Anti–TNF‐α Immunotherapy Is Associated With Increased Gingival Inflammation Without Clinical Attachment Loss in Subjects With Rheumatoid Arthritis

Pers, Jacques‐Olivier; Saraux, Alain; Pierre, Roselyne; Youinou, Pierre

doi:10.1902/jop.2008.070616

Cited by 115 publications

(122 citation statements)

References 17 publications

Supporting

Mentioning

106

Contrasting

Unclassified

Order By: Relevance

“…In addition to reducing TNF-a levels and ameliorating AIA parameters, such as cell infiltration and cartilage destruction, the anti-TNF-a Ab prevented the development of AIA-induced PD. In contrast, Pers et al (29) indicated that infliximab tended to aggravate gingival inflammation in patients, although it induced a decrease in attachment loss. Indeed, the absence of the TNF-a receptor p55 results in an impairment in protective immunity to A. actinomycetemcomitans infection in mice, leading to an increase in bacterial load (18), which could explain the gingival inflammation in those patients.…”

Section: Discussionmentioning

confidence: 93%

See 1 more Smart Citation

Experimental Arthritis Triggers Periodontal Disease in Mice: Involvement of TNF-α and the Oral Microbiota

Queiroz-Junior

Madeira

Coelho

et al. 2011

The Journal of Immunology

View full text Add to dashboard Cite

Rheumatoid arthritis (RA) and periodontal disease (PD) are prevalent chronic inflammatory disorders that affect bone structures. Individuals with RA are more likely to experience PD, but how disease in joints could induce PD remains unknown. This study aimed to experimentally mimic clinical parameters of RA-induced PD and to provide mechanistic findings to explain this association. Chronic Ag-induced arthritis (AIA) was triggered by injection of methylated BSA in the knee joint of immunized mice. Anti–TNF-α was used to assess the role of this cytokine. Intra-articular challenge induced infiltration of cells, synovial hyperplasia, bone resorption, proteoglycan loss, and increased expression of cytokines exclusively in challenged joints. Simultaneously, AIA resulted in severe alveolar bone loss, migration of osteoclasts, and release of proinflammatory cytokines in maxillae. Anti–TNF-α therapy prevented the development of both AIA and PD. AIA did not modify bacterial counts in the oral cavity. PD, but not AIA, induced by injection of Ag in immunized mice was decreased by local treatment with antiseptic, which decreased the oral microbiota. AIA was associated with an increase in serum C-reactive protein levels and the expression of the transcription factors RORγ and Foxp3 in cervical lymph nodes. There were higher titers of anti-collagen I IgG, and splenocytes were more responsive to collagen I in AIA mice. In conclusion, AIA-induced PD was dependent on TNF-α and the oral microbiota. Moreover, PD was associated with changes in expression of lymphocyte transcription factors, presence of anti-collagen Abs, and increased reactivity to autoantigens.

show abstract

Section: Discussionmentioning

confidence: 93%

“…The role of TNF-a in inflammatory RA and PD is widely known (18,27); indeed, some clinical studies addressed the role of anti-TNF-a therapies in the reduction of periodontal parameters in patients with RA (28,29). In these individuals, this therapy reduced periodontal indices and TNF-a levels in gingival crevicular fluid (28).…”

Section: Discussionmentioning

confidence: 99%

Experimental Arthritis Triggers Periodontal Disease in Mice: Involvement of TNF-α and the Oral Microbiota

Queiroz-Junior

Madeira

Coelho

et al. 2011

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…This may partly explain why anti-TNF treatment can protect against the development of bone erosions, an effect that may be independent of inflammation itself (Vis et al 2006). An analysis of periodontal bone loss in patients with gingivitis receiving anti-TNF treatment is instructive (Pers et al 2008). These patients experienced very little deterioration in periodontal bone damage during their anti-TNF treatment compared with similar patients not receiving anti-TNF.…”

