Dryness of the oral cavity is considered one cause of oral malodor. However, it is unclear which of the factors regulating the wetness of the oral cavity are involved in oral malodor development. This study investigated the effects of salivary flow and oral mucosal moisture on oral malodor.The study population comprised 119 patients (48 men and 71 women, mean age of 50.6 ± 15.4 years) with complaint of oral malodor. After the oral malodor level had been evaluated by the organoleptic test and gas chromatography, the rates of stimulated saliva and resting saliva and the moisture levels of the tongue and buccal mucosa were measured. The plaque index, bleeding on pocket probing, probing pocket depth, and tongue coating score were also assessed. Strong oral malodor was defined as an organoleptic test score of ≥3.The flow rate of resting saliva in women was significantly lower than in men. The flow rate of resting saliva and the moisture levels of the tongue and buccal mucosa showed significant negative correlations with age. The flow rate of resting saliva was significantly lower in patients with strong oral malodor than in those with no or weak oral malodor. The flow rate of stimulated saliva and the moisture levels of the tongue and buccal mucosa had no relationship with strong oral malodor. Logistic regression analysis showed that a ≥5-mm probing pocket depth with bleeding on pocket probing, an increased tongue coating score, and decreased resting salivary flow were strong explanatory factors in clinical findings for oral malodor.This study suggests that the flow rate of resting saliva is a significant modulating factor for oral malodor.
Ameloblastoma is the most common benign odontogenic tumor in Japan. It is believed that it expands in the jaw bone through peritumoral activation of osteoclasts by receptor activator of nuclear factor kappa-B ligand (RANKL) released from the ameloblastoma, as in bone metastases of cancer cells. However, the clinical features of ameloblastoma, including its growth rate and patterns of invasion, are quite different from those of bone metastasis of cancer cells, suggesting that different underlying mechanisms are involved. Therefore, in the present study, we examined the possible mechanisms underlying the invasive expansion of ameloblastoma in the jaw bone. Expression levels of RANKL assessed by western blotting were markedly lower in ameloblastoma (AM-1) cells than in highly metastatic oral squamous cell carcinoma (HSC-3) cells. Experiments coculturing mouse macrophages (RAW264.7) with AM-1 demonstrated low osteoclastogenic activity, as assessed by tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cell formation, probably because of low release of RANKL, whereas cocultures of RAW264.7 with HSC-3 cells exhibited very high osteoclastogenic activity. Thus, RANKL release from AM-1 appeared to be too low to generate osteoclasts. However, AM-1 cultured directly on calcium phosphate-coated plates formed resorption pits, and this was inhibited by application of bafilomycin A1. Furthermore, vacuolar-type H+-ATPase (V-ATPase) and H+/Cl- exchange transporter 7 (CLC-7) were detected on the surface of AM-1 cells by plasma membrane biotinylation and immunofluorescence analysis. Immunohistochemical analysis of clinical samples of ameloblastoma also showed plasma membrane-localized V-ATPase and CLC-7 in the epithelium of plexiform, follicular and basal cell types. The demineralization activity of AM-1 was only 1.7% of osteoclasts demineralization activity, and the growth rate was 20% of human normal skin keratinocytes and HSC-3 cells. These results suggest that the slow expansion of several typical types of ameloblastomas in jaw bone is attributable to its slow growth and low demineralization ability.
Abstract Acute joint inflammation was produced in BALB/c mice by a single intravenous injection of synthetic muramyl dipeptide (MDP), its stereoisomers and 6‐ O ‐acyl derivatives of MDP. Four adjuvant‐active, but not five adjuvant‐inactive MDP analogs induced acute swelling and erythema of the ankles and wrists which were detected around 6–10 hr, reached the maximum severity by 18–24 hr and subsided by days 3 to 4 after injection. Introduction of the stearoyl group, but not the α‐branched long chain fatty acid group into the C‐9 hydroxyl group of MDP enhanced and prolonged the joint lesions compared with MDP.
Background: Porphyromonas gingivalis is one of the most important periodontopathogens. It produces cysteine proteinases named gingipains. We previously examined the effect of gingipains on abscess formation in a murine model. The rgpA rgpB double and kgp mutants induced smaller abscesses than the wild type. Moreover, the rgpA rgpB kgp triple (gingipain‐null) mutant hardly showed lesion formation at all under the experimental conditions used, indicating that genes encoding gingipains are important for P. gingivalis virulence . Objectives: Here, we further report the humoral immune responses induced by P. gingivalis strains. Methods: After the lesions were apparently cured, sera were collected from the mice and immunoglobulin G (IgG) responses against the whole cell antigens of wild‐type P. gingivalis were measured . Results: Wild‐type strain was found to induce a strong antibody reaction. On the other hand, the rgpA rgpB kgp triple and kgp mutants induced significantly lower antibody responses compared to the wild type. Western blotting analysis confirmed the differences in antibody production. Next, these mice were re‐infected with wild‐type strain. Mice that were first infected with wild‐type strain showed significantly smaller lesion formation than control mice that were first infected with medium only. On the other hand, mice that were first infected with mutant strains devoid of gingipain activities did not show resistance to re‐infection and immunoglobulins directed against gingipains may be protective. Conclusions: These results suggest that gingipains play an important role in abscess formation in mice, and humoral immune responses seem to be partly responsible for the resistance to re‐infection by P. gingivalis .
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