that for each square centimetre of periodontal disease burden, there was a 1.4-times higher likelihood of greater changes in the left atrio-ventricular valves, plus 1.2 and 1.4 times higher likelihood for greater liver and kidney pathology, respectively.
A landmark epidemiological study of over 164,000 dogs with periodontal disease examined the association with chronic kidney disease (CKD).[9] The hazard ratio for azotemic CKD increased with increasing severity of periodontal disease: stage 1 showed a hazard ratio of 1.8, stage 2 a ratio of 2.0, and stage 3/4 a ratio of 2.7. Critically, treatment of periodontal disease was associated with a 23% reduction in the risk of azotemic CKD, providing evidence that intervention can modify systemic disease risk.
Cardiovascular associations have also been documented. Research has found that periodontal disease is associated with endocarditis and cardiovascular changes in dogs.[10,11] Interestingly, type C P. gulae has been found prevalent in dogs with mitral regurgitation, suggesting a potential link between specific periodontal pathogens and cardiac disease.[12]
The Gut-Oral Axis: Bidirectional Communication

Oral-to-Gut Pathway
The most direct route of communication between the oral cavity and gut is through swallowing. Dogs produce and swallow approximately 0.75 to 1.5 litres of saliva daily, continuously delivering oral bacteria, their metabolic products, and host-derived inflammatory mediators to the gastrointestinal tract. This constant microbial seeding means that oral dysbiosis can directly influence gut microbial composition and function.
Oral pathogens that survive transit through the acidic stomach environment can colonise the intestine, potentially contributing to gut dysbiosis and inflammation. Studies in humans and animal models have demonstrated that periodontal pathogens can indeed be detected in the gut, and that oral infection can alter intestinal barrier function and trigger local immune responses. While direct evidence in dogs is still emerging, the mechanistic framework established in other species suggests similar pathways operate in canines.
Gut-to-Oral Pathway
Communication also flows from gut to mouth. The intestinal microbiome influences systemic immune function, and this immune modulation affects how the oral environment responds to bacterial challenges.[14,20] A healthy gut microbiome promotes balanced immune responses, helping to prevent the excessive inflammation that characterises periodontal disease.
Metabolites produced by gut bacteria, particularly short-chain fatty acids (SCFAs) like acetate, propionate, and butyrate, enter systemic circulation and can influence oral tissue health.[14,20] These compounds have well-documented anti-inflammatory properties and can modulate immune cell function throughout the body, including in the periodontal tissues.
Inflammatory Signalling
Periodontal disease generates a chronic inflammatory response characterised by elevated levels of pro-inflammatory cytokines including interleukin-1β (IL-1β), interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), and cyclooxygenase-2 (COX-2).[11,12] These inflammatory mediators don’t remain localised – they enter systemic circulation and can influence distant organ systems, including the gut.
This systemic inflammatory burden helps explain the associations between periodontal disease and organ pathology.[7,8,11] Chronic low-grade inflammation is increasingly recognised as a driver of multiple disease processes, and the mouth represents a significant potential source of this inflammatory load. Reducing periodontal inflammation through appropriate treatment and nutritional support can therefore benefit overall health beyond the oral cavity.
Metabolite Exchange
The relationship between SCFAs and periodontal health presents an interesting paradox. While gut-derived SCFAs circulating systemically exert anti-inflammatory effects, locally produced SCFAs in periodontal pockets may actually contribute to tissue damage by acidifying the environment and providing substrate for pathogenic bacteria.[20] This complexity highlights the importance of considering the entire gut-oral axis rather than focusing on single metabolites in isolation.
Other bacterial metabolites including trimethylamine, hydrogen sulphide, and various toxins can also travel between oral and gut compartments. Understanding these complex metabolic exchanges provides opportunities for targeted nutritional interventions that can modulate the biochemical environment at both ends of the axis.
Nutritional Strategies for Gut-Oral Axis Support
Prebiotics and Fibre
Prebiotic fibres that selectively nourish beneficial gut bacteria can influence oral health through multiple mechanisms.[14,17] By promoting a healthy gut microbiome, prebiotics support optimal immune function that helps maintain oral homeostasis. Different fibre types have been shown to modulate the canine gut microbiome in specific ways, with beet pulp, fructooligosaccharides (FOS), and mannan-oligosaccharides (MOS) among the most studied.
