Disease relevance of Periodontitis

• Inhibition of OPG-L may thus have therapeutic value to prevent alveolar bone and/or tooth loss in human periodontitis [1].
• The oral anaerobic bacterium Porphyromonas gingivalis, a major pathogen of advanced adult periodontitis, produces a novel class of cysteine proteinases in both cell-associated and secretory forms [2].
• These findings suggest that generation of bradykinin in inflammatory lesions of rheumatoid arthritis and periodontitis may contribute to the bone resorptive process seen in the joints and alveolar bone; however, bradykinin does not directly activate chondrocytes into a catabolic state [3].
• This failure to ameliorate the complications of periodontitis in patients with primary SS was associated with high levels of BAFF in their saliva compared with the levels in xerostomia controls (7.4 +/- 2.1 versus 1.0 +/- 0.4 ng/ml [P < 0.002]) [4].
• Culture supernatants from Treponema maltophilum associated with periodontitis in humans and Treponema brennaborense found in a bovine cattle disease accompanied with cachexia caused a dose-dependent TNF-alpha synthesis in human monocytes increasing with culture time [5].

Psychiatry related information on Periodontitis

• Metronidazole in periodontitis (IV). The effect of patient compliance on treatment parameters [6].
• BACKGROUND: Increased physical activity improves insulin sensitivity and glucose metabolism, and may therefore affect incidence of periodontitis [7].
• METHODS: Using the Heft-Parker self-assessment pain scale, 52 adults with moderate periodontitis evaluated their pain before and after SRP conducted with local anesthetic [8].

High impact information on Periodontitis

• Most PLS patients display both periodontitis and hyperkeratosis [9].
• These results indicate that RGP-1 is the major VPE factor of P. gingivalis, inducing this activity through PK activation and subsequent BK release, resulting in GCF production at sites of periodontitis caused by infection with this organism [10].
• Furthermore, mice protected in the lesion and periodontitis models had a predominant P. gingivalis-specific IL-4 response, whereas mice with disease had a predominant IFN-gamma response [11].
• To study an involvement of the periodontitis pathogen and neuropeptides in pulp inflammation, we investigated human dental pulp cell neuropeptide release by arginine-specific cysteine protease (RgpB), a cysteine proteinase of P. gingivalis, and participating signaling pathways [12].
• Thus, elevated VEGF secretion in HGFs under the HG condition may play a role in the development of the severe periodontitis observed in diabetic patients [13].

Chemical compound and disease context of Periodontitis

• Our results indicate that the more phagocytosis-resistant invasive strains accumulate less 125I-C3 than the noninvasive strain; moreover, invasive strains degrade complement C3 in a dose-dependent manner, inhibitable by rabbit antiserum or adult periodontitis serum [14].
• The effect of two arginine-specific cysteine proteinases (gingipain Rs) from Porphyromonas gingivalis, a causative bacterium of adult periodontitis, on human blood coagulation was investigated [15].
• Opsonization and C3 accumulation on strain A7436 were both facilitated by pretreatment with rabbit antiserum, certain adult periodontitis sera, protease inhibitors (p-chloromercuriphenylsulfonic acid, N alpha-p-tosyl-L-lysine chloromethyl ketone, diisopropylfluorophosphate), heat (60 degrees C, 15 min), and were Mg2+ dependent [14].
• Periodontitis in estrogen-deficient women [16].
• The results indicate that in patients who are allergic to penicillin, cefixime and ciprofloxacin may be useful alternative antibiotics in combination with metronidazole for the treatment of A. actinomycetemcomitans-associated periodontitis [17].

Biological context of Periodontitis

• Extracellular cysteine proteinases, referred to as gingipains, are considered important virulence factors for Porphyromonas gingivalis, a bacterium recognized as a major etiologic agent of chronic periodontitis [18].
• Analysis of the nucleotide sequences of the TCR demonstrated that human hsp60-reactive T-cell clones and periodontitis lesion-infiltrating T cells have the same receptors, suggesting that hsp60-reactive T cells accumulate in periodontitis lesions [19].
• Sixty-nine EOP patients, including 11 with localized juvenile periodontitis (LJP), 19 who had LJP, 15 with LJP-rapidly progressing periodontitis (RPP), and 24 with RPP, were examined for the Gm and Km allotypes by a hemagglutination inhibition test [20].
• Neutrophil chemotaxis was evaluated in nine patients with juvenile periodontitis, with normal subjects and patients with the adult form of periodontitis as controls [21].
• Accordingly, we examined cell motility of PMNs and MNs from 27 patients with rapidly progressive periodontitis, 5 patients with juvenile periodontitis, and 37 normal control subjects by using a microchamber technique and the synthetic peptide N-formylmethionyl-leucyl-phenylalanine (FMLP) as the chemoattractant [22].

Anatomical context of Periodontitis

• Examination of human gingival tissue sections from subjects with chronic adult periodontitis with in situ hybridization revealed marked expression of MMP-13 in basal cells of some epithelial rete ridges expanding into connective tissue [23].
• Anti-neutrophil cytoplasmic Abs targeting proteinase 3 (PR3) have been detected in relation to a wide range of inflammatory conditions such as periodontitis, and interaction of anti-PR3 Abs with endothelial and epithelial cells provokes cell activation, although the underlying mechanism has been unclear [24].
• Studies of anaerobic periodontal infections have shown that active MMP-8 in gingival crevicular fluid is associated with the degradation of periodontal tissues in progressive periodontitis whereas the latent enzyme is predominant in gingivitis [25].
• Circulating promyelocytes and low levels of CD16 expression on polymorphonuclear leukocytes accompany early-onset periodontitis [26].
• The sum of these activities may result in the recruitment of differential cell types to sites of inflammation since IL-8 preferentially recruits neutrophils and IP-10 attracts activated T cells and may be relevant to the pathogenesis of periodontitis [27].

Gene context of Periodontitis

• We found a higher frequency of allele 2 carriage in IL-1A, IL-1B, and IL-1RN in periodontitis patients who were non-smokers and in whom P. gingivalis and A. actinomycetemcomitans could not be detected (42.1% vs. 11.3% in controls; P = 0.0068; OR 5.7, 95% CI: 1.6-19.8) [28].
• This study provides evidence for a major role of TNF-alpha in chronic adult periodontitis [29].
• FOXP3, a characteristic marker for CD4+CD25+ Tr cells, TGF-beta1 and IL-10 were expressed more highly in periodontitis compared with gingivitis [30].
• We hypothesized that functional CD14 and TLR4 polymorphisms contribute to periodontitis susceptibility [31].
• Activated matrix metalloproteinase-3 (MMP-3) can contribute to periodontal ligament destruction in adult periodontitis [32].

Analytical, diagnostic and therapeutic context of Periodontitis

• Fourteen patients with periodontitis, who harbored P. gingivalis in their subgingival plaque, were treated by root planing and with metronidazole to suppress any detectable P. gingivalis [33].
• We determined sCD14 concentrations in the sera of 38 periodontitis patients and 25 healthy controls by enzyme-linked immunosorbent assay [34].
• Twenty-five sera from subjects with adult periodontitis (diseased group) and 25 sera from healthy subjects (control group) were used for the study [35].
• The immunoreactivities of sera from humans with (n = 24) or without (n = 25) periodontitis to the 26 LPSC and other H+LPS determinants were analyzed by Western blot [36].
• We previously examined the distribution of P. gingivalis in terms of fimA genotypes in periodontitis patients using a fimA type-specific PCR assay [37].

References