Dental infection didn’t raise rheumatoid arthritis risk

Arthralgia patients who later developed rheumatoid arthritis were no more likely to show signs of dental infection with Porphyromonas gingivalis than were those who didn’t develop the disease, according to a small case-control study.

Previous studies have suggested an association between periodontitis and rheumatoid arthritis (RA), which has been theorized to occur potentially through the ability of P. gingivalis to convert the amino acid arginine to citrulline. This interaction might thereby lead to the production of anticitrullinated protein antibodies (ACPA), which are known to precede the development of RA.

Dr. Menke de Smit of the Center for Dentistry and Oral Hygiene at the University of Groningen, the Netherlands, and associates studied the prognostic potential of using anti–P. gingivalis antibody levels to predict the development of RA in a cohort of 289 adults with a mean age of 50 years (79% women) who were at risk for RA by virtue of having arthralgia with seropositivity for immunoglobulin M–rheumatoid factor (IgM-RF) and/or ACPA. They had a median follow-up period of 30 months (Ann. Rheum. Dis. 2014 Jan. 13 [doi:10.1136/annrheumdis-2013-204594]).

The investigators used reference groups for anti–P. gingivalis antibody levels, including 36 healthy control patients and 117 severe periodontitis patients without systemic disease. Cultures for P. gingivalis tested positive in 42% of the reference group patients with periodontitis, but in none of the healthy controls. IgM levels of anti–P. gingivalis did not differ between the two reference groups, but culture-positive patients with periodontitis had significantly higher levels of IgA and IgG anti–P. gingivalis than did healthy controls and culture-negative patients with periodontitis.

The 33% of seropositive arthralgia patients who developed RA after a follow-up period of 12 months did not have higher anti–P. gingivalis levels than seropositive arthralgia patients who didn’t develop the disease.

Significantly more seropositive arthralgia patients who did not develop RA had elevated levels of IgA (25%) and IgG anti–P. gingivalis (37%), based on a cut-off value of twice the standard deviation of levels found in healthy controls, compared with those who did have RA (11% and 26%, respectively).

However, there was a weak yet statistically significant correlation (r = .23) between IgM anti–P. gingivalis and ACPA levels in seropositive arthralgia patients who later developed RA.

In all seropositive arthralgia patients combined, IgA and IgG anti–P. gingivalis levels were higher than in healthy controls, but were lower than in patients with periodontitis. IgM anti–P. gingivalis levels were similar across all three groups. In the seropositive arthralgia patients, none of the anti–P. gingivalis immunoglobulin levels differed according to ACPA status.

Positivity for anti–P. gingivalis did not significantly predict the development of RA in a multivariate Cox proportional hazards model, but ACPA positivity, IgM-RF positivity, number of tender joints, and HLA-DRB1 SE carrier status all were independent predictors of RA.

"Within the limitations of this study, we conclude that anti–P. gingivalis antibody levels are not prognostic for development of RA," they wrote.

The study was funded by the authors’ institutions. The authors had no financial conflicts of interest to disclose.

[email protected]

Arthralgia patients who later developed rheumatoid arthritis were no more likely to show signs of dental infection with Porphyromonas gingivalis than were those who didn’t develop the disease, according to a small case-control study.

Previous studies have suggested an association between periodontitis and rheumatoid arthritis (RA), which has been theorized to occur potentially through the ability of P. gingivalis to convert the amino acid arginine to citrulline. This interaction might thereby lead to the production of anticitrullinated protein antibodies (ACPA), which are known to precede the development of RA.

Dr. Menke de Smit of the Center for Dentistry and Oral Hygiene at the University of Groningen, the Netherlands, and associates studied the prognostic potential of using anti–P. gingivalis antibody levels to predict the development of RA in a cohort of 289 adults with a mean age of 50 years (79% women) who were at risk for RA by virtue of having arthralgia with seropositivity for immunoglobulin M–rheumatoid factor (IgM-RF) and/or ACPA. They had a median follow-up period of 30 months (Ann. Rheum. Dis. 2014 Jan. 13 [doi:10.1136/annrheumdis-2013-204594]).

The investigators used reference groups for anti–P. gingivalis antibody levels, including 36 healthy control patients and 117 severe periodontitis patients without systemic disease. Cultures for P. gingivalis tested positive in 42% of the reference group patients with periodontitis, but in none of the healthy controls. IgM levels of anti–P. gingivalis did not differ between the two reference groups, but culture-positive patients with periodontitis had significantly higher levels of IgA and IgG anti–P. gingivalis than did healthy controls and culture-negative patients with periodontitis.