Research has demonstrated that prebiotic supplementation can increase beneficial bacterial populations and SCFA production in dogs.[14,17] While direct effects on oral health require further investigation, the systemic anti-inflammatory benefits of a well-nourished gut microbiome likely extend to periodontal tissue health.
Probiotics and Postbiotics
Probiotic supplementation in dogs has demonstrated benefits for gut health and immune function.[17,18,19] While probiotics typically cannot permanently colonise the gut due to competition with established microbiota, they can still exert beneficial effects through the production of antimicrobial peptides, metabolites that modify the local microbiota, and interaction with the host immune system.[20]
Specific probiotic strains studied in dogs include Enterococcus faecium, Lactobacillus species, Bifidobacterium species, and Bacillus species including B. subtilis/B. velezensis.[17,18] These organisms support gut barrier function, compete with pathogenic bacteria, and modulate immune responses.
Postbiotics – the beneficial compounds produced by probiotic bacteria or released upon their inactivation – offer another approach to supporting the gut-oral axis.[19] These include heat-treated bacterial preparations that retain immune-modulating properties without requiring live organisms. Postbiotics may offer advantages in terms of stability and consistency of effect.
Marine Bioactives
The brown seaweed Ascophyllum nodosum has emerged as a promising natural intervention for canine oral health.[15,16] A placebo-controlled, double-blind, randomised study demonstrated that 90-day supplementation with treats containing A. nodosum significantly improved plaque index, calculus index, and volatile sulphur compound (VSC) concentration compared to placebo.[15]
The mechanisms underlying these benefits are not fully elucidated, but research suggests that active ingredients from the seaweed may be absorbed in the small intestine and then secreted into the oral cavity via saliva – a perfect example of gut-to-oral communication.[15,16] Metabolomic analysis of dog saliva following A. nodosum supplementation revealed clear changes in metabolite profiles, supporting this hypothesis.
Ascophyllum nodosum contains numerous biologically active compounds including polysaccharides (ascophyllan, fucoidan, laminarin), polyphenols, minerals, and vitamins.[16] Clinical trials have demonstrated its effectiveness in both dogs and cats, with the strongest preventive action observed when administered as a powder.[16]
Anti-inflammatory Nutrients
Omega-3 polyunsaturated fatty acids, particularly EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), represent powerful anti-inflammatory nutrients with documented benefits for periodontal health.[21,22] These fatty acids modulate the inflammatory response through multiple mechanisms: they incorporate into cell membrane phospholipids, compete with arachidonic acid for cyclooxygenase and lipoxygenase enzymes, and serve as precursors for specialised pro-resolving mediators including resolvins, protectins, and maresins.
Systematic reviews and meta-analyses of human studies have demonstrated that omega-3 supplementation as an adjunct to periodontal therapy significantly improves clinical attachment level and probing depth.[21,22] While direct canine studies are more limited, the anti-inflammatory mechanisms are conserved across species, and omega-3 supplementation is well-established in veterinary practice for various inflammatory conditions.
EPA and DHA also demonstrate antibacterial properties, with research showing inhibition of periodontal pathogens including Porphyromonas gingivalis, Fusobacterium nucleatum, and Prevotella intermedia.[22] Given the similarity between P. gingivalis and canine P. gulae, similar antibacterial effects may benefit dogs.[5]
Plant-based polyphenols and antioxidants provide additional anti-inflammatory support. Compounds found in turmeric, green tea, and various fruits and vegetables can modulate oxidative stress and inflammatory pathways relevant to both oral and gut health.
Practical Implementation for Dog Owners
Supporting your dog’s gut-oral axis doesn’t require complicated interventions. Here are evidence-based strategies that can be implemented at home:
- Choose a complete diet with gut-oral axis support: Look for diets containing prebiotic fibres, omega-3 fatty acids from algal or marine sources, and probiotic or postbiotic ingredients. Plant-based diets rich in fibre and antioxidants naturally support both gut and oral microbiome health.
- Consider targeted supplementation: Supplements containing Ascophyllum nodosum seaweed, probiotics, and omega-3s can provide additional support beyond what diet alone provides, particularly for dogs at higher risk of periodontal disease.[15,16]
- Maintain regular dental care: Daily tooth brushing remains the gold standard for mechanical plaque removal, achieving up to 37.4% plaque reduction and 80.2% calculus reduction compared to non-brushed teeth.[15] Combine mechanical cleaning with nutritional support for optimal results.
