Anti‐B lymphocyte immunotherapy is associated with improvement of periodontal status in subjects with rheumatoid arthritis

Abstract

Anti-B lymphocyte therapy could be beneficial to improve periodontitis suggesting a major role of B cells in this disease.

Interaction of biologic therapy with apical periodontitis and periodontitis: a systematic review

“…Quality of information in non‐randomized clinical studies was considered high level in seven articles and moderate in the remaining studies . Quality of information in the In vivo animal studies was considered moderate in five articles and high in seven studies .…”

“…registered a positive effect on the periodontium at 6 months in patients with AS and on anti‐TNF‐α, but not in patients with RA. Therapies based on anti‐IL‐6, anti‐IL‐1 and anti‐CD20 also show a delay in the progression of P, as well as an improvement of the periodontal status of the patients (Table ). In accordance with the clinical studies, most experimental in vivo animal studies show that anti‐cytokines BMs were consistently associated with improvement of the periodontal status expressed as reduction of inflammatory infiltrate, level of local and systemic cytokines number of osteoclasts, alveolar bone loss, lesion size and preservation of collagen network .…”

“…This was discussed in two articles where BMs had positive effects on the alveolar bone and connective architecture, but not on gingival inflammation, which could worsen, suggesting two separate, overlapped, pathways of tissue damage and control of inflammation. Both these pathways seemed to be inhibited by the use of Rituximab, a BM which blocking the activity of B lymphocytes inhibits more widely the inflammatory cascade, whereas the selective blockade of TNF‐α and IL‐1 can be compensated by cytokine pathways (IL‐6, IL‐17/IL‐23) …”

The aggravation of arthritis by periodontitis is dependent of IL‐17 receptor A activation

“…Case-control studies found a more prevalent and severe periodontal disease (PD) status in RA patients (Al-Shammari, Al-Khabbaz, Al-Ansari, Neiva, & Wang, 2005;Bozkurt, Yetkin Ay, Berker, Tepe, & Akkus, 2006), as well as a reduction in the clinical parameters of active RA following effective periodontal treatment and control of periodontal infection (Al-Katma, Bissada, Bordeaux, Sue, & Askari, 2007;Bıyıkoğlu et al, 2013;Ortiz et al, 2009). On the other hand, clinical parameters of periodontal disease were improved in RA patients under treatment with anti-B lymphocyte therapy (Coat et al, 2015). However, it is remains unclear whether there is an etiological link between these two chronic inflammatory diseases, or whether the epidemiological results are due to statistical bias reinforced by the common risk factors (Farquharson, Butcher, & Culshaw, 2012).…”

Comment on “The B Cell–Stimulatory Cytokines BLyS and APRIL Are Elevated in Human Periodontitis and Are Required for B Cell–Dependent Bone Loss in Experimental Murine Periodontitis.”

“…IgD-deficient mice have a delay in B cell affinity maturation, exhibit diminished B cell activation, and are significantly protected against periodontal bone loss versus WT controls (9). 6) Importantly, a clinical trial showed that anti-B cell therapy with anti-CD20 mAb in individuals with arthritis significantly reduced indices of clinical periodontal inflammation and tissue destruction, thus implicating B cells in periodontal pathogenesis (10). Together, B cells are not only abundant and a major source of RANKL (3) but they are also causally involved in periodontitis.…”