Porphyromonas gingivalis infection in the oral cavity is associated with elevated galactose-deficient IgA1 and increased nephritis severity in IgA nephropathy.

BACKGROUND: The relationship between the major periodontal bacteria, Porphyromonas gingivalis, and the pathogenesis of IgA nephropathy (IgAN)-particularly with respect to galactose-deficient IgA1 (Gd-IgA1)-has not been fully elucidated. METHODS: Saliva samples from 30 IgAN patients and 44 patients with chronic kidney disease (CKD) were subjected to analysis of P. gingivalis status via polymerase chain reaction using a set of P. gingivalis-specific primers. The associations between P. gingivalis presence and clinical parameters, including plasma Gd-IgA1, were analyzed in each group. RESULTS: Compared with the CKD group, the IgAN group demonstrated significantly higher plasma Gd-IgA1 levels (p < 0.05). Compared with the P. gingivalis-negative subgroup, the P. gingivalis-positive subgroup exhibited significantly higher plasma Gd-IgA1 levels in both IgAN and CKD patients (p < 0.05). Additionally, among IgAN patients, the P. gingivalis-positive subgroup displayed significantly higher plasma Gd-IgA1 and urine protein levels, compared with the P. gingivalis-negative subgroup (p < 0.05). With respect to renal biopsy findings, the frequencies of segmental glomerulosclerosis and tubular atrophy/interstitial fibrosis were significantly greater in the P. gingivalis-positive subgroup than in the P. gingivalis-negative subgroup, according to the Oxford classification of IgAN (p < 0.05). CONCLUSION: Our findings suggest an association between the presence of P. gingivalis in the oral cavity and the pathogenesis of IgAN, mediated by increased levels of Gd-IgA1.

Detection of Helicobacter pylori from Extracted Teeth of a Patient with Idiopathic Thrombocytopenic Purpura.

Immune thrombocytopenic purpura (ITP) is an autoimmune disease characterized by isolated cryptogenic thrombocytopenia due to a transient or persistent reduction in platelet count. Many patients with ITP have shown improved platelet count after Helicobacter pylori eradication therapy. However, there have been no studies regarding H. pylori in the oral cavity of patients with ITP. Here, we describe a patient with ITP whose oral samples exhibited H. pylori. A 64-year-old woman with ITP came to our hospital with chief complaints that required oral surgery, including tooth extraction and cystectomy. Bacterial DNA from H. pylori was confirmed on the extracted tooth, but was not detected in the saliva taken at the time. Bacterial DNA from H. pylori was detected on the suture around the extraction socket, which was removed at 10 days post-operation. However, H. pylori DNA was not detected in other oral samples at 10 or 30 days post-operation. A urea breath test was carried out in the gastrointestinal clinic at 60 days post-operation, which revealed no presence of H. pylori in the gastrointestinal tract. These results suggest that teeth with severe bacterial infections may be a potential reservoir of H. pylori for patients with ITP.

A Case of X-Linked Hypophosphatemic Rickets with Dentin Dysplasia in Mandibular Third Molars.

X-linked hypophosphatemic rickets (XLH) is a disease characterized by impaired bone mineralization, and its dental features include gingival abscesses and large pulp spaces due to dentin dysplasia. A 20-year-old woman with XLH was referred to oral surgery for extraction of mandibular third molars. She was diagnosed with XLH at approximately 1 year of age and was treated thereafter. There was no history of gingival abscesses, and panoramic radiographic and computed tomographic examinations revealed no evidence of dentin dysplasia. However, histopathological examination of the extracted teeth showed dentin dysplasia, including interglobular dentin. In this XLH patient, dentin dysplasia was revealed histologically even though no obvious abnormality was found on visual and radiographic examinations. These findings suggest that in patients with XLH, oral management must take dentin dysplasia of the permanent teeth into consideration even if the patient's general condition is well controlled with conventional therapy.

Contribution of Severe Dental Caries Induced by Streptococcus mutans to the Pathogenicity of Infective Endocarditis.

Streptococcus mutans, a major pathogen of dental caries, is regarded as a causative agent of infective endocarditis (IE), which mainly occurs in patients with underlying heart disease. However, it remains unknown whether severe dental caries that extend to pulp space represent a possible route of infection. In the present study, we evaluated the virulence of S. mutans for IE development using rats with concurrent severe dental caries and heart valve injury. Dental caries was induced in rats through the combination of a caries-inducing diet and the administration of S. mutans into the oral cavity. Then, the heart valves of a subset of rats were injured using a sterile catheter and wire under general anesthesia. The rats were euthanized at various times with various stages of dental caries. The number of teeth affected by dental caries with pulp exposure was increased in the rats in a time-dependent manner. S. mutans was recovered from injured heart tissue, which was mainly observed in rats with higher number of S. mutans bacteria in mandibular bone and a larger number of teeth in which caries extended to pulp. Dental caries was more severe in rats with heart injury than in rats without heart injury. Sequencing analysis targeting 16S rRNA revealed that specific oral bacteria appeared only in rats with heart injury, which may be related to the development of dental caries. Our findings suggest that dental caries caused by the combination of S. mutans infection and sucrose intake may contribute to S. mutans colonization in injured heart tissue.

Inhibition of Porphyromonas gulae and periodontal disease in dogs by a combination of clindamycin and interferon alpha.

Porphyromonas gulae is a major periodontal pathogen in dogs, which can be transmitted to their owners. A major virulence factor of P. gulae consists of a 41-kDa filamentous appendage (FimA) on the cell surface, which is classified into three genotypes: A, B, and C. Thus far, inhibition of periodontal disease in dogs remains difficult. The present study assessed the inhibitory effects of a combination of clindamycin and interferon alpha (IFN-α) formulation against P. gulae and periodontal disease. Growth of P. gulae was significantly inhibited by clindamycin; this inhibition had a greater effect on type C P. gulae than on type A and B isolates. In contrast, the IFN-α formulation inhibited the expression of IL-1ß and COX-2 elicited by type A and B isolates, but not that elicited by type C isolates. Furthermore, periodontal recovery was promoted by the administration of both clindamycin and IFN-α formulation to dogs undergoing periodontal treatment; moreover, this combined treatment reduced the number of FimA genotypes in oral specimens from treated dogs. These results suggest that a combination of clindamycin and IFN-α formulation inhibit P. gulae virulence and thus may be effective for the prevention of periodontal disease induced by P. gulae.