Current Molecular, Cellular and Genetic Aspects of Peri-Implantitis Disease: A Narrative Review
Abstract
:1. Introduction
2. Materials and Methods
3. Literature Search Results
3.1. Types of Peri-Implant Disease and Criteria for Implant Health and Peri-Implantitis
3.2. Risk Factors Associated with Peri-Implantitis
3.3. Molecular Factors Contributing to Peri-Implantitis Development
3.3.1. Pro-Inflammatory Cytokines
Interleukin-6 (IL-6)
Interleukin-1β (IL-1β)
Tumor Necrosis Factor α (TNFα)
Interleukin-8 (IL-8)
Interleukin-17 (IL-17)
Collagenase-2 (MMP-8/aMMP-8)
Other Metalloproteinases and Activated Metalloproteinases (MMPs/aMMPs)
3.3.2. Anti-Inflammatory Cytokines
Interleukin-10 (IL-10)
Tissue Metalloproteinase Inhibitors (TIMPs)
RANKL, OPG and RANKL/OPG Ratio
3.4. Genetic Differences Increasing Risk of Peri-Implantitis
3.4.1. IL-1β (+3953/+3954)
3.4.2. IL-1β (−511)
3.4.3. IL-1α (−889)
3.4.4. TNFα (+308)
3.4.5. MMP-8
3.4.6. IL-10 (+1082), (+819) and (+592)
3.4.7. IL-17R and IL-1RN
3.4.8. SERPINs
3.4.9. Other Important Genetic Factors: RUNX-2, GSK3B and MiR-1297
3.4.10. Peri-Implantitis’ Genetic Link to Other Diseases
3.5. Cellular Factors
3.6. Diagnostic Opportunities (aMMP-8, TNFα, IL-1β, IL-6)
4. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
References
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Number [Citation] | Authors | Journal | Date of Publication | Type | Results |
---|---|---|---|---|---|
1 [7] | Liu C. et al. | Advanced Science | 2021 | Review | Most well-known pro-inflammatory cytokines are IL-1, IL-6, IL-8, IL-12, IL-18, IFN-α/γ, and TNF- α. The anti-inflammatory cytokines are IL-1 RA, IL-4, IL-6, IL-10, IL-11, IL-13, and TGF-β. There are many ways of cytokine detection like ELISA assay, PoC testing, multiplex detection, flow cytometry, Luminex assays and MSD assays. |
2 [22] | E Silva R. et al. | Brazilian Dental Journal | 2020 | Article | Smoking, alcoholism, lack of hygene, type 2 diabetes and thin gingival biotype increase the risk of peri-implantitis. RANK, RANKL and OPG polymorphisms did not increase the risk of peri-implantitis in amazon population. |
3 [23] | Thierbach R. et al. | Journal of Clinical and Diagnostic Research | 2016 | Article | Although treatment decreases MMP-8 levels, the inflammatory levels are still present. Risk alleles were present in 54% examined patients. |
4 [24] | Astolfi V. et al. | International Journal of Environmental Research and Public Health | 2022 | Article | Smoking, lack of regular follow-up visits and previous periodontal problems increase the chance of peri-implantitis, external abutment connection increases the risk of peri-implantitis |
5 [25] | Plemmenos G. et al. | Life | 2022 | Review | Hyperglycemia and smoking have an adverse effect on peri-implant tissues, type 2 diabetes promotes AGE production, past periodontal problems make peri-implant tissues more sensitive to AGE and oxidative stress |
6 [26] | Petkovic-Curcin A. et al. | The International Jounral of Oral & Maxillofacial Implants | 2017 | Article | Smoking and previous periodontitis increase the chance of peri-implantitis. Patients with peri-implantitis had more frequently IL-10 (−1082), IL-1RN and TNFα (308) genetic polymorphisms. Smoking elevates the risk if combined with mentioned polymorphisms. |
7 [27] | Insua A. et al. | Journal of Biomedical Materials Research | 2017 | Narrative Review | The effects of systemic levels of cholesterol, fatty acids and vitamin D may be responsible factors for early implant loss and long-term implant stability. Immune cells have prolific impact on dental implant osseointegration and maintenance. |
