Soft‐Tissue Phenotype as a Risk Indicator of Peri‐Implantitis and Peri‐Implant Soft‐Tissue Dehiscence—A Cross‐Sectional Study
ABSTRACT Aim To investigate the association, as well as to characterize the associated panel of pro‐ and anti‐inflammatory markers, between the different components of the peri‐implant phenotype and the presence of peri‐implantitis/peri‐implant soft‐tissue dehiscence (PISTD). Materials and Methods A...
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| Veröffentlicht in: | Journal of clinical periodontology 2024-11, Vol.51 (11), p.1443-1457 |
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| creator | Isler, Sila Cagri Romandini, Mario Akca, Gulcin Bakirarar, Batuhan Unsal, Berrin Romanos, Georgios Sculean, Anton |
| description | ABSTRACT
Aim
To investigate the association, as well as to characterize the associated panel of pro‐ and anti‐inflammatory markers, between the different components of the peri‐implant phenotype and the presence of peri‐implantitis/peri‐implant soft‐tissue dehiscence (PISTD).
Materials and Methods
A total of 324 implants in 112 patients were included. The following components of the peri‐implant phenotype were clinically measured through the use of a manual periodontal probe or a digital calliper: keratinized mucosa width (PIKM‐W), mucosal thickness (MT), attached mucosa (AM) and vestibulum depth (VD). The presence of peri‐implantitis and PISTD was assessed through clinical and radiographic examination. Mixed‐models logistic regression analyses were performed to analyse the association between peri‐implant phenotype and the presence of peri‐implantitis or PISTD, adjusting for relevant confounders. Multiplex immunoassays were employed to evaluate the peri‐implant crevicular fluid levels of a panel of pro‐ and anti‐inflammatory markers.
Results
Peri‐implant health, peri‐implant mucositis and peri‐implantitis were diagnosed in 36.6%, 21.4% and 42% of the patients (classified according to their worst implant) and 35.2%, 34.3%, and 30.5% of the implants, respectively. In the multi‐level multiple regression model, the absence of PIKM‐W (odds ratio [OR] = 9.24; 95% CI: 2.73–31.28), the absence of attached mucosa (OR = 19.58; 95% CI: 6.12–62.56) and a reduced ( |
| doi_str_mv | 10.1111/jcpe.14059 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_3097494734</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3117694250</sourcerecordid><originalsourceid>FETCH-LOGICAL-c2829-fdd3a90921daa45083e9be800204ba9b7dbe746bde2382a85bf0a3cab87b81ba3</originalsourceid><addsrcrecordid>eNp90ctKxDAUBuAgio6XjQ8gATciVE-adtosZbyNCA6OgruSNKeYsdPUpkVm59adC5_QJzHjqKALswkkHz_n8BOyzeCA-XM4yWs8YBHEYon0WB8ggJjdLZMecOBBXyRijaw7NwFgCed8laxxwVIRx9AjL2NbtO_PrzfGuQ7p6B4r285qpNJRSa-Ne6DDSptctrahtqAjbIznw2ldyqo1rfGs0n-e6e_QY7w3Lscqx_fntyM6aKxz_neMeWtsJUs6bjs92yQrhSwdbn3dG-T29ORmcB5cXp0NB0eXQR6moQgKrbkUIEKmpYxiSDkKhSlACJGSQiVaYRL1lcaQp6FMY1WA5LlUaaJSpiTfIHuL3Lqxjx26NpvOpyv94Gg7l3EQSSSihEee7v6hE9s1fmKvGEv6Igpj8Gp_ofL5Yg0WWd2YqWxmGYNsXlA2Lyj7LMjjna_ITk1R_9DvRjxgC_BkSpz9E5VdDEYni9APgF2iaA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3117694250</pqid></control><display><type>article</type><title>Soft‐Tissue Phenotype as a Risk Indicator of Peri‐Implantitis and Peri‐Implant Soft‐Tissue Dehiscence—A Cross‐Sectional Study</title><source>Wiley Online Library - AutoHoldings Journals</source><creator>Isler, Sila Cagri ; Romandini, Mario ; Akca, Gulcin ; Bakirarar, Batuhan ; Unsal, Berrin ; Romanos, Georgios ; Sculean, Anton</creator><creatorcontrib>Isler, Sila Cagri ; Romandini, Mario ; Akca, Gulcin ; Bakirarar, Batuhan ; Unsal, Berrin ; Romanos, Georgios ; Sculean, Anton</creatorcontrib><description>ABSTRACT
Aim
To investigate the association, as well as to characterize the associated panel of pro‐ and anti‐inflammatory markers, between the different components of the peri‐implant phenotype and the presence of peri‐implantitis/peri‐implant soft‐tissue dehiscence (PISTD).
