19 June 2019

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Periodontitis and rheumatoid arthritis: a common responsible

Alessandra Abbà

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Periodontitis is a chronic inflammatory disease characterized by an irreversible loss of connective tissue attachment and alveolar bone and it is a major cause of tooth loss.
Reumatoid Arthritis (RA) is a chronic destructive multifactorial disease of unknown etiology in which genetic susceptibility, environmental and hormonal factors interact in complex ways. It’s characterized by the accumulation and persistence of an inflammatory infiltrate in the synovial membrane, resulting in synovitis and joint architecture destruction.  

So what do they share?

Porphyromonas gingivalis (Pg) is a key factor in the pathogenesis both of rheumatoid arthritis (RA) and periodontitis. An increasing number of studies have demonstrated this association. Pg can induce anticyclic-citrullinated peptide autoantibodies (anti-CCP antibodies),responsible of the development of RA. Periodontitis and RA also share genetic and environmental risk factors.  
In this prospective cross-sectional study, published in JPIS in 2018, authors aimed to evaluate the relationships and the clinical implications between the two diseases in Korean adults.

MATERIALS AND METHODS 
The RA group included 260 patients who satisfied the 1987 American College of Rheumatology classification criteria for RA. Serologic analyses were performed for them. An age- and sex-matched control group of 86 volunteers without arthritis was enrolled too.    In order to evaluate periodontal conditions, the following data were registered:  

• plaque index (PI)
• gingival index (GI)
•  probing pocket depth (PPD)
•  bleeding on probing (BOP)
• clinical attachment level (CAL) 

Periodontal indices and the prevalence and amount of periodontal pathogens were recorded and compared between the groups. Correlations between periodontal and RA indices were examined.  

RESULTS
Statistacally significant higher values were registered for the RA group (P<0.05) for all periodontal indices except the number of teeth. The severity of periodontitis in all participants was slight or more than slight. The RA group showed also a significantly higher prevalence of moderate-to-severe periodontitis (64.2% vs. 34.9%, P<0.001).
The GI, BOP, and PPD showed positive relationships with several RA indices. The anti-Pg antibody titer had positive relationships with PPD, BOP, CAL, and periodontitis severity (table 1).

CONCLUSIONS
Even if there was no significant difference in the prevalence of periodontal pathogens between the two groups, RA was associated with higher values of periodontal indices and periodontitis severity. In conclusion, alteration of periodontal indices could be used as a warning sign of disease development in RA patients and at the same time an increasing anti-Pg antibody titer could be considered as a risk indicator in RA patients suffering with periodontitis.

For additional informations: 
Periodontal pathogens and the association between periodontitis and rheumatoid arthritis in Korean adults