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Abstract
Discussion Forum (0)
The following report summarises the third paper presented during the Bone biology: where do we stand? session, at the EAO's 25th annual Scientific Meeting in Paris, 2016.
This session was devoted to recent advances in bone biology and how they can be applied to osseointegration. The first presentation focused on implant concepts influenced by recent bone research; the second provided new insights into the bone-implant interface; the third painted a modern vision of osseointegration and discussed peri-implantitis.
Peri-implantitis is a controversial topic, with a discrepancy between the high reported rates in recent publications and the experience of clinicians. The definition of peri-implantitis as a common infectious disease similar to periodontitis is problematic in several ways.
Fundamental differences between the interface of teeth and implants with bone make them react differently. A study by Becker et al. on the transcriptomic profiling of both concludes that periodontitis and peri-implantitis exhibit different mRNA signatures:
While in peri-implantitis tissue the regulation of transcripts related to innate immune responses and defence responses were dominating, in periodontitis tissues bacterial response systems prevailed (Becker et al. 2014)
A recent clinical study of marginal bone loss in areas surrounding implants and teeth also seems to illustrate this, finding that bone loss in both areas behaved differently (Cecchinato et al. 2016). The authors conclude: 'marginal bone loss at implants and teeth … might be independent phenomena'. It has been shown that periodontal markers such as bleeding on probing (BoP) and periodontal disease (PD) are not reliable tools for diagnosing implant disease (Coli et al. 2016; De Bruyn et al. 2016).
In contrast to periodontitis, the onset of marginal bone resorption around oral implants is unrelated to bacteria or plaque. Rather, it is an aseptic reaction which arises as a complication of treatment. Sometimes it progresses and becomes problematic, and sometimes it remains in equilibrium, dormant for decades (Figure 1).
Figure 1
There is also evidence that contradicts the allegedly high incidence of peri-implantitis. Jemt et al. documented marginal bone levels around implants in the cohort of 182 patients evaluated by Fransson and co-workers 9 years earlier (Jemt et al. 2013; Fransson et al. 2008). They found that 91.4% of the allegedly affected implants had suffered no further significant bone loss than was initially reported, and that 95.3% still survived. The authors offered another intriguing conclusion: 'Treated patients did not perform better than untreated patients with regard to bone loss or implant failure'. To better understand these issues, we must go back to osseointegration as it was originally conceptualised.
Body defence mechanisms can respond to the insertion of an implant in two ways: the implant fails and is expelled (primary failure), as happens in 1–2% of cases, or the implant is accepted and becomes encapsulated by a bone envelope. Secondary marginal bone loss depends on immunological phenomena, resulting in a delayed expulsion of the implant or late failure. This remodelling response may result in:
- minor bone resorption taking place over decades
- later complications, potentially resulting in infections
- aseptic loosening (Figure 2)
Figure 2
The balance of osteoblasts and osteoclasts is not only an expression of bone homeostasis, but the cells themselves are also part of the immune system (Takanayagi H. 2007; Takanayagi H. 2012). Marginal bone loss may be the result of multiple factors that cumulatively activate the immune system (with complement, macrophages, B- and T-cells), tilting the delicate balance between osteoblasts and osteoclasts towards resorption (Figure 3). However, even if immunological reactions result in bone resorption, we cannot ignore the fact that bacteria may plan an additional role in this process (Trindade et al. 2016).
Figure 3
Albrektsson T, Canullo L, Cochran D, De Bruyn H. “Peri-Implantitis”: A Complication of a Foreign Body or a Man-Made “Disease”. Facts and Fiction. Clin Implant Dent Relat Res. 2016 Aug;18(4):840–9. doi: 10.1111/cid.12427. Epub 2016 May 30.
Becker ST, Beck-Broichsitter BE, Graetz C, Dörfer CE, Wiltfang J, Häsler R. Peri-implantitis versus periodontitis: functional differences indicated by transcriptome profiling. Clin Implant Dent Relat Res. 2014 Jun;16(3):401–11. doi: 10.1111/cid.12001. Epub 2012 Sep 11.