Section: Other Therapiesmentioning

confidence: 99%

Bone loss in inflammatory disorders

Hardy

Cooper

2009

Journal of Endocrinology

310

244

View full text Add to dashboard Cite

Chronic inflammatory diseases of almost any cause are associated with bone loss. Bone loss is due to direct effects of inflammation, poor nutrition, reduced lean body mass, immobility and the effects of treatments, especially glucocorticoids. These mechanisms are complex and interrelated but are ultimately mediated through effects on the bone remodelling cycle. Inflammatory disease can increase bone resorption, decrease bone formation but most commonly impacts on both of these processes resulting in an uncoupling of bone formation from resorption in favour of excess resorption. This review will illustrate these interactions between inflammation and bone metabolism and discuss how these are, and might be, manipulated as therapies for inflammation related bone loss.

show abstract

“…TNF-α inhibitors have been demonstrated to inhibit bone loss caused by periodontal disease (17,18). Similarly, TNF blockers improved the clinical condition of arthritis in an experimental arthritis model (13). A recent study demonstrated that TNF-α mediated the destruction of temporomandibular joint cartilage and bone in RA patients (19).…”

Section: Introductionmentioning

confidence: 99%

“…Complete understanding of disease pathogenesis of RA is challenging owing to itsplay major roles in the pathogenesis of RA and periodontitis. Besides, both diseases are chronic inflammatory diseases sharing certain pathogenetic mechanisms such as increased proinflammatory cytokines, such as interleukin (IL)-1, IL-6, IL-11, IL-17, prostaglandin E2 (PGE2), and tumor necrosis factor (TNF)-α, resulting in bone loss (11)(12)(13)(14). Among these proinflammatory cytokines, TNF-α is particularly important as it plays a crucial role in hard and soft tissue destruction in both RA and chronic periodontitis (CP) (15,16).…”

Section: Introductionmentioning

confidence: 99%

Assessment of local and systemic 25-hydroxy-vitamin D, RANKL, OPG, and TNF levels in patients with rheumatoid arthritis and periodontitis

et al. 2017

View full text Add to dashboard Cite

The present study aimed to evaluate proinflammatory cytokine and vitamin D levels in rheumatoid arthritis (RA) and chronic periodontitis (CP) patients and healthy individuals before and after initial periodontal treatment. Overall, 17 CP patients with RA (RA + CP), 18 systemically healthy CP patients (CP), and 18 healthy controls (C) were included. Clinical periodontal measurements were recorded and gingival crevicular fluid (GCF) and blood samples were recorded. RA + CP and CP patients received nonsurgical periodontal treatment. Vitamin D, tumor necrosis factor (TNF)-α, receptor activator of nuclear factor-KB ligand (RANKL), and OPG levels were determined in GCF and serum. Baseline clinical parameters were similar in all periodontitis groups (P > 0.05) but were higher than that in controls (P < 0.05). Periodontal treatment improved clinical parameters in all periodontitis groups (P < 0.05). GCF vitamin D levels were higher in RA + CP and CP groups than in healthy controls, but these levels decreased in the RA + CP group after periodontal treatment (P < 0.05). Serum RANKL and GCF TNF-α levels in RA patients decreased after periodontal treatment (P < 0.05). Within the limitations of this study, the results suggested that GCF vitamin D levels are increased in RA patients and decrease after periodontal treatment; therefore, local vitamin D levels might be an important indicator of periodontal bone loss.

show abstract

Anti–TNF‐α Immunotherapy Is Associated With Increased Gingival Inflammation Without Clinical Attachment Loss in Subjects With Rheumatoid Arthritis

Abstract: Inflammation and destruction constitute two interrelated yet separate components of periodontitis in patients with RA. Therefore, TNF-alpha blockade could be beneficial in the treatment of periodontitis.

Cited by 115 publications

References 17 publications

Experimental Arthritis Triggers Periodontal Disease in Mice: Involvement of TNF-α and the Oral Microbiota

Experimental Arthritis Triggers Periodontal Disease in Mice: Involvement of TNF-α and the Oral Microbiota

Bone loss in inflammatory disorders

Assessment of local and systemic 25-hydroxy-vitamin D, RANKL, OPG, and TNF levels in patients with rheumatoid arthritis and periodontitis

Contact Info

Product

Resources

About