Disease relevance of Periodontal Diseases

• Purification and characterization of a novel arginine-specific cysteine proteinase (argingipain) involved in the pathogenesis of periodontal disease from the culture supernatant of Porphyromonas gingivalis [1].
• Members of the matrix metalloproteinase (MMP) family have been implicated in disease states such as arthritis, periodontal disease, and tumor cell invasion and metastasis [2].
• The chronic inflammatory diseases in humans have been intensively investigated, however the immune mechanisms underlying diseases such as rheumatoid arthritis (RA), inflammatory bowel disease, and periodontal disease (PD) remain elusive [3].
• The goal of this study was to determine the prevalence and incidence of periodontal disease and its relationship with non-insulin-dependent diabetes mellitus (NIDDM) [4].
• These findings, taken together with those of other groups, suggest that butyrate and propionate, end products of dental plaque metabolism, may have an etiological role in periodontal disease [5].

Psychiatry related information on Periodontal Diseases

• Gender and smoking-related risk reduction of periodontal disease with variant myeloperoxidase alleles [6].
• Dental health behaviors and periodontal disease indicators in Danish youths. A 10-year epidemiological follow-up [7].
• As background, principles of diagnostic decision-making and conceptual shifts during the 1970's and 1980's are reviewed in brief. "Diseases" that appeared in many classification schemes for periodontal diseases in the early 1970's--for example, "periodontosis" and "occlusal trauma"--do not appear in most current classifications [8].
• The degree of mental retardation and the occurrence of epilepsy and more severe forms of neuromuscular disorder appeared to influence the extent of gingival and periodontal disease [9].

High impact information on Periodontal Diseases

• Products of human blood monocytes (mononuclear cell factor, MCF) have been implicated in the pathogenesis of inflammatory diseases such as rheumatoid arthritis and periodontal disease [10].
• The nonsteroidal anti-inflammatory drug, flurbiprofen, a potent cyclooxygenase inhibitor, significantly decreases the resorption of alveolar bone in naturally occurring chronic destructive periodontal disease in beagles [11].
• Deficiency in saliva LL-37 accords with occurrence of periodontal disease in patients with morbus Kostmann [12].
• Overproduction of IL-6, a proinflammatory cytokine, is associated with a spectrum of age-related conditions including cardiovascular disease, osteoporosis, arthritis, type 2 diabetes, certain cancers, periodontal disease, frailty, and functional decline [13].
• To elucidate the role of T cells in periodontal disease, a system of cell transfer with TCR/CD28-dependent Th1 or Th2 clones was developed in rats [14].

Chemical compound and disease context of Periodontal Diseases

• The arginine-specific protease activity of Porphyromonas gingivalis is considered to be an important factor in the pathogenic potential of this organism in destructive periodontal disease [15].
• METHODS: A total of 135 postmenopausal women (aged 41-70 years) with no evidence of moderate or severe periodontal disease were randomized to receive daily oral conjugated estrogen (Premarin; 0.625 mg) alone or in combination with medroxyprogesterone acetate (Prempro; 0.625 and 2.5 mg, respectively) or placebo [16].
• The most important of the other factors is regular tooth brushing, which results in the removal of the bacterial plaque that causes caries and periodontal diseases and makes fluoride (which is contained in every advanced toothpaste) available for maintenance of the hard dental tissues and for remineralization wherever demineralization has occurred [17].
• Arg-gingipain (Rgp) and Lys-gingipain (Kgp) are cysteine proteinases produced by Porphyromonas gingivalis, a major etiological bacterium of periodontal diseases [18].
• Although periodontal disease was common in nondiabetic Pima Indians, in whom most of the incident cases occurred, diabetes clearly conferred a substantially increased risk [4].

Biological context of Periodontal Diseases

• Absence of exogenous interleukin-4-induced apoptosis of gingival macrophages may contribute to chronic inflammation in periodontal diseases [19].
• Porphyromonas gingivalis is one of the pathogens associated with periodontal diseases, and its lipopolysaccharide (LPS) has been suggested as a possible virulence factor, acting by stimulation of host cells to secrete proinflammatory mediators [20].
• Recent developments suggest that interleukin (IL)-1 genetic polymorphisms may identify certain individuals who have a predisposed susceptibility to periodontal breakdown and that elevated levels of IL-1 are found in individuals with periodontal disease [21].
• Single-nucleotide polymorphism in the CD14 promoter and periodontal disease expression in a Japanese population [22].
• Features of natural masticatory function, of physiological attrition, both occlusal and approximal, and of continuing tooth eruption in adult life need to be borne in mind in considering how the chronic inflammatory periodontal diseases and dental caries have become so widespread [23].

Anatomical context of Periodontal Diseases

• Drugs that inhibit the formation or activity of osteoclasts are valuable for treating osteoporosis, Paget's disease, and inflammation of bone associated with rheumatoid arthritis or periodontal disease [24].
• These results suggest that Rgps activated human gingival fibroblasts to secrete HGF in the inflamed sites and the mechanism(s) involved may actively participate in both inflammatory and reparative processes in periodontal diseases [25].
• Fractal concepts have also been usefully incorporated into models of biological processes, including epithelial cell growth, blood vessel growth, periodontal disease and viral infections [26].
• Partial characterization of an interleukin-1-like factor in human gingival crevicular fluid from patients with chronic inflammatory periodontal disease [27].
• Epithelial cells play a critical role in periodontal disease through the secretion of pro-inflammatory cytokines such as interleukin-1 beta (IL-1 beta) and interleukin-18 (IL-18) [28].

Gene context of Periodontal Diseases

• The potential involvement of the inducible cyclooxygenase isoform (COX-2) and the role of novel lipid mediators were investigated in the pathogenesis of periodontal disease [29].
• These results indicate that LTAs act as antagonists or agonists via a CD14-dependent mechanism, probably due to the heterogeneous structure of LTAs, and that an antagonistic LTA might be a useful agent for suppressing the periodontal disease caused by gram-negative bacteria [30].
• In addition, IL-17 cooperates with bacterial components involved in periodontal disease to up-regulate LIX expression [31].
• This novel function of TLR2 as a signaling receptor for pathogen-induced activation of CD11b-CD18 may play a significant role in infection-driven chronic inflammatory conditions, such as periodontal disease or atherosclerosis, where P. gingivalis has been implicated [32].
• The two polypeptides, MRP8 and MRP14, identified in GCF represent the major difference between the 2-D PAGE patterns of serum and GCF, and we hypothesize that they may play an important role in the gingival sulcus and could represent possible markers for periodontal diseases [33].

Analytical, diagnostic and therapeutic context of Periodontal Diseases

• RESEARCH DESIGN AND METHODS: In a prospective longitudinal study of 628 subjects aged > or =35 years, we examined the effect of periodontal disease on overall and cardiovascular disease mortality in Pima Indians with type 2 diabetes [34].
• A recent study with animal models suggests the involvement of RANKL in the pathogenesis of this periodontal disease [35].
• These were assigned to eight groups: caries, periodontal diseases, eruption problems, prosthetics, trauma, orthodontics, occlusal problems, and other reasons [36].
• The aim of this study was to test effects of preventive regimes using fluoride and chlorhexidine to prevent caries and periodontal diseases in 34 patients with overdentures [37].
• RESULTS: Severe periodontal disease was more common in the spontaneous preterm birth group (49%) than in the indicated preterm (25%, P =.02) and term control groups (30%, P =.045) [38].

References