The efficacy of tinidazole in naturally occurring periodontitis in dogs: bacteriological and clinical results

Sarkiala, E.; Asikainen, Sirkka; Kanervo, A.; Junttila, Juha; Jousimies‐Somer, Hannele

doi:10.1016/0378-1135(93)90094-n

Cited by 19 publications

(12 citation statements)

References 26 publications

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“…In fact, strains with type II fimA were more virulent that those with type I fimA in a mouse abscess model [14]. Earlier studies obtained P. gingivalis-like isolates (likely P. gulae) from both healthy and diseased gingival pockets in dogs [1,16]. In our previous study, P. gulae was detected in approximately 90% of oral swab specimens from Japanese dogs, which came to veterinary clinics for health checkups and vaccinations [9].…”

Section: Discussionmentioning

confidence: 99%

Diversity of Fimbrillin among <i>Porphyromonas gulae</i> Clinical Isolates from Japanese Dogs

Nomura

Shirai

Kato

et al. 2012

The Journal of Veterinary Medical Science

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ABSTRACT. Porphyromonas gulae, a gram-negative black-pigmented anaerobe, is a pathogen for periodontitis in dogs. An approximately 41-kDa fimbrial subunit protein (FimA) encoded by fimA is regarded as associated with periodontitis. In the present study, the fimA genes of 17 P. gulae strains were sequenced, and classified into two major types. The generation of phylogenetic trees based on the deduced amino acid sequence of FimA of P. gulae strains along with sequences from several strains of Porphyromonas gingivalis, a major cause of human periodontitis, revealed that the two types of FimA (types A and B) of P. gulae were similar to type I FimA and types II and III FimA of P. gingivalis, respectively. A PCR system for classification was established based on differences in the nucleotide sequences of the fimA genes. Analysis of 115 P. gulae-positive oral swab specimens from dogs revealed that 42.6%, 22.6%, and 26.1% of them contained type A, type B, and both type A and B fimA genes, respectively. Experiments with a mouse abscess model demonstrated that the strains with type B fimA caused significantly greater systemic inflammation than those with type A. These results suggest that the FimA proteins of P. gulae are diverse with two major types and that strains with type B fimA could be more virulent. Periodontal diseases are characterized by gingivitis, a reversible condition involving gingival inflammation, and periodontitis, the irreversible destruction of periodontal tissues such as cementum, periodontal ligaments, and supportive bone [15]. In dogs, the prevalence of gingivitis is 95-100% and that of periodontitis, 50-70%, and the severity of periodontal disease tends to worsen with age, as in humans [8,10].Numerous periodontitis-related bacterial species have been reported in humans, with Porphyromonas gingivalis, a gram-negative black-pigmented anaerobe, considered a major species [15]. The 41-kDa cell surface protein fimbrillin (FimA), a subunit of fimbriae, is an important virulence factor of periodontitis, associated with adhesion to and invasion of gingival cells [4]. There are six genotypes of fimA encoding FimA (I through V and Ib), among which types II/ IV/Ib and I/III/V are considered invasive and non-invasive, respectively [2,3,[11][12][13][14]17].A previous analysis of 11 periodontitis-related bacterial species in oral swab specimens collected from 26 pet dogs in Japan showed that the isolation frequency of P. gingivalis was extremely low in dogs [9]. In contrast, Porphyromonas gulae was frequently detected in these specimens, accounting for approximately 70% of all Porphyromonas isolates. A recent study revealed the presence of a 41-kDa FimA, similar to that in P. gingivalis, in P. gulae [7]. In the present study, we performed molecular analyses of fimA in many clinical strains of P. gulae focusing on the association between the gene's diversity and virulence. Table 1 lists the P. gulae strains analyzed in the present study, 10 of which were isolated in Tokyo, Japan, previously [9]. The 7 new clinic...

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Section: Discussionmentioning

confidence: 99%

Diversity of Fimbrillin among <i>Porphyromonas gulae</i> Clinical Isolates from Japanese Dogs

Nomura

Shirai

Kato

et al. 2012

The Journal of Veterinary Medical Science

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“…gingiualis would live free in nature. Also, human isolates of these species are phenotypically and genetically distinct from those recovered from other mammals, such as monkeys, cats, and dogs (17,60,71,78,112,128). In humans, the highest frequencies and levels of A. actinomycetemcomitans and l ?…”

Section: The Natural Habitat Of a Actinomycetemcomitans And €! Gingimentioning

confidence: 99%

Oral ecology and person‐to‐person transmission of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis

