Pro‐inflammatory profiles in cardiovascular disease patients with peri‐implantitis

Abstract

Background To investigate the pro‐inflammatory cytokine profiles in patients with or without cardiovascular disease (CVD) and with or without peri‐implantitis. Methods Serum, peri‐implant crevicular fluid (PICF), and gingival crevicular fluid (GCF) were collected from patients with (n = 82) or without CVD (n = 46) at the most severe peri‐implantitis site including sites with periodontitis. A panel of proinflammatory molecules including high‐sensitivity C‐reactive protein (hsCRP), fibrinogen, interleukin‐1 beta (IL‐1β), IL‐6, plasma tumor necrosis factor‐alpha (TNF‐α), matrix metallo‐proteinase‐8 (MMP‐8), osteoprotegerin (OPG), vascular endothelial growth factor (VEGF), IL‐17, IL‐8, tissue inhibitor of metalloproteinase‐2 (TIMP‐2), myeloperoxidase (MPO), and prostaglandin E2 (PGE2) were analyzed using human custom Quantibody arrays. Krunskal‐Wallis test was used to compare groups. The diagnostic ability of each biomarker was assessed using chi‐square test and ROC analysis. Results Serum IL‐1β, TNF‐α and fibrinogen were significantly higher in CVD patients than those without. Serum fibrinogen displayed a trend of higher concentration in patients with radiographic bone loss (RBL) ≥2 mm (P = 0.08). PICF TNF‐α exhibited a significantly higher detection level in the CVD patients that is coincided with the local peri‐implant inflammation. In addition, PICF MMP‐8 was significantly higher in the RBL ≥2 mm sites than the healthy implants; whereas IL‐1β, IL‐8, MMP‐8, and TIMP‐2 proved to be the significant predictors for peri‐implant disease. GCF TNF‐α collected from patients with periodontitis was significantly associated with CVD cases. Conclusion The augmented expression of local and systemic pro‐inflammatory cytokines found in the current study supports the weak association between the chronic peri‐implantitis with increasing severity and CVD.

A GP130-Targeting Small Molecule, LMT-28, Reduces LPS-Induced Bone Resorption around Implants in Diabetic Models by Inhibiting IL-6/GP130/JAK2/STAT3 Signaling

“…Furthermore, the levels of IL-1β and TNF-α in lung tissues from mice with sepsis were markedly decreased by LMT-28 [28]. As inflammatory biomarkers, the variations of IL-1β, IL-6, and TNF-α are the most commonly studied functional polymorphisms for periimplantitis and peri-implant bone loss [18,33,34]. Thus, the multiple effects of LMT-28 are anticipated to be appropriate for tissue repair in many bone-related diseases and organs.…”

“…Moreover, the combination of IL-6/IL-6R and GP130 in osteoblasts, which subsequently activated the JAK signaling pathway and preferentially induced tyrosine phosphorylation of STAT3, also correlated with RANKL levels. The JAK2/STAT3 signal transduction pathway is one of the main pathways through which IL-6 exerts its biological roles and plays a critical part in inflammatory bone disease [33]. To study the role of the JAK2/STAT3 signaling pathway in the expression of RANKL, we used LPS, AGEs, LMT-28, and the JAK2 inhibitor baricitinib to treat osteoblasts, and we observed that LPS and AGEs stimulated the expression of p-STAT3, p-JAK2, and RANKL, which were inhibited by baricitinib and LMT-28.…”

Bibliometric research on analysis of links between periodontitis and cardiovascular diseases

“…Hom-Lay Wang's studies showed that 64.6% of peri-implantitis was found in CVD patients, while only 56.5% of peri-implantitis was found in the controls ( 65 ). Moreover, IL-1β and TNF-α were significantly higher in CVD patients, which were significant markers for peri-implantitis ( 66 ). Inflammation plays a crucial role in the pathogenesis of atherosclerosis, the underlying cause of many cardiovascular diseases.…”

Effects of customized CAD/CAM abutments on cytokine levels in peri-implant crevicular fluid during early implant healing: a pilot study

“…In both abutment groups, a significant decrease in the expression of CRP, IL-6, MIP - 1α, osteopontin, and osteoactivin in PICF during the 6-month observation period was measured; this suggests a reduction of the inflammation process. While CRP is known as a marker for systemic inflammation, it has also been detected in PICF at peri-implantitis sites [ 18 ]. As a classical pro-inflammatory cytokine, IL-6 has been used to assess peri-implant inflammation in PICF [ 19 ].…”