8 [28] | D’Ambrosio F. et al. | Dentistry Journal | 2022 | Review | Tobacco smoking, alcohol consumption, unhealthy diets, chronic stress and depression are promoting dysbiosis, immunologic deficiencies and inflammatory environment, increasing the chance of peri-implantitis. SARS-CoV-2 virus promoted disregulated production of especially IL-1beta, IL-6 and IFN-γ. |
9 [29] | Mancini L. et al. | Frontiers in Oral Health | 2022 | Mini Review | COVID-19 infection may increase the production of MMP-8, leading to increased chance of peri-implant diseases when combined with poor oral hygene |
10 [30] | Sahoo S.K. et al. | Journal of Pharmacy & Bioallied Sciences | 2021 | Article | In peri-implantitis IL-1β level is greatly increased. IL-8 and MMP-1 is decreased compared with healthy patients. Herpesviridae (HHV-4, HHV-6 and HHV-7) increase the expression of pro-inflammatory cytokines. |
11 [31] | Baseri M. et al. | BioMed Research International | 2020 | Review | Increase in local macrophage and T-limphocytes may be due to type 4 hypersensitivity towards titanium particles, in periimplantitis macrophages balance shift towards pro-inflammatory M1 form, levels of IL-1β, IL-2, IL-8, IL-17, MMP-7, MMP-8, MMP-9 are increased in peri-implantitis, the RANKL/OPG ratio favours osteoclastogenesis, IL-1β can be used as earl diagnostic cytokine |
12 [32] | Corrêa M. et al. | Brazilian Oral Research | 2019 | Review | In peri-implantitis there are elevated levels of IL-1β, TNFα, IL-8, IL-17, IL-23, MMP-1, MMP-8, RANKL and decreased levels of PPARγ, IL-10, TIMP-1, OPG, BMP-7, RUNX, IL-1RA. Furthermore, the polymorphisms of IL-1β (−511), MMP-1 (G-1607GG), TNFα (308) may increase the risk of peri-implantitis. TNFα and IL-1β can have diagnostic potential. |
13 [33] | Al-Majid A. et al. | International Journal of Dentistry | 2018 | Review | aMMP-8 can detect subclinical periimplantitis stages, MMP-8 levels correlate positively with the bacteria infection, TIMP/MMP-8 tests are more sensitive and precise than sole MMP-8 tests, smokers have decreased levels of MMP-8, obesity increases MMP-8 levels |
14 [34] | Nickles K. et al. | Journal of Clinical Medicine | 2022 | Case Report | In patients with Papillon-Lefevre syndrome, regular dental appointments delay the peri-implantitis |
15 [35] | Al.-Askar M. et al. | Medical Principles and Practise | 2018 | Article | Increased Hb1c levels and improper oral hygene lead to increased IL-1β and IL-6 levels in saliva. |
16 [36] | Fernandes M.H. et al. | Journal of Oral and Maxillofacial Research | 2016 | Review | Bone loss process is both direct and indirect. IL-1β, IL-6, TNFα, IL-17, IL-12, IL-8 are elevated, whereas IL-4, OPG and IL-10 are decreased. RUNX2, BMP-7 production is decreased, MMP-8 and MMP-7 are increased. Fibroblasts can restrain the immunological response, however LPS increases the production of IL-1, IL-6 and IL-8. |
17 [37] | Alassy H. et al. | Diagnostics | 2019 | Review | PICF in peri-implantitis contains more aMMP-8, IL-6, TNFα and IL-1β. IL-10 levels decreased in peri-implantitis. The disproportion between MMP-1/TIMP-1 and MMP-8 levels can serve for diagnostic purposes. IL-1β levels can serve as predictor marker for peri-implantitis. Peri-implantitis tissues contain more CD138, CD68 and MPO-positive cells than in periodontitis. |
18 [38] | Martins L. et al. | International Journal of Environmental Research and Public Health | 2022 | Brief Report | Increased level of AhR, IL-6 and GAPDH gene expression in peri-implantitis group |
