Table 3.
Study | Patients (number) | Sex (M/F) | Age (years, mean ± SD) | RA duration (years, mean ± SD | DAS28 (baseline) | Follow‐up | RA treatment (number of patients) | Cytokine(s) investigated in GCF | Same cytokine(s) investigated in serum | Periodontal assessment | Periodontal classification | Difference in periodontal status between study groups | Difference in concentrations of cytokines in GCF between study groups | Difference in concentrations of cytokines in serum between study groups | |||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Baseline | Pretreatment versus post‐treatment | Baseline | Pretreatment versus post‐treatment | Baseline | Pretreatment versus post‐treatment | ||||||||||||
Cosgarea et al., (2019) | RA + CP (18) | 4/14 | 52 ± 11 | 15 ± 6 | median 4.8 (IQR 3.9–5.7 |
6 months (15 RA + CP, 18 HC + CP) |
NSAIDs (13), DMARDS (18), sulfasalasin (2), steroids (6), anti‐cytokine therapy (3) | MMP−8, IL−1β, IL−10, | no | PD, BOP, CAL, PI | Armitage 1999 |
Similar values in BOP, CAL, PI. PD higher in HC + CP |
Significant improvements in PD, BOP, CAL. No difference in PI for RA + CP |
Significantly higher amount MMP−8 and IL−1β in RA + CP (no concentrations assessed) | RA + CP: no significant differences | ‐ | ‐ |
HC + CP (18) | 8/10 | 44 ± 11 | – | – | – | HC + CP: significantly higher Il−10 post‐treatment | |||||||||||
Balci Yuce et al., (2017) | RA + CP (17) | 6/11 | 51 ± 8 | n.a. | – | 6 weeks | Maintenance therapy, not specified |
TNF‐α, RANKL, OPG, 25‐hydroxyvitamin D |
TNF‐α, RANKL, OPG, 25‐hydroxyvitamin D |
CAL, GI, PI | Armitage 1999 | Similar values in CAL, GI, PI between RA + CP and HC + CP, but higher than in HC | Significant improvements in CAL, PI, GI in both CP groups, but still higher than in HC |
25‐hydroxyvitamin D levels higher in RA + CP and CP No significant differences in TNF‐α, RANKL, levels Higher OPG levels in HC |
Reduction of 25‐hydroxyvitamin D and TNF‐α levels in RA + CP only Reduce |
Similar values of 25‐hydroxyvitamin D levels Higher OPG levels in RA + CP |
Increase in OPG in CP, decrease in RANKL in RA + CP, but no significant increase in OPG/RANKL |
HC + CP 18) | 9/9 | 50 ± 9 | – | ||||||||||||||
HC (18) | 9/9 | 49 ± 10 | – | ||||||||||||||
Kurgan et al., (2017) | RA + CP (15) | 6/9 | 49 ± 13 | n.a. | mean 3.0 SD 1.4 | 3 months | Maintenance therapy, not specified | t‐PA, PAI−2 | no | PD, BOP, CAL, GI, PI | Armitage 1999 | Similar values in PD, BOP, GI, PI, but higher than in HC | Significant improvements in PD, BOP, CL, PI, GI in both CP groups, but still higher than in HC | Higher t‐PA and PAI‐levels in RA + CP and HC + CP compared to HC | Reduction of t‐PA levels in RA + CP | – | – |
HC + CP (15) | 7/8 | 42 ± 7 | |||||||||||||||
HC (15) | 6/9 | 39 ± 7 | |||||||||||||||
Kurgan et al., (2016) | RA + CP (13) | 4/9 | 49 ± 14 | n.a. | median 2.6 (IQR 2.4–4.0) | 3 months | NSAIDs (10), MTX (10), sulfasalasin (2), steroids (9) | MMP−8, PGE2, IL−6 | no | PD, BOP, GI, PI | Armitage 1999 |
Similar values in PD, BOP, GI, PI |
Significant improvements in PD, BOP and GI in both groups | Significantly higher amount PGE2 in RA + CP (no concentrations assessed | RA + CP: significantly lower amount of all assessed cytokines post‐treatment | – | – |
HC + CP (13) | 7/6 | 41 ± 7 | – | – | – | HC + CP: MMP−8 amount significantly lower post‐treatment | |||||||||||
Bıyıkoğlu et al., (2013) | RA + CP (15) | 6/9 | 47 ± 8 | 6 ± 4 | mean 4.2 SD 1.0 | 6 months (10 RA + CP, 13 HC + CP) | MTX (15), leflunomide (2), prednisolone (14), chloroquine12), sulfasalasin (3), anti‐CD20 (1), anti‐TNF‐α (1) | IL−1β, TNF‐α | yes | PD, BOP, CAL, PI | Armitage 1999 | Similar values in PD, BOP, CAL, PI | Significant improvements in PD, CAL, BOP and PI in both groups | No significant differences | RA + CP: TNF‐α significantly higher post‐treatment |
Higher TNF‐α in RA + CP |
No significant differences in both groups |
HC + CP (15) | 9/6 | 47 ± 7 | – | – | – | HC + CP: TNF‐α significantly higher post‐treatment, IL1‐β significantly lower post‐treatment |
Abbreviations: Armitage 1999 (Armitage, 2000); BOP: bleeding on probing; CAL: clinical attachment level; DAS28: disease activity score 28 joint count; DMARDs: disease‐modifying anti‐rheumatic drugs; GI: gingivitis index; HC + CP: healthy controls with CP; IL: interleukin; MMP: matrix metalloproteinase; MTX: methotrexate; n.a.: not assessed; NSAIDs: non‐steroidal anti‐inflammatory drugs; OPG: osteoprotegerin; PAI‐2: plasminogen activator inhibitor‐2; PD: periodontal pocket depth; PGE2: prostaglandin E2; PI: plaque index; RA + CP: RA patients with chronic periodontitis (CP); RANKL; receptor activator of nuclear factor‐kappa β ligand; TNF‐α: tumor necrosis factor‐α; t‐PA: tissue/blood vessel‐type plasminogen activator.