Table 1: Adipokines and periodontal disease.
| Adipokine | Role | Mechanism of action | Highlights |
|---|---|---|---|
| OM-1 | Anti-inflammatory | 1. Salivary OM-1 is a remarkable inhibitor of inflammation, acting through multiple cellular signalling pathways and molecular mechanisms. 2. It effectively blocks TNF-α induced by cyclooxygenase-2, superoxide production and the expression of adhesion molecules in endothelial cells, thus disrupting the ERK/NF-κB pathway. 3. It exerts its anti-inflammatory effects by directly suppressing the expression of proinflammatory mediators, including TNF-α, IL-6 and monocyte chemotactic protein-1, through the AMPK/ AKT pathway. 4. OM-1 promotes signalling pathways that stimulate the proliferation of human osteoblasts, suggesting that it plays a significant role as a regulator of bone remodelling |
1. Lower salivary OM-1 levels were identified in patients with chronic periodontitis and associated with increased levels of periodontal parameters. 2. Higher salivary OM-1 levels after non-surgical periodontal therapy were also concomitant with an improvement in the periodontal health status. 3. It may be concluded that OM-1 has an anti-inflammatory role in periodontitis, and its expression may have a potential role in the immunopathogenesis of chronic periodontitis |
| APN | Anti-inflammatory | 1. APN, when binding to its receptors, exhibits strong anti-inflammatory effects. It can counteract proinflammatory responses in different cell types. For instance, APN increases the expression of chemokines in epithelial cells through NF-κB signalling but paradoxically prevents LPS-induced NF-κB nuclear translocation, thereby inhibiting the expression of inflammatory cytokines such as IL-1β, IL-6 and IL-8 in human GECs. 2. APN effects are also influenced by the context; it initially promotes TNF-α production through the ERK1/2→EGR-1 and NF-κB-dependent pathways, subsequently boosting IL-10 expression, which dampens the inflammatory response in LPS-exposed macrophages. 3. This adipokine contributes to bone metabolism by enhancing osteoblast recruitment, differentiation and proliferation while inhibiting osteoclast differentiation and activity |
1. APN alleviates periodontitis partly due to its action in inflammation and bone and can mediate different stages of bone metabolism. 2. The level of APN has an inverse association with periodontitis. 3. The underlying mechanisms may include the functions of APN in suppressing inflammation and promoting bone regeneration |
| Resistin | Proinflammatory | 1. Resistin is expressed mainly by macrophages in response to bacterial and inflammatory challenges, suggesting that it plays a role in inflammation. Moreover, it plays a role in bone remodelling as it enhances the proliferation of preosteoblast cells and in osteoclastogenesis since it increases the number of differentiated osteoclasts. 2. Resistin expression in PDL cells is upregulated in the presence of the proinflammatory mediator IL-1β. Thus, resistin has the potential to increase the expression of IL-6 and IL-8 in periodontal cells. 3. In addition, resistin induces downregulation of hard tissue (BMP2, RUNX2 and OCN) and matrix (POSTN and COL1) markers and growth factors (TGF-β1 and VEGF) in periodontal cells |
1. Resistin is produced by periodontal cells and tissues. 2. Microbial and inflammatory stimuli increase resistin expression and production in the periodontium. 3. Resistin seems to interfere with soft and hard tissue metabolism by reducing alkaline phosphatase activity and markers related to bone tissue and matrix formation |
| Leptin | Proinflammatory | 1. The decrease in leptin is associated with an increase in VEGF. This inverse correlation between leptin and VEGF in human gingiva supports that leptin has no pro-angiogenic effects on periodontal tissues. 2. TGF-β1, another important growth factor, comprises three isoforms and promotes wound healing by its stimulatory effects on the migration, chemotaxis, and proliferation of monocytes/macrophages, fibroblasts, and endothelial cells and keratinocyte migration and re-epithelialization. 3. Leptin abrogated the stimulatory actions of EMD on the aforementioned growth and transcription factors as well as matrix molecules, suggesting that leptin may interfere with the EMD-induced effects on both periodontal soft and hard tissue regeneration |
1. Leptin production is under the control of the obesity gene. It is an adipokine entirely produced in the adipocytes, with the fundamental function of controlling appetite and regulating food intake and energy expenditure. 2. Leptin negatively interferes with the regenerative capacity of PDL cells, suggesting leptin as a pathomechanistic link between obesity and compromised periodontal healing |
| Visfatin | Proinflammatory | 1. Visfatin is thought to have insulin-l ike effects, particularly those that lower plasma glucose levels. 2. The relationship between the serum and GCF concentrations of visfatin and periodontal diseases has been evaluated, concluding that visfatin concentration increased with disease severity in the serum and GCF. 3. Higher expression of visfatin, NF-κB, PI3k, TNF-α, and IL-1β in patients with gingivitis and periodontitis suggest that increased visfatin levels play a role in the pathogenesis of periodontitis. 4. TNF-α and IL-6, which are known as tissue destruction mediators, function as proinflammatory cytokines, and their levels increase during inflammation. 5. In patients with severe periodontitis, corpuscles and adipocytes in the liver have been proposed as sources of IL-6. This information helps us to understand the high level of GCF IL-6 in individuals who are obese |
1. Higher expression of visfatin is observed in patients with gingivitis and periodontitis. 2. Visfatin and IL-6 levels might play a role in the pathogenesis of periodontal disease and can be used as reliable markers for monitoring the course of periodontitis. 3. Visfatin may accelerate periodontal inflammation and bone destruction via the production of MMP-1 and CCL2 |
AKT = protein kinase B; AMPK = 5' adenosine monophosphate-activated protein kinase; APN = adiponectin; Bcl-2 = B-cell lymphoma 2; CCL2 = chemokine ligand 2; COL1 = collagen type 1; EGR-1 = early growth response-1; EMD = enamel matrix derivative; ERK = extracellular signal-regulated protein kinase; GCF = gingival crevicular fluid; GEC = gingival epithelial cell; IL = interleukin; LPS = lipopolysaccharide; MMP-1 = matrix metalloproteinase-1; NF-κB = nuclear factor kappa-light-chain-enhancer of activated B cells; OCN = osteocalcin; OM-1 = omentin-1; OPG = osteoprotegerin; PDL = periodontal ligament; PI3k = phosphatidylinositol 3-kinase; POSTN = periostin; RANK = receptor activator of NF-κB; RUNX2 = runt-related transcription factor-2; TGF-β1 = transforming growth factor-beta 1; TNF-α = tumour necrosis factor-alpha; VEGF = vascular endothelial growth factor; ZFP36 = zinc finger protein 36.