Materials and Methods
A total of 324 implants in 112 patients were included. The following components of the peri‐implant phenotype were clinically measured through the use of a manual periodontal probe or a digital calliper: keratinized mucosa width (PIKM‐W), mucosal thickness (MT), attached mucosa (AM) and vestibulum depth (VD). The presence of peri‐implantitis and PISTD was assessed through clinical and radiographic examination. Mixed‐models logistic regression analyses were performed to analyse the association between peri‐implant phenotype and the presence of peri‐implantitis or PISTD, adjusting for relevant confounders. Multiplex immunoassays were employed to evaluate the peri‐implant crevicular fluid levels of a panel of pro‐ and anti‐inflammatory markers.
Results
Peri‐implant health, peri‐implant mucositis and peri‐implantitis were diagnosed in 36.6%, 21.4% and 42% of the patients (classified according to their worst implant) and 35.2%, 34.3%, and 30.5% of the implants, respectively. In the multi‐level multiple regression model, the absence of PIKM‐W (odds ratio [OR] = 9.24; 95% CI: 2.73–31.28), the absence of attached mucosa (OR = 19.58; 95% CI: 6.12–62.56) and a reduced (<4 mm) vestibulum depth (OR = 2.61; 95% CI: 1.05–6.48) were associated with peri‐implantitis. Similarly, the absence of PIKM‐W (OR = 6.32; 95% CI: 1.67–23.83), a thin (<2 mm) mucosa (OR = 157.75; 95% CI: 14.06–1769.9) and a reduced vestibulum depth (OR = 3.32; 95% CI: 1.02–10.84) were associated with the presence of PISTD. Implants with PIKM‐W = 0 mm showed statistically significantly higher levels of interferon‐γ in both regular (≥2 maintenance/year) and irregular (<2 maintenance/year) compliers (p = 0.046 and p = 0.012). In irregular compliers, the absence of PIKM‐W was also associated with statistically significantly higher levels of interleukin (IL)‐1β and IL‐21 (p = 0.016, p = 0.046). These associations were independent of the effect of relevant confounders (e.g., plaque, compliance with maintenance, etc.).