19 [39] | Lähteenmäki H. et al. | Clinical and Experimental Dental Research | 2022 | Article | The levels of IL-6, MMP-8, aMMP-8, calprotectin was elevated in peri-implantitis, MMP-8 has the best diagnostic value from the measured cytokines |
20 [40] | Kalsi A.S. et al. | Journal of Periodontal and Implant Science | 2021 | Review | In peri-implantitis there are elevated levels of RANKL/sRANKL, TNFα, IL-6, IL-8, MMP-8, MMP-1 and decrease in IL-10, TIMP-1, TIMP-2, OPG, IL-10. Additionally, aquaporin-1 disregulation inhibits cell growth and cell homeostasis. |
21 [41] | Jiang J. et al. | Journal of Clinical Laboratory Analysis | 2021 | Article | SERPINs taking part in inflammatory process in peri-implantitis are SERPINB1, SERPINB3, SERPINB4 and SERPINB5. The increase in IL-6 and TNFα is positively correlated with SERPINs level increase. |
22 [41] | Jiang J. et al. | Journal of Clinical Laboratory Analysis | 2021 | Article | SERPINs taking part in inflammatory process in peri-implantitis are SERPINB1, SERPINB3, SERPINB4 and SERPINB5. The increase in IL-6 and TNFα is positively correlated with SERPINs level increase. |
23 [42] | Figueiredo L. et al. | International Journal of Environmental Research and Public Health | 2020 | Article | IL-1β levels are significantly more elevated in peri-implantitis than in periodontitis or control group. IL-6, TNFα, MMP-1, MMP-8, MMP-2, MMP-9, TIMP-1 and TIMP-2 levels are similar between peri-implantitis and periodontitis. |
24 [43] | Ata-Ali J. et al. | BMC Oral Health | 2015 | Article | Peri-implantitis group showed increased levels of IL-1β, IL-6, TNFα. The IL-1β/IL-10 ratio was significantly higher in peri-implantitis. Improper microbial control can lead to increased bone loss through inflammation. |
25 [44] | Gleiznys D. et al. | Medical Science Monitor | 2019 | Article | In peri-implant tissues IL-10 levels decrease and IL-1β increase. Highest increase of IL-1 is in the beginning of inflammatory process. |
26 [45] | Aleksandrowicz P. et al. | BMC Oral Health | 2021 | Article | The levels of IL-1β and TNFα are higher in periodontitis than in peri-implantitis, CXCL8 is dependent on the stage of periodontitis/ peri-implantitis and on patient susceptibility. Both IL-1β and TNFα can be used as diagnostic markers in periodontics |
27 [46] | Ghaasib I. et al. | Clinical Implant Dentistry and Related Research | 2019 | Systematic Review | Il-1β, IL-6, TNFα and MMP-8 levels were elevated in PICF. IL-1β and IL-6 level measurements can be used to differentiate healthy patients, mucositis and peri-implantitis. |
28 [47] | Yaghobee S. et al. | Journal of Dentistry of Teheran University of Medical Science | 2013 | Article | IL-1β levels positively correlate with PD, GI, BL, PL. The levels of IL-1β in PICF is higher than in GCF. |
29 [48] | Gao X. et al. | Medicine | 2018 | Observational Study | Higher levels of IL-1β and MMP-8 were detected in Han population than in Uygr population, whereas MMP-13 levels was higher in Uygr population. This may lead to different progression of peri-implantitis between the two groups. |
30 [49] | Eckert M. et al. | Molecular Oral Microbiology | 2018 | Pilot Study | Comparing teeth with implants, the levels of IL-1β in periodontitis exceeded those in peri-implantitis. The anti-inflammatory IL-10 was lower in periodontitis and peri-implantitis in comparison with gingivitis and mucositis. Expression of miropsin-1 was positively associated with levels of IL-1β and negatively associated with those of IL-10. Additionally, miropin may play a regulatory role in a multispecies dysbiotic biofilm forming on teeth and implant surfaces and may contribute to the initiation and/or progression of both periodontal and peri-implant diseases. |