Cecchinato D, Marino M, Lindhe J. Bone loss at implants and teeth in the same segment of the dentition in partially dentate subjects. Clin Oral Implants Res. 2017 May;28(5):626–630. doi: 10.1111/clr.12847. Epub 2016 Mar 27
Coli P, Christiaens V, Sennerby L, Bruyn H. Reliability of periodontal diagnostic tools for monitoring peri-implant health and disease. Periodontol 2000. 2017 Feb;73(1):203–217. doi: 10.1111/prd.12162.
De Bruyn H, Christiaens V, Doornewaard R, Jacobsson M, Cosyn J, Jacquet W, Vervaeke S. Implant surface roughness and patient factors on long‐term peri‐implant bone loss. Periodontol 2000. 2017 Feb;73(1):218–227. doi: 10.1111/prd.12177.
Fransson C, Wennström J, Berglundh T. Clinical characteristics at implants with a history of progressive bone loss. Clin Oral Implants Res. 2008 Feb;19(2):142–7. doi: 10.1111/j.1600-0501.2007.01448.x.
Jemt T, Gyzander V, Britse AÖ. Incidence of surgery related to problems with peri-implantitis: a retrospective study on patients followed up between 2003 and 2010 at one specialist clinic. Clin Implant Dent Relat Res. 2015 Apr;17(2):209–20. doi: 10.1111/cid.12097. Epub 2013 Jun 10.
Takanayagi H. Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems. Nat Rev Immunol. 2007 Apr;7(4):292–304.
Takanayagi H. New developments in osteoimmunology. Nat Rev Rheumatol. 2012 Nov;8(11):684–9. doi: 10.1038/nrrheum.2012.167. Epub 2012 Oct 16.
Trindade R, Albrektsson T, Tengvall P, Wennerberg A. Foreign Body Reaction to Biomaterials: On Mechanisms for Buildup and Breakdown of Osseointegration. Clin Implant Dent Relat Res. 2016 Feb;18(1):192–203. doi: 10.1111/cid.12274. Epub 2014 Sep 25.
This summary was prepared by the EAO Congress Scientific Report rapporteurs and approved by the speaker.
View the full publication at: www.eao.org
This session was devoted to recent advances in bone biology and how they can be applied to osseointegration. The first presentation focused on implant concepts influenced by recent bone research; the second provided new insights into the bone-implant interface; the third painted a modern vision of osseointegration and discussed peri-implantitis.
What is osseointegration in 2016 and why are we losing bone around dental implants?
'Peri-implantitis' – a foreign body reaction or a man-made 'disease' (Albrektsson et al. 2016)
Peri-implantitis is a controversial topic, with a discrepancy between the high reported rates in recent publications and the experience of clinicians. The definition of peri-implantitis as a common infectious disease similar to periodontitis is problematic in several ways.
Fundamental differences between the interface of teeth and implants with bone make them react differently. A study by Becker et al. on the transcriptomic profiling of both concludes that periodontitis and peri-implantitis exhibit different mRNA signatures:
While in peri-implantitis tissue the regulation of transcripts related to innate immune responses and defence responses were dominating, in periodontitis tissues bacterial response systems prevailed (Becker et al. 2014)
A recent clinical study of marginal bone loss in areas surrounding implants and teeth also seems to illustrate this, finding that bone loss in both areas behaved differently (Cecchinato et al. 2016). The authors conclude: 'marginal bone loss at implants and teeth … might be independent phenomena'. It has been shown that periodontal markers such as bleeding on probing (BoP) and periodontal disease (PD) are not reliable tools for diagnosing implant disease (Coli et al. 2016; De Bruyn et al. 2016).
In contrast to periodontitis, the onset of marginal bone resorption around oral implants is unrelated to bacteria or plaque. Rather, it is an aseptic reaction which arises as a complication of treatment. Sometimes it progresses and becomes problematic, and sometimes it remains in equilibrium, dormant for decades (Figure 1).