Conclusions
Within their limits, the present findings indicate that (a) peri‐implant soft‐tissue phenotype appears to be associated with the presence of peri‐implantitis and PISTD, and (b) in the absence of PIKM‐W, the inflammatory response seems to be dysregulated and the soft‐tissue remodelling up‐regulated.</description><identifier>ISSN: 0303-6979</identifier><identifier>ISSN: 1600-051X</identifier><identifier>EISSN: 1600-051X</identifier><identifier>DOI: 10.1111/jcpe.14059</identifier><identifier>PMID: 39189550</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>cytokines ; Dehiscence ; dental implants ; Genotype & phenotype ; Inflammation ; keratinized mucosa ; Mucosa ; Mucositis ; multiplex immunoassay ; peri‐implant diseases ; Phenotypes ; Regression analysis ; Transplants & implants</subject><ispartof>Journal of clinical periodontology, 2024-11, Vol.51 (11), p.1443-1457</ispartof><rights>2024 The Author(s). published by John Wiley & Sons Ltd.</rights><rights>2024 The Author(s). Journal of Clinical Periodontology published by John Wiley & Sons Ltd.</rights><rights>2024. This article is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2829-fdd3a90921daa45083e9be800204ba9b7dbe746bde2382a85bf0a3cab87b81ba3</cites><orcidid>0000-0001-5646-083X ; 0000-0001-5419-9658</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjcpe.14059$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjcpe.14059$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39189550$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Isler, Sila Cagri</creatorcontrib><creatorcontrib>Romandini, Mario</creatorcontrib><creatorcontrib>Akca, Gulcin</creatorcontrib><creatorcontrib>Bakirarar, Batuhan</creatorcontrib><creatorcontrib>Unsal, Berrin</creatorcontrib><creatorcontrib>Romanos, Georgios</creatorcontrib><creatorcontrib>Sculean, Anton</creatorcontrib><title>Soft‐Tissue Phenotype as a Risk Indicator of Peri‐Implantitis and Peri‐Implant Soft‐Tissue Dehiscence—A Cross‐Sectional Study</title><title>Journal of clinical periodontology</title><addtitle>J Clin Periodontol</addtitle><description>ABSTRACT
Aim
To investigate the association, as well as to characterize the associated panel of pro‐ and anti‐inflammatory markers, between the different components of the peri‐implant phenotype and the presence of peri‐implantitis/peri‐implant soft‐tissue dehiscence (PISTD).
Materials and Methods
A total of 324 implants in 112 patients were included. The following components of the peri‐implant phenotype were clinically measured through the use of a manual periodontal probe or a digital calliper: keratinized mucosa width (PIKM‐W), mucosal thickness (MT), attached mucosa (AM) and vestibulum depth (VD). The presence of peri‐implantitis and PISTD was assessed through clinical and radiographic examination. Mixed‐models logistic regression analyses were performed to analyse the association between peri‐implant phenotype and the presence of peri‐implantitis or PISTD, adjusting for relevant confounders. Multiplex immunoassays were employed to evaluate the peri‐implant crevicular fluid levels of a panel of pro‐ and anti‐inflammatory markers.
Results
Peri‐implant health, peri‐implant mucositis and peri‐implantitis were diagnosed in 36.6%, 21.4% and 42% of the patients (classified according to their worst implant) and 35.2%, 34.3%, and 30.5% of the implants, respectively. In the multi‐level multiple regression model, the absence of PIKM‐W (odds ratio [OR] = 9.24; 95% CI: 2.73–31.28), the absence of attached mucosa (OR = 19.58; 95% CI: 6.12–62.56) and a reduced (<4 mm) vestibulum depth (OR = 2.61; 95% CI: 1.05–6.48) were associated with peri‐implantitis. Similarly, the absence of PIKM‐W (OR = 6.32; 95% CI: 1.67–23.83), a thin (<2 mm) mucosa (OR = 157.75; 95% CI: 14.06–1769.9) and a reduced vestibulum depth (OR = 3.32; 95% CI: 1.02–10.84) were associated with the presence of PISTD. Implants with PIKM‐W = 0 mm showed statistically significantly higher levels of interferon‐γ in both regular (≥2 maintenance/year) and irregular (<2 maintenance/year) compliers (p = 0.046 and p = 0.012). In irregular compliers, the absence of PIKM‐W was also associated with statistically significantly higher levels of interleukin (IL)‐1β and IL‐21 (p = 0.016, p = 0.046). These associations were independent of the effect of relevant confounders (e.g., plaque, compliance with maintenance, etc.).