The 33% of seropositive arthralgia patients who developed RA after a follow-up period of 12 months did not have higher anti–P. gingivalis levels than seropositive arthralgia patients who didn’t develop the disease.

Significantly more seropositive arthralgia patients who did not develop RA had elevated levels of IgA (25%) and IgG anti–P. gingivalis (37%), based on a cut-off value of twice the standard deviation of levels found in healthy controls, compared with those who did have RA (11% and 26%, respectively).

However, there was a weak yet statistically significant correlation (r = .23) between IgM anti–P. gingivalis and ACPA levels in seropositive arthralgia patients who later developed RA.

In all seropositive arthralgia patients combined, IgA and IgG anti–P. gingivalis levels were higher than in healthy controls, but were lower than in patients with periodontitis. IgM anti–P. gingivalis levels were similar across all three groups. In the seropositive arthralgia patients, none of the anti–P. gingivalis immunoglobulin levels differed according to ACPA status.

Positivity for anti–P. gingivalis did not significantly predict the development of RA in a multivariate Cox proportional hazards model, but ACPA positivity, IgM-RF positivity, number of tender joints, and HLA-DRB1 SE carrier status all were independent predictors of RA.

"Within the limitations of this study, we conclude that anti–P. gingivalis antibody levels are not prognostic for development of RA," they wrote.

The study was funded by the authors’ institutions. The authors had no financial conflicts of interest to disclose.

[email protected]

Arthralgia patients who later developed rheumatoid arthritis were no more likely to show signs of dental infection with Porphyromonas gingivalis than were those who didn’t develop the disease, according to a small case-control study.

Previous studies have suggested an association between periodontitis and rheumatoid arthritis (RA), which has been theorized to occur potentially through the ability of P. gingivalis to convert the amino acid arginine to citrulline. This interaction might thereby lead to the production of anticitrullinated protein antibodies (ACPA), which are known to precede the development of RA.

Dr. Menke de Smit of the Center for Dentistry and Oral Hygiene at the University of Groningen, the Netherlands, and associates studied the prognostic potential of using anti–P. gingivalis antibody levels to predict the development of RA in a cohort of 289 adults with a mean age of 50 years (79% women) who were at risk for RA by virtue of having arthralgia with seropositivity for immunoglobulin M–rheumatoid factor (IgM-RF) and/or ACPA. They had a median follow-up period of 30 months (Ann. Rheum. Dis. 2014 Jan. 13 [doi:10.1136/annrheumdis-2013-204594]).

The investigators used reference groups for anti–P. gingivalis antibody levels, including 36 healthy control patients and 117 severe periodontitis patients without systemic disease. Cultures for P. gingivalis tested positive in 42% of the reference group patients with periodontitis, but in none of the healthy controls. IgM levels of anti–P. gingivalis did not differ between the two reference groups, but culture-positive patients with periodontitis had significantly higher levels of IgA and IgG anti–P. gingivalis than did healthy controls and culture-negative patients with periodontitis.

The 33% of seropositive arthralgia patients who developed RA after a follow-up period of 12 months did not have higher anti–P. gingivalis levels than seropositive arthralgia patients who didn’t develop the disease.

Significantly more seropositive arthralgia patients who did not develop RA had elevated levels of IgA (25%) and IgG anti–P. gingivalis (37%), based on a cut-off value of twice the standard deviation of levels found in healthy controls, compared with those who did have RA (11% and 26%, respectively).

However, there was a weak yet statistically significant correlation (r = .23) between IgM anti–P. gingivalis and ACPA levels in seropositive arthralgia patients who later developed RA.

In all seropositive arthralgia patients combined, IgA and IgG anti–P. gingivalis levels were higher than in healthy controls, but were lower than in patients with periodontitis. IgM anti–P. gingivalis levels were similar across all three groups. In the seropositive arthralgia patients, none of the anti–P. gingivalis immunoglobulin levels differed according to ACPA status.

Positivity for anti–P. gingivalis did not significantly predict the development of RA in a multivariate Cox proportional hazards model, but ACPA positivity, IgM-RF positivity, number of tender joints, and HLA-DRB1 SE carrier status all were independent predictors of RA.

"Within the limitations of this study, we conclude that anti–P. gingivalis antibody levels are not prognostic for development of RA," they wrote.

The study was funded by the authors’ institutions. The authors had no financial conflicts of interest to disclose.

[email protected]