31 [50] | Darabi E. et al. | Iranian Journal of Allergy, Asthma and Immunology | 2013 | Article | TNFα and IL-17 levels were greatly increased compared with healthy patients, IL-17 levels are positively correlated with probing depth |
32 [51] | Gomes A.M. et al. | Journal of Applied Oral Science | 2019 | Article | The peri-implant maintenance therapy significantly lowered TNFα levels. Increased salivary TNFα levels was associated with worse peri-implant clinical condition. |
33 [52] | Alassiri S. et al. | Disease Markers | 2018 | Review | Periimplantitis site has elevated MMP-8 levels, MMP-8 PoC/Chairside tests have 76–90% sensitivity and 96% specificity |
34 [53] | Farhad S.Z. et al. | International Journal of Preventive Denstistry | 2019 | Article | The highest levels of IL-17 were detected in peri-implant mucositis, followed by peri-implantitis. IL-10 level was the highest in peri-implantitis group. |
35 [54] | Zhang H. et al. | Experimental and Therapeutic Medicine | 2017 | Article | IL-6, TLR-4, N1, IL1β, MMP9, CXCL8, CXCR4, CXCL1, PECAM1, and SPP1 genes are upregulated in peri-implantitis. Key genes in peri-implantitis are IL-6 and IL-1β |
36 [55] | Zhang X. et al. | BioMed Research International | 2021 | Research Article | In periimplantitis there are 2 upregulated DEGs that are also upregulated in Alzheimer's Disease, HSP90AA1 and NFκB are also upregulated modulating osteoclasts, OPG and RANK |
37 [56] | Mohammadi H. et al. | Pathogens | 2021 | Review | Periimplantitis is noted more frequently if IL-1β (+3954), IL-1α (−889) are present. |
38 [57] | Jin Q. et al. | PLoS ONE | 2021 | Research Article | IL-1α (−889), IL-1β (+3954) and IL-1β (−511) may be more frequently found in periimplantitis. TNFα genotypes did not have direct influence in increasing periimplantitis risk. |
39 [58] | Mo Y.Y. et al. | Medicine | 2016 | Systematic Review | TNFα (308) gene polymorphism is associated with higher risk of peri-implantitis. The risk is of implant failure is further elevated by smoking. IL-1α (−889) and IL-1β (+3954) are potentially seen as risk factors in peri-implantitis. |
40 [59] | Hamdy A.A. et al. | Journal of Oral Implantology | 2011 | Article | Combination of IL-1α (−889) and Il-1β (+3954) polymorphisms may act as risk factor for tissue destruction and peri-implantitis. Furthermore, IL-1 gene polymorphisms can have negative effect on treatment response and result in genotype-positive patients. |
41 [60] | Lafuente-Ibáñez de Mendoza I. et al. | International Journal of Implant Dentistry | 2022 | Review | There is no direct evidence that IL-1β (+3954), IL-10 (−1081), IL-6 (−174) or TNFα (308) have higher risk of developing peri-implantitis, however composite genotypes IL-1α(−889)/IL-1β (+3954) IL-1α(−889)/IL-1β (+3953) combined with smoking >20 cigarettes a day significantly increase the bone loss and contributes to peri-implantitis. |
42 [61] | Laine M.L. et al. | Clinical Oral Implants Research | 2006 | Article | IL-1β (+3954), IL-1α (−889), IL-1RN polymorphisms were detected more often in peri-implantitis patients and can be assumed to represent as risk factors for peri-implantitis. Smoking increases the chance of peri-implantitis. |
43 [62] | Jamshidy L. et al. | International Journal of Environmental Research and Public Health | 2021 | Review | TNFα (308) gene polymorphism is associated with higher risk of peri-implantitis, especially in Asian ethnicity population |