Conclusions
Within their limits, the present findings indicate that (a) peri‐implant soft‐tissue phenotype appears to be associated with the presence of peri‐implantitis and PISTD, and (b) in the absence of PIKM‐W, the inflammatory response seems to be dysregulated and the soft‐tissue remodelling up‐regulated.</description><subject>cytokines</subject><subject>Dehiscence</subject><subject>dental implants</subject><subject>Genotype & phenotype</subject><subject>Inflammation</subject><subject>keratinized mucosa</subject><subject>Mucosa</subject><subject>Mucositis</subject><subject>multiplex immunoassay</subject><subject>peri‐implant diseases</subject><subject>Phenotypes</subject><subject>Regression analysis</subject><subject>Transplants & implants</subject><issn>0303-6979</issn><issn>1600-051X</issn><issn>1600-051X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><recordid>eNp90ctKxDAUBuAgio6XjQ8gATciVE-adtosZbyNCA6OgruSNKeYsdPUpkVm59adC5_QJzHjqKALswkkHz_n8BOyzeCA-XM4yWs8YBHEYon0WB8ggJjdLZMecOBBXyRijaw7NwFgCed8laxxwVIRx9AjL2NbtO_PrzfGuQ7p6B4r285qpNJRSa-Ne6DDSptctrahtqAjbIznw2ldyqo1rfGs0n-e6e_QY7w3Lscqx_fntyM6aKxz_neMeWtsJUs6bjs92yQrhSwdbn3dG-T29ORmcB5cXp0NB0eXQR6moQgKrbkUIEKmpYxiSDkKhSlACJGSQiVaYRL1lcaQp6FMY1WA5LlUaaJSpiTfIHuL3Lqxjx26NpvOpyv94Gg7l3EQSSSihEee7v6hE9s1fmKvGEv6Igpj8Gp_ofL5Yg0WWd2YqWxmGYNsXlA2Lyj7LMjjna_ITk1R_9DvRjxgC_BkSpz9E5VdDEYni9APgF2iaA</recordid><startdate>202411</startdate><enddate>202411</enddate><creator>Isler, Sila Cagri</creator><creator>Romandini, Mario</creator><creator>Akca, Gulcin</creator><creator>Bakirarar, Batuhan</creator><creator>Unsal, Berrin</creator><creator>Romanos, Georgios</creator><creator>Sculean, Anton</creator><general>Blackwell Publishing Ltd</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5646-083X</orcidid><orcidid>https://orcid.org/0000-0001-5419-9658</orcidid></search><sort><creationdate>202411</creationdate><title>Soft‐Tissue Phenotype as a Risk Indicator of Peri‐Implantitis and Peri‐Implant Soft‐Tissue Dehiscence—A Cross‐Sectional Study</title><author>Isler, Sila Cagri ; Romandini, Mario ; Akca, Gulcin ; Bakirarar, Batuhan ; Unsal, Berrin ; Romanos, Georgios ; Sculean, Anton</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2829-fdd3a90921daa45083e9be800204ba9b7dbe746bde2382a85bf0a3cab87b81ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>cytokines</topic><topic>Dehiscence</topic><topic>dental implants</topic><topic>Genotype & phenotype</topic><topic>Inflammation</topic><topic>keratinized mucosa</topic><topic>Mucosa</topic><topic>Mucositis</topic><topic>multiplex immunoassay</topic><topic>peri‐implant diseases</topic><topic>Phenotypes</topic><topic>Regression analysis</topic><topic>Transplants & implants</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Isler, Sila Cagri</creatorcontrib><creatorcontrib>Romandini, Mario</creatorcontrib><creatorcontrib>Akca, Gulcin</creatorcontrib><creatorcontrib>Bakirarar, Batuhan</creatorcontrib><creatorcontrib>Unsal, Berrin</creatorcontrib><creatorcontrib>Romanos, Georgios</creatorcontrib><creatorcontrib>Sculean, Anton</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of clinical periodontology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Isler, Sila Cagri</au><au>Romandini, Mario</au><au>Akca, Gulcin</au><au>Bakirarar, Batuhan</au><au>Unsal, Berrin</au><au>Romanos, Georgios</au><au>Sculean, Anton</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Soft‐Tissue Phenotype as a Risk Indicator of Peri‐Implantitis and Peri‐Implant Soft‐Tissue Dehiscence—A Cross‐Sectional Study</atitle><jtitle>Journal of clinical periodontology</jtitle><addtitle>J Clin Periodontol</addtitle><date>2024-11</date><risdate>2024</risdate><volume>51</volume><issue>11</issue><spage>1443</spage><epage>1457</epage><pages>1443-1457</pages><issn>0303-6979</issn><issn>1600-051X</issn><eissn>1600-051X</eissn><abstract>ABSTRACT
Aim
To investigate the association, as well as to characterize the associated panel of pro‐ and anti‐inflammatory markers, between the different components of the peri‐implant phenotype and the presence of peri‐implantitis/peri‐implant soft‐tissue dehiscence (PISTD).