There is also evidence that contradicts the allegedly high incidence of peri-implantitis. Jemt et al. documented marginal bone levels around implants in the cohort of 182 patients evaluated by Fransson and co-workers 9 years earlier (Jemt et al. 2013; Fransson et al. 2008). They found that 91.4% of the allegedly affected implants had suffered no further significant bone loss than was initially reported, and that 95.3% still survived. The authors offered another intriguing conclusion: 'Treated patients did not perform better than untreated patients with regard to bone loss or implant failure'. To better understand these issues, we must go back to osseointegration as it was originally conceptualised.
Osseointegration revisited
Body defence mechanisms can respond to the insertion of an implant in two ways: the implant fails and is expelled (primary failure), as happens in 1–2% of cases, or the implant is accepted and becomes encapsulated by a bone envelope. Secondary marginal bone loss depends on immunological phenomena, resulting in a delayed expulsion of the implant or late failure. This remodelling response may result in:
- minor bone resorption taking place over decades
- later complications, potentially resulting in infections
- aseptic loosening (Figure 2)
The balance of osteoblasts and osteoclasts is not only an expression of bone homeostasis, but the cells themselves are also part of the immune system (Takanayagi H. 2007; Takanayagi H. 2012). Marginal bone loss may be the result of multiple factors that cumulatively activate the immune system (with complement, macrophages, B- and T-cells), tilting the delicate balance between osteoblasts and osteoclasts towards resorption (Figure 3). However, even if immunological reactions result in bone resorption, we cannot ignore the fact that bacteria may plan an additional role in this process (Trindade et al. 2016).
References
Albrektsson T, Canullo L, Cochran D, De Bruyn H. “Peri-Implantitis”: A Complication of a Foreign Body or a Man-Made “Disease”. Facts and Fiction. Clin Implant Dent Relat Res. 2016 Aug;18(4):840–9. doi: 10.1111/cid.12427. Epub 2016 May 30.
Becker ST, Beck-Broichsitter BE, Graetz C, Dörfer CE, Wiltfang J, Häsler R. Peri-implantitis versus periodontitis: functional differences indicated by transcriptome profiling. Clin Implant Dent Relat Res. 2014 Jun;16(3):401–11. doi: 10.1111/cid.12001. Epub 2012 Sep 11.
Cecchinato D, Marino M, Lindhe J. Bone loss at implants and teeth in the same segment of the dentition in partially dentate subjects. Clin Oral Implants Res. 2017 May;28(5):626–630. doi: 10.1111/clr.12847. Epub 2016 Mar 27
Coli P, Christiaens V, Sennerby L, Bruyn H. Reliability of periodontal diagnostic tools for monitoring peri-implant health and disease. Periodontol 2000. 2017 Feb;73(1):203–217. doi: 10.1111/prd.12162.
De Bruyn H, Christiaens V, Doornewaard R, Jacobsson M, Cosyn J, Jacquet W, Vervaeke S. Implant surface roughness and patient factors on long‐term peri‐implant bone loss. Periodontol 2000. 2017 Feb;73(1):218–227. doi: 10.1111/prd.12177.
Fransson C, Wennström J, Berglundh T. Clinical characteristics at implants with a history of progressive bone loss. Clin Oral Implants Res. 2008 Feb;19(2):142–7. doi: 10.1111/j.1600-0501.2007.01448.x.
Jemt T, Gyzander V, Britse AÖ. Incidence of surgery related to problems with peri-implantitis: a retrospective study on patients followed up between 2003 and 2010 at one specialist clinic. Clin Implant Dent Relat Res. 2015 Apr;17(2):209–20. doi: 10.1111/cid.12097. Epub 2013 Jun 10.
Takanayagi H. Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems. Nat Rev Immunol. 2007 Apr;7(4):292–304.
Takanayagi H. New developments in osteoimmunology. Nat Rev Rheumatol. 2012 Nov;8(11):684–9. doi: 10.1038/nrrheum.2012.167. Epub 2012 Oct 16.
Trindade R, Albrektsson T, Tengvall P, Wennerberg A. Foreign Body Reaction to Biomaterials: On Mechanisms for Buildup and Breakdown of Osseointegration. Clin Implant Dent Relat Res. 2016 Feb;18(1):192–203. doi: 10.1111/cid.12274. Epub 2014 Sep 25.
This summary was prepared by the EAO Congress Scientific Report rapporteurs and approved by the speaker.