44 [63] | Schminke B. et al. | Journal of Dental Resarch | 2015 | Research Report | In periimplantitis IL-8, MMP-8 and -9 are upregulated, BMP-9 and PPARγ are downregulated, RUNX levels decrease with the bone destruction progression |
45 [64] | Kadkhodazadeh M. et al. | Acta Medica Iranica | 2013 | Report | IL-17RA polymorphism doesn't increase the chance of periimplantitis incidence |
46 [65] | Ingendoh-Tsakmakidis A. et al. | Cellular Microbiology | 2019 | Research Article | In peri-implantitis, upregulated genes were related either linked to cell division (FIGN, HMGA2, CDC25A, and ERCC6L) or to DNA repair/damage (CLSPN, POLQ, and FANCA). The pathway analysis of the downregulated genes related to this signal transduction (MDM2, IL2RG, TLR4, and F2R). S. oralis modulated response of tissues in a way to modulate the peri-implant tissue process. |
47 [66] | Mijiritsky E. et al. | Journal of Clinical Medicine | 2020 | Article | Connective tissue in peri-implantitis has a large number of neutrophils and the structure of the tissue is disorganized, collagen type III production is increased, osteogenic pathways were downregulated, ROS pathways were upregulated |
48 [67] | Li Y. et al. | BMC Medical Genetics | 2020 | Research Article | GSK3B and miR-1297 may have important significance in the immune microenvironment and pathogenesis of peri-implantitis. |
49 [68] | Yu T. et al. | PeerJ | 2019 | Article | There are 92 common genes between periimplantitis and type 2 diabetes, 3 of which (IL6, NFKB1, PIK3CG) are the same, IL-17 expression |
50 [69] | Dionigi C. et al. | Journal of Clinical Periodontology | 2020 | Article | Compared to periodontitis, periimplantitis has increased neutrophil, macrophage and iNOS-positive cells. Epithelium and connective tissue were thicker in periimplantitis than periodontitis. |
51 [70] | Li Y. et al. | Frontiers in Immunology | 2021 | Review | Inflammasomes can be a target point for drugs, periimplantitis tissues have elevated IL-1β and IL-18. Increased NLRP3 levels if P. gingivalis or C. albicans are present |
52 [71] | Galarraga-Vinuenza M. et al. | Clinical Oral Investigations | 2021 | Article | Enhanced M1 macrophages polarization and higher M1/M2 ratio are found in peri-implantitis sites. M1 phenotype leads to exacerbated osteolysis and inflammatory response, accelerating the peri-implantits progression. |
53 [72] | Tzah-Nahman R. et al. | Scientific Reports | 2017 | Article | Increased PDLF levels stimulate TNFα and IL-1β production as well as spontaneous production of IL-6 by macrophages. Blocking IL-6 or IL-10 production reduced fibroblasts modulatory effect and promoted macrophage phagocytosis when bacterial challenge occurred |
54 [73] | Aleksandrowicz P. et al. | Medicators of Infammation | 2017 | Research Article | Monitoring of MMP-8 level in PISF could help to diagnose mucositis/peri-implantitis in an early stage, prior to clinical manifestations, which may allow for quick start of appropriate therapy. |
55 [74] | Guarneri R. et al. | Journal of Personalized Medicine | 2022 | Article | The initial high level of aMMP8 can be considered as indicators of the subsequent progression of peri-implant bone loss. MMP-8 could be used as biomarker for identifying implants and patients that could present a high bone loss |
Peri-Implant Health | Peri-Implantitis | Peri-Implantitis in the Absence of Previous Examinations |
---|---|---|
No clinical sign of inflammation | No sign or visible inflammation | No sign or visible inflammation |
No bleeding/suppuration on gentle probing | Bleeding/suppuration on gentle probing | Bleeding/suppuration on gentle probing |