Materials and Methods
A total of 324 implants in 112 patients were included. The following components of the peri‐implant phenotype were clinically measured through the use of a manual periodontal probe or a digital calliper: keratinized mucosa width (PIKM‐W), mucosal thickness (MT), attached mucosa (AM) and vestibulum depth (VD). The presence of peri‐implantitis and PISTD was assessed through clinical and radiographic examination. Mixed‐models logistic regression analyses were performed to analyse the association between peri‐implant phenotype and the presence of peri‐implantitis or PISTD, adjusting for relevant confounders. Multiplex immunoassays were employed to evaluate the peri‐implant crevicular fluid levels of a panel of pro‐ and anti‐inflammatory markers.
Results
Peri‐implant health, peri‐implant mucositis and peri‐implantitis were diagnosed in 36.6%, 21.4% and 42% of the patients (classified according to their worst implant) and 35.2%, 34.3%, and 30.5% of the implants, respectively. In the multi‐level multiple regression model, the absence of PIKM‐W (odds ratio [OR] = 9.24; 95% CI: 2.73–31.28), the absence of attached mucosa (OR = 19.58; 95% CI: 6.12–62.56) and a reduced (<4 mm) vestibulum depth (OR = 2.61; 95% CI: 1.05–6.48) were associated with peri‐implantitis. Similarly, the absence of PIKM‐W (OR = 6.32; 95% CI: 1.67–23.83), a thin (<2 mm) mucosa (OR = 157.75; 95% CI: 14.06–1769.9) and a reduced vestibulum depth (OR = 3.32; 95% CI: 1.02–10.84) were associated with the presence of PISTD. Implants with PIKM‐W = 0 mm showed statistically significantly higher levels of interferon‐γ in both regular (≥2 maintenance/year) and irregular (<2 maintenance/year) compliers (p = 0.046 and p = 0.012). In irregular compliers, the absence of PIKM‐W was also associated with statistically significantly higher levels of interleukin (IL)‐1β and IL‐21 (p = 0.016, p = 0.046). These associations were independent of the effect of relevant confounders (e.g., plaque, compliance with maintenance, etc.).
Conclusions
Within their limits, the present findings indicate that (a) peri‐implant soft‐tissue phenotype appears to be associated with the presence of peri‐implantitis and PISTD, and (b) in the absence of PIKM‐W, the inflammatory response seems to be dysregulated and the soft‐tissue remodelling up‐regulated.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>39189550</pmid><doi>10.1111/jcpe.14059</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-5646-083X</orcidid><orcidid>https://orcid.org/0000-0001-5419-9658</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Wiley Online Library - AutoHoldings Journals |
| subjects | cytokines Dehiscence dental implants Genotype & phenotype Inflammation keratinized mucosa Mucosa Mucositis multiplex immunoassay peri‐implant diseases Phenotypes Regression analysis Transplants & implants |
| title | Soft‐Tissue Phenotype as a Risk Indicator of Peri‐Implantitis and Peri‐Implant Soft‐Tissue Dehiscence—A Cross‐Sectional Study |
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