Periodontitis in systemic rheumatic diseases

Abstract

Periodontitis is a chronic inflammatory disease that is characterized by loss of the periodontal ligament and alveolar bone, and is a major cause of tooth loss. Results from clinical and epidemiologic studies have suggested that periodontitis and tooth loss are more prevalent in individuals with rheumatoid arthritis (RA). However, the strength and temporality of the association are uncertain. Several biologically plausible causal and noncausal mechanisms might account for this association between periodontitis and RA. There is evidence to suggest that periodontitis could indeed be a causal factor in the initiation and maintenance of the autoimmune inflammatory response that occurs in RA. If proven, chronic periodontitis might represent an important modifiable risk factor for RA. In addition, patients with RA might show an increased risk of developing periodontitis and tooth loss through various mechanisms. Moreover, exposure to common genetic, environmental or behavioral factors might contribute to a noncausal association between both conditions.

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

“…15,16 Experimental studies reinforce the noncausal shared genetic susceptibility hypothesis as mouse lines phenotype selected for the acute inflammatory reactivity maximum (AIRmax) or minimal (AIRmin) share the susceptibility or resistance phenotype to both chronic models of pristane-induced arthritis (PIA) and Actinobacillus actinomycetemcomitansinduced PD. [24][25][26][27][28] AIRmax and AIRmin mice were developed through bidirectional genetic selection, starting from a highly polymorphic population (F0) derived from the intercrossing of eight inbred mouse strains (A, DBA2, P, SWR, CBA, SJL, BALB/c, and C57BL/6), and the progressive divergence of the AIRmax and AIRmin lines during successive generations of selective breeding reached 20-and 2.5-fold differences in leukocyte infiltration and exudated protein concentrations, respectively.…”

“…10,13 Furthermore, in both diseases, these cytokines present a catabolic function over the periodontal tissues, mediated by the production of matrix metalloproteinases (MMPs) and the osteoclastogenic factor RANKL. 10,[13][14][15][16][17][18][19][20] On the other hand, Th2-and anti-inflammatory cytokines such as IL-4 and IL-10 exert the reverse effect, mediating the direct downregulation of inflammatory cytokines and their signaling pathways, and also upregulating the expression of TIMPs and OPG, the endogenous inhibitors of MMPs and RANKL, respectively. 10,13,19,21,22 However, a major unanswered question is how a joint lesion could influence the host response at periodontal environment to affect PD outcome.…”

“…Among the hypothesis raised, considering the common immune and inflammatory features of both diseases, conceptual models link both diseases by causal and noncausal pathways. [14][15][16]23 Noncausal hypothesis considers that environmental or host factors increase susceptibility to both RA and PD, whereas causal assumption is that RA and PD can actively interfere in the pathogenesis of each other.…”

Defining the gut microbiota in individuals with periodontal diseases: an exploratory study

“…Among those, periodontal diseases are complex polymicrobial inflammatory diseases associated with dysbiosis of the dental biofilm that induces a long-lasting chronic inflammation of the periodontal supporting tissues, leading to alveolar bone destruction, and eventual tooth loss [6]. Over the years, strong evidence has accumulated to indicate that the pathogenic microbiota and the chronic inflammation established in periodontitis contribute to the onset and/or progression of several systemic inflammatory diseases such as cardiovascular diseases [7,8], diabetes [9], obesity [10], metabolic syndrome [11], respiratory disease [12], cancer [13], chronic kidney disease (CKD) [14] and rheumatoid arthritis (RA) [15]. Most research on the periodontitis-systemic disease relationship, however, has not determined causality, and the link between these diseases are bi-directional associations [16].…”

Chronic periodontitis and rheumatoid arthritis – microbiological aspects

“…Patients with RA show prevalence of CP 8 times higher (9,10). It has been estimated that moderate and severe forms of CP predominate in more than 75% of the patients with RA in comparison to the control group (6).…”