- Schedule professional dental assessments: Regular veterinary dental examinations allow early detection of periodontal disease. The American Animal Hospital Association recommends complete dental prophylaxis by 1 year of age for small and medium breeds.
- Monitor for warning signs: Bad breath (halitosis), red or swollen gums, reluctance to eat hard food, pawing at the mouth, and visible tartar accumulation all warrant veterinary attention.
Supporting Your Dog’s Gut-Oral Axis: The Bonza Approach
Bonza’s “One Gut. Whole Dog.” philosophy recognises that oral health and gut health are not separate concerns:the daily swallowing of up to 1.5 litres of bacteria-laden saliva makes the mouth the gut’s primary microbial gateway, and the gut microbiome reciprocally determines which oral bacterial communities can establish and thrive. The gut-oral axis is one of the eight gut-organ axes underpinning Bonza’s formulation framework, informing both Superfoods & Ancient Grains and the Bioactive Bites supplement range. The daily food provides foundational gut-oral axis support through Calsporin®, TruPet™ postbiotic, prebiotic chicory, yeast-derived MOS and beta-glucans, DHAgold® algae-derived omega-3, and the PhytoPlus® botanical blend, working together through the Biotics Triad to maintain the gut microbiome balance and systemic inflammatory control that reciprocally influences oral bacterial community composition and periodontal tissue integrity.
For dogs requiring targeted gut-oral axis support, Biotics Bioactive Bites is formulated to address the gut foundation of oral health, combining the complete Biotics Triad at therapeutic concentrations: TruPet™ postbiotic (285mg), Calsporin® (4.5 × 10⁴ CFU), and Lactobacillus helveticus (2.7 × 10⁹ CFU), alongside L-glutamine and zinc glycinate for gut barrier repair to reduce the endotoxin translocation that drives systemic inflammation affecting periodontal tissues, and clinoptilolite for direct endotoxin binding within the gut lumen. Used together with Superfoods & Ancient Grains, Biotics addresses the gut-oral axis at both ends simultaneously, from the gut microbiome that reciprocally shapes oral bacterial communities to the systemic inflammatory burden that determines whether periodontal disease remains localised or drives organ-level consequences throughout the body.
Frequently Asked Questions
While nutrition plays an important role in supporting oral health through the gut-oral axis, diet alone cannot completely prevent periodontal disease. The most effective approach combines appropriate nutrition with regular dental care, including tooth brushing and professional cleanings. However, diets and supplements that support the gut-oral axis can reduce disease severity and support overall oral health.
Small and toy breeds have proportionally smaller jaws relative to tooth size, leading to tooth crowding that creates ideal conditions for plaque accumulation.[4,6] Additionally, some small breeds may have genetic predispositions affecting their oral microbiome or immune responses to periodontal pathogens.
Research has demonstrated that increasing severity of periodontal disease is associated with increased risk of chronic kidney disease in dogs.[9] The mechanisms likely involve chronic bacteraemia (bacteria entering the bloodstream), immune complex formation affecting kidney tissue, and systemic inflammation damaging renal structures. Importantly, treatment of periodontal disease has been associated with reduced risk of kidney disease.
Common signs include persistent bad breath (halitosis), red or bleeding gums, visible tartar on teeth, difficulty eating or preference for soft foods, drooling, pawing at the mouth, loose or missing teeth, and facial swelling. However, early periodontal disease often has no obvious signs, making regular veterinary dental examinations essential.
Probiotics support oral health indirectly through the gut-oral axis by promoting optimal immune function, reducing systemic inflammation, and supporting a healthy gut microbiome that influences the body’s response to oral pathogens.[17,18,19] While probiotics are not a replacement for dental care, they represent a valuable component of a comprehensive oral health strategy.
Ascophyllum nodosum seaweed contains bioactive compounds that, when absorbed through the gut, appear to be secreted into saliva and modify the oral environment in ways that reduce plaque and calculus formation.[15,16] Clinical studies have demonstrated significant improvements in oral health indices with daily supplementation.
Dental health attention should begin in puppyhood. Establishing good oral hygiene habits early, including introducing tooth brushing and providing appropriate nutrition from the start, sets the foundation for lifelong oral health. Professional dental assessment is recommended by one year of age for small breeds and two years for larger breeds.