Stable probing depth between examinations | Increased probing depth compared to previous examinations | Probing depth ≥ 6 mm |
No crestal bone changes apart from initial bone remodeling | Crestal bone loss other than initial bone remodeling | Bone levels ≥ 3 mm apical of the most coronal portion of the intraosseous part of the implant |
Pro-Inflammatory Cytokines | Anti-Inflammatory Cytokines |
---|---|
Interleukin-6 | Interleukin-10 |
Interleukin-1 | Tissue Metalloproteinase Inhibitors (TIMPs) |
Tumor Necrosis Factor α | Osteoprotegrin |
Interleukin-8 | Interleukin-1RN |
Interleukin-17 | Serase Protease Inhibitors (SERPINs) |
Metalloproteinase-8 (MMP-8) and other MMPs |
Cytokine | Function |
---|---|
Interleukin-6 | Stimulating acute phase protein synthesis, neutrophils production, fever mediation, B-cell growth stimulation |
Interleukin-1α | Part of epithelial barrier, epithelium integrity preservation |
Interleukin-1β | Modulating inflammatory response, pyrogen, pain hypersensitivity, cell proliferation |
Tumor Necrosis Factor α | Immune cells modulation, cell signaling, inflammation regulation, response to bacterial lipopolysaccharide |
Interleukin-8 | Neutrophil chemotaxis, phagocytosis stimulation |
Interleukin-17 | Recruitment of immune cells (mainly neutrophils and monocytes) via chemokines, promotes inflammatory responses of IL-1β and TNF-α |
Interleukin-10 | Anti-inflammatory agent, blocks NFkB activity resulting in decrease in osteoclasts formation, TNF-α regulation |
MMP-8 | Catalyzes the degradation of collagen type III and I |
MMP-2 | Collagen type IV degradation, cell-cell clustering |
MMP-9 | Collagen type IV and V degradation, cooperation with MMP-2 in ECM remodeling |
MMP-7 | Gelatin, fibronectin and proteoglycan degradation, probably plays role in wound healing |
MMP-13 | Collagen type I, II and III degradation, tissue remodeling |
TIMP-1 | MMPs inhibition, cell proliferation promotion |
TIMP-2 | MMPs inhibition, complements TIMP-1 in maintaining tissues hemostasis |
RANKL | Bone remodeling and regeneration control, cell proliferation, with RANK binding promotes osteoclasts formation and maturation |
Osteoprotegrin | Suppression of osteoclasts formation by competitive binding to RANK |
Cells Type | Function and Disfunction |
---|---|
Epithelial cells | Apical proliferation, γ-H2AX, iNOS, NOX2, MPO expression |
Fibroblasts | Lowered collagen production, mainly type I and III |
Macrophages | Tissue infiltration, cytokine production, phagocytosis |
Neutrophyls | Tissue infiltration, cytokine production, NETosis, ROS production |
Osteocytes | Bone matrix production reduction, inability to repair the damages |
Osteoclasts | Bone destruction, influence the bone metabolism |
Plasma cells | Maintaining inflammation process, humoral immunity |
T-type lymphocytes | Maintaining inflammation process, cellular immunity |
Dendritic cells | Inflammation modulation, affect Langerhans cells response |
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Chmielewski, M.; Pilloni, A. Current Molecular, Cellular and Genetic Aspects of Peri-Implantitis Disease: A Narrative Review. Dent. J. 2023, 11, 134. https://doi.org/10.3390/dj11050134
Chmielewski M, Pilloni A. Current Molecular, Cellular and Genetic Aspects of Peri-Implantitis Disease: A Narrative Review. Dentistry Journal. 2023; 11(5):134. https://doi.org/10.3390/dj11050134
Chicago/Turabian StyleChmielewski, Marek, and Andrea Pilloni. 2023. "Current Molecular, Cellular and Genetic Aspects of Peri-Implantitis Disease: A Narrative Review" Dentistry Journal 11, no. 5: 134. https://doi.org/10.3390/dj11050134