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Response to: ‘Response to: ‘Alcohol is not the missing link between Porphyromonas gingivalis related periodontitis and radiologic progression in early Rheumatoid arthritis’ by Hillion et al’ by Marotte and Paul
  1. Alexandre Bellier1,
  2. Xavier Romand2,
  3. Athan Baillet2
  1. 1Unité de Qualité et d’Evaluation Médicale, CHU Grenoble Alpes, La Tronche, Grenoble, France
  2. 2Univ Grenoble Alpes, CNRS, CHU Grenoble Alpes, Grenoble INP, TIMC-IMAG, Grenoble, France
  1. Correspondence to Professor Athan Baillet, Univ.Grenoble Alpes, CNRS, CHU Grenoble Alpes, Grenoble 38000, France; abaillet{at}chu-grenoble.fr

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We thank Marotte et al1 for their interest in our study.2 They suggested to check interactions between Porphyromonasgingivalis serology, smoking and human leucocyte antigen (HLA) status as in the Etude et Suivi des Polyarthrites Indifférenciées Récentes (ESPOIR) cohort and the association between P. gingivalis serology status and radiological progression. In the ESPOIR cohort, P. gingivalis serology was increased in patients who are non-smokers and with structural damage.3

As suggested, we checked interactions with smoking and HLA status. We could not find any significant interaction between alcohol intake, P. gingivalis serology and structural progression in the non-smoking population (table 1). We also ran a multivariate analysis showing that shared epitope,4 alcohol intake and P. gingivalis serology are not independently associated with structural progression in patient with early RA of ESPOIR cohort (table 2).

Table 1

Interactions between gender, Porphyromonas gingivalis infection and radiological progression of American College of Rheumatology/European League Against Rheumatism 2010 patients with early rheumatoid arthritis in the ESPOIR cohort

Table 2

Porphyromonas gingivalis serology is not an independent predictor of structural progression in the multivariate logistic regression results

Hence, in the ESPOIR cohort, we could not show any influence of P. gingivalis serology on structural progression, even in the non-smoking population of early rheumatoid arthritis.

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Footnotes

  • Collaborators We also wish to thank Nathalie Rincheval (CHU Montpellier and EA 2415) who did expert monitoring and data management and all the investigators who recruited and followed the patients (F Berenbaum, Paris-Saint Antoine; MC Boissier, Paris-Bobigny; A Cantagrel, Toulouse; B Combe, Montpellier; M Dougados, Paris-Cochin; P Fardelone, P Boumier Amiens, B Fautrel, Paris-La Pitié; RM Flipo, Lille; Ph Goupille, Tours; F Liote, Paris-Lariboisière; O Vittecoq, Rouen; X Mariette, Paris Bicetre; O Meyer and Ph Dieude, Paris Bichat; A Saraux, Brest; Th Schaeverbeke, Bordeaux; J Sibilia, Strasbourg), V Devauchelle and C Lukas for expert X-ray reading and S Martin (Paris Bichat) who did all the central dosages of CRP, IgA and IgM rheumatoid factor and anti-CCP antibodies.

  • Contributors XR and AB critically reviewed the study proposal and critically reviewed the study proposal; AB generated statistical analysis and critically reviewed the study proposal.

  • Funding This study was funded by Direction de la Recherche Clinique Grenoble.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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