Gingivitis (early gum inflammation without bone loss) is reversible with appropriate treatment and improved oral care. However, periodontitis involving bone loss is generally irreversible, though it can be controlled and further progression prevented. This underscores the importance of early intervention and preventive strategies including nutritional support for the gut-oral axis.
Conclusion
The gut-oral axis represents a frontier in understanding and supporting canine health. The evidence linking periodontal disease to systemic conditions including kidney disease, liver pathology, and cardiovascular changes underscores that dental health cannot be viewed in isolation.[7,8,9,10,11] What happens in your dog’s mouth affects their entire body, and what happens in their gut influences their oral microbiome.
This bidirectional communication opens opportunities for nutritional interventions that traditional dental care alone cannot provide. By supporting the gut microbiome with prebiotics, probiotics, and postbiotics, and by providing anti-inflammatory nutrients like omega-3 fatty acids and bioactive compounds from sources like Ascophyllum nodosum seaweed, we can influence oral health from the inside out.[14,15,16,17,21]
The most effective approach combines these nutritional strategies with regular mechanical dental care and professional veterinary oversight. Together, these interventions support the entire gut-oral axis, promoting optimal health for your dog from mouth to gut and beyond.
References
- Dewhirst FE, Klein EA, Thompson EC, et al. The canine oral microbiome. PLoS One. 2012;7(4):e36067. doi:10.1371/journal.pone.0036067
- Ruparell A, Inui T, Staunton R, et al. The canine oral microbiome: variation in bacterial populations across different niches. BMC Microbiol. 2020;20(1):42. doi:10.1186/s12866-020-1704-3
- Wallis C, Marshall M, Colyer A, et al. A longitudinal assessment of changes in bacterial community composition associated with the development of periodontal disease in dogs. Vet Microbiol. 2015;181(3-4):271-282. doi:10.1016/j.vetmic.2015.09.003
- Wallis C, Holcombe LJ. A review of the frequency and impact of periodontal disease in dogs. J Small Anim Pract. 2020;61(9):529-540. doi:10.1111/jsap.13218
- Lenzo JC, O’Brien-Simpson NM, Orth RK, et al. Porphyromonas gulae has virulence and immunological characteristics similar to those of the human periodontal pathogen Porphyromonas gingivalis. Infect Immun. 2016;84(9):2575-2585. doi:10.1128/IAI.01500-15
- Shirahata S, Iwashita N, Sasaki R, Nomura R, Murakami M, Yasuda J, Yasuda H, Nakajima K, Inaba H, Matsumoto-Nakano M, Nakano K, Uchiyama J and Fukuyama T (2023) Possible association of fimA genotype of Porphyromonas gulae with the severity of periodontal disease and the number of permanent teeth in dogs. Front. Vet. Sci. 10:1022838. doi: 10.3389/fvets.2023.1022838
- DeBowes LJ, Mosier D, Logan E, et al. Association of periodontal disease and histologic lesions in multiple organs from 45 dogs. J Vet Dent. 1996;13(2):57-60.
- Pavlica Z, Petelin M, Juntes P, et al. Periodontal disease burden and pathological changes in organs of dogs. J Vet Dent. 2008;25(2):97-105. doi:10.1177/089875640802500210
- Glickman LT, Glickman NW, Moore GE, et al. Association between chronic azotemic kidney disease and the severity of periodontal disease in dogs. Prev Vet Med. 2011;99(2-4):193-200. doi:10.1016/j.prevetmed.2011.01.011
- Glickman LT, Glickman NW, Moore GE, et al. Evaluation of the risk of endocarditis and other cardiovascular events on the basis of the severity of periodontal disease in dogs. J Am Vet Med Assoc. 2009;234(4):486-494. doi:10.2460/javma.234.4.486
- Pereira Dos Santos JD, Cunha E, Nunes T, et al. Relation between periodontal disease and systemic diseases in dogs. Res Vet Sci. 2019;125:136-140. doi:10.1016/j.rvsc.2019.06.007
- Nomura R, Inaba H, Yasuda H, et al. Inhibition of Porphyromonas gulae and periodontal disease in dogs by a combination of clindamycin and interferon alpha. Sci Rep. 2020;10(1):3113. doi:10.1038/s41598-020-59730-9
- Davis IJ, Wallis C, Deusch O, et al. A cross-sectional survey of bacterial species in plaque from client owned dogs with healthy gingiva, gingivitis or mild periodontitis. PLoS One. 2013;8(12):e83158. doi:10.1371/journal.pone.0083158
- Pilla R, Suchodolski JS. The gut microbiome of dogs and cats, and the influence of diet. Vet Clin North Am Small Anim Pract. 2021;51(3):605-621. doi:10.1016/j.cvsm.2021.01.002
- Gawor JP, Jank M, Jodkowska K, et al. Effects of edible treats containing Ascophyllum nodosum on the oral health of dogs: a double-blind, randomized, placebo-controlled single-center study. Front Vet Sci. 2018;5:168. doi:10.3389/fvets.2018.00168
- Gawor J, Jank M. Ascophyllum nodosum as a nutrient supporting oral health in dogs and cats: a review. Pol J Vet Sci. 2023 Sep 20;26(3):511-520. doi: 10.24425/pjvs.2023.145053. PMID: 37727971.