Asikainen¹,

Chen²

1999

Periodontology 2000

130

111

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The ecological characteristics of the oral cavity are dissimilar for A. actinomycetemcomitans and for P. gingivalis, as judged by differences in their colonization preferences and patterns, associations with periodontal disease parameters, relationships with the subgingival microbiota and the type of periodontitis and their clonal persistence in the oral cavity. These features also suggest that as a periodontal pathogen, A. actinomycetemcomitans is different from P. gingivalis. Probably in most infected individuals, low levels of A. actinomycetemcomitans can persist for years in equilibrium with the host and the resident oral microbiota. However, it is well established that A. actinomycetemcomitans can cause disease in some individuals or in some circumstances when the regulatory mechanisms are unable to maintain homeostasis in the ecosystem. Elevated A. actinomycetemcomitans proportions of the biota can be regarded as a sign of ecological imbalance, leading to increased risk of periodontal destruction. There is also evidence showing elevated pathogenic potential of certain A. actinomycetemcomitans clones. Although A. actinomycetemcomitans seems to be relatively rarely transmitted between cohabiting adults, transmission can occur to periodontally healthy children of A. actinomycetemcomitans-positive parents. Parents and children may share factors that promote successful oral colonization of A. actinomycetemcomitans, or the window of opportunity is in childhood. Therefore, to prevent parent-child transmission of A. actinomycetemcomitans, bacterium-positive parents of young children are optimal targets for enhanced information and treatment. In selected populations, screening for specific clones of A. actinomycetemcomitans has been employed in prevention of peridontitis. Future research aiming at finding the reasons which cause the changes in the oral homeostasis to allow the growth of A. actinomycetemcomitans may give insight into novel prevention strategies for A. actinomycetemcomitans-associated periodontitis. Compared with A. actinomycetemcomitans, P. gingivalis shows a different pattern of coexistence with the host. In periodontal health or in children, P. gingivalis is absent or only rarely detected. When present, P. gingivalis is commonly recovered in high numbers from dentitions exhibiting inflamed periodontitis and poor oral hygiene. Contrary to A. actinomycetemcomitans, the data on the vertical transmission of P. gingivalis are limited. The major infection route of P. gingivalis seems to be between adults, indicating that P. gingivalis commonly colonizes in an established oral microbiota. These characteristics suggest that the degree of tolerance between P. gingivalis and the host is inferior to that between A. actinomycetemcomitans and the host. It appears that the association of P. gingivalis with disease is a rule rather than an accidental incident. On these grounds, it seems that the host-P. gingivalis relationship approaches antibiosis. Since P. gingivalis infection is related to a typical periodonta...

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“…The experimental periodontal diseases/periodontal pockets studied in dogs, were either induced by placing ligatures around the teeth for a certain period of time (94) or occurred spontaneously in old dogs (45,151). In different studies, ligatures placed around the teeth into the sulcus of the canine to establish chronic periodontal defects were maintained from 1 week to 20 weeks (78,155).…”

Section: Chronic Defect Model In Dogsmentioning

confidence: 99%

Description of the periodontal pocket in preclinical models: limitations and considerations

Donos¹,

Park²,

Vajgel³

et al. 2017

Periodontology 2000

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Establishment of periodontal health and regeneration of the lost periodontal tissues are always the ultimate goal of periodontal treatment. The development of new therapeutic approaches raises the necessity for appropriate experimental models that present periodontal structures and healing capability comparable to humans. Preclinical research and extrapolation of the data to human conditions remains a stage of great importance before the clinical application of the new biomaterials and techniques. Periodontal pockets/defects in preclinical models can be induced experimentally through acute or chronic or a combination of both (induced) modalities. The features of the created defects and those of humans vary greatly mostly due to the nature of the periodontal disease. This is an important point to take into account, since it is well recognized that the potential of periodontal therapy may be dependent on both the biological background and the defect morphology. This review provides insight into the commonly used preclinical models for the reproduction of the periodontal pocket and discusses the advantages and disadvantages of each model in terms of similarity to human conditions, standardization and reproducibility.

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The efficacy of tinidazole in naturally occurring periodontitis in dogs: bacteriological and clinical results

Cited by 19 publications

References 26 publications

Diversity of Fimbrillin among <i>Porphyromonas gulae</i> Clinical Isolates from Japanese Dogs

Diversity of Fimbrillin among <i>Porphyromonas gulae</i> Clinical Isolates from Japanese Dogs

Oral ecology and person‐to‐person transmission of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis

Description of the periodontal pocket in preclinical models: limitations and considerations

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