- Schmitz S, Suchodolski J. Understanding the canine intestinal microbiota and its modification by pro-, pre- and synbiotics – what is the evidence? Vet Med Sci. 2016;2(2):71-94. doi:10.1002/vms3.17
- Lee D, Goh TW, Kang MG, et al. Perspectives and advances in probiotics and the gut microbiome in companion animals. J Anim Sci Technol. 2022;64(2):197-217. doi:10.5187/jast.2022.e8
- Yang Q, Wu Z. Gut Probiotics and Health of Dogs and Cats: Benefits, Applications, and Underlying Mechanisms. Microorganisms. 2023 Sep 29;11(10):2452. doi: 10.3390/microorganisms11102452. PMID: 37894110; PMCID: PMC10609632.
- Pilla R, Suchodolski JS. The role of the canine gut microbiome and metabolome in health and gastrointestinal disease. Front Vet Sci. 2020;6:498. doi:10.3389/fvets.2019.00498
- Stańdo M, Pleskacz M, Csupor D, et al. Omega-3 polyunsaturated fatty acids as an adjunct to non-surgical treatment of periodontitis. Eur J Lipid Sci Technol. 2020;122(2):1800345. doi:10.1002/ejlt.201800345
- Kruse AB, Kowalski CD, Leuthold S, Vach K, Ratka-Krüger P, Woelber JP. What is the impact of the adjunctive use of omega-3 fatty acids in the treatment of periodontitis? A systematic review and meta-analysis. Lipids Health Dis. 2020 May 21;19(1):100. doi: 10.1186/s12944-020-01267-x. PMID: 32438906; PMCID: PMC7240972.
- Oh C, Lee K, Cheong Y, et al. Comparison of the oral microbiomes of canines and their owners using next-generation sequencing. PLoS One. 2015;10(7):e0131468. doi:10.1371/journal.pone.0131468
- Sturgeon A, Stull JW, Costa MC, Weese JS. Metagenomic analysis of the canine oral cavity as revealed by high-throughput pyrosequencing of the 16S rRNA gene. Vet Microbiol. 2013;162(2-4):891-898. doi:10.1016/j.vetmic.2012.11.018
- Kwack KH, Jang EY, Kim C, Choi YS, Lee JH, Moon JH. Porphyromonas gulae and canine periodontal disease: Current understanding and future directions. Virulence. 2025 Dec;16(1):2449019. doi: 10.1080/21505594.2024.2449019. Epub 2025 Jan 21. PMID: 39834343; PMCID: PMC11756583.
Editorial Information
| Field | Detail |
|---|---|
| Published | 22 January 2026 |
| Last Updated | 21 March 2026 (image added) |
| Reviewed by | Glendon Lloyd Dip.Canine.Nutrition Dip.Dog.Nutrigenomics |
| Next Review | January 2027 |
| Author | Glendon Lloyd Dip.Canine.Nutrition Dip.Dog.Nutrigenomics |
| Disclaimer | This article is for informational purposes only and does not constitute veterinary advice. Always consult a qualified veterinarian before making changes to your dog’s diet or supplement regimen. |
One note: the article currently carries its own expanded disclaimer at the bottom (the longer version referencing heart disease, medications, pregnancy etc.), which is good practice for this topic given the systemic disease associations discussed. You may want to keep that as a separate clinical disclaimer block distinct from the Editorial Information table, since the locked table disclaimer is the shorter, standardised version. Worth flagging for consistency across the hub.