View the full publication at: www.eao.org
The following report summarises the third paper presented during the Bone biology: where do we stand? session, at the EAO's 25th annual Scientific Meeting in Paris, 2016.
This session was devoted to recent advances in bone biology and how they can be applied to osseointegration. The first presentation focused on implant concepts influenced by recent bone research; the second provided new insights into the bone-implant interface; the third painted a modern vision of osseointegration and discussed peri-implantitis.
Peri-implantitis is a controversial topic, with a discrepancy between the high reported rates in recent publications and the experience of clinicians. The definition of peri-implantitis as a common infectious disease similar to periodontitis is problematic in several ways.
Fundamental differences between the interface of teeth and implants with bone make them react differently. A study by Becker et al. on the transcriptomic profiling of both concludes that periodontitis and peri-implantitis exhibit different mRNA signatures:
While in peri-implantitis tissue the regulation of transcripts related to innate immune responses and defence responses were dominating, in periodontitis tissues bacterial response systems prevailed (Becker et al. 2014)
A recent clinical study of marginal bone loss in areas surrounding implants and teeth also seems to illustrate this, finding that bone loss in both areas behaved differently (Cecchinato et al. 2016). The authors conclude: 'marginal bone loss at implants and teeth … might be independent phenomena'. It has been shown that periodontal markers such as bleeding on probing (BoP) and periodontal disease (PD) are not reliable tools for diagnosing implant disease (Coli et al. 2016; De Bruyn et al. 2016).
In contrast to periodontitis, the onset of marginal bone resorption around oral implants is unrelated to bacteria or plaque. Rather, it is an aseptic reaction which arises as a complication of treatment. Sometimes it progresses and becomes problematic, and sometimes it remains in equilibrium, dormant for decades (Figure 1).
Figure 1
There is also evidence that contradicts the allegedly high incidence of peri-implantitis. Jemt et al. documented marginal bone levels around implants in the cohort of 182 patients evaluated by Fransson and co-workers 9 years earlier (Jemt et al. 2013; Fransson et al. 2008). They found that 91.4% of the allegedly affected implants had suffered no further significant bone loss than was initially reported, and that 95.3% still survived. The authors offered another intriguing conclusion: 'Treated patients did not perform better than untreated patients with regard to bone loss or implant failure'. To better understand these issues, we must go back to osseointegration as it was originally conceptualised.
Body defence mechanisms can respond to the insertion of an implant in two ways: the implant fails and is expelled (primary failure), as happens in 1–2% of cases, or the implant is accepted and becomes encapsulated by a bone envelope. Secondary marginal bone loss depends on immunological phenomena, resulting in a delayed expulsion of the implant or late failure. This remodelling response may result in:
- minor bone resorption taking place over decades
- later complications, potentially resulting in infections
- aseptic loosening (Figure 2)
Figure 2
The balance of osteoblasts and osteoclasts is not only an expression of bone homeostasis, but the cells themselves are also part of the immune system (Takanayagi H. 2007; Takanayagi H. 2012). Marginal bone loss may be the result of multiple factors that cumulatively activate the immune system (with complement, macrophages, B- and T-cells), tilting the delicate balance between osteoblasts and osteoclasts towards resorption (Figure 3). However, even if immunological reactions result in bone resorption, we cannot ignore the fact that bacteria may plan an additional role in this process (Trindade et al. 2016).
Figure 3
Albrektsson T, Canullo L, Cochran D, De Bruyn H. “Peri-Implantitis”: A Complication of a Foreign Body or a Man-Made “Disease”. Facts and Fiction. Clin Implant Dent Relat Res. 2016 Aug;18(4):840–9. doi: 10.1111/cid.12427. Epub 2016 May 30.
Becker ST, Beck-Broichsitter BE, Graetz C, Dörfer CE, Wiltfang J, Häsler R. Peri-implantitis versus periodontitis: functional differences indicated by transcriptome profiling. Clin Implant Dent Relat Res. 2014 Jun;16(3):401–11. doi: 10.1111/cid.12001. Epub 2012 Sep 11.
Cecchinato D, Marino M, Lindhe J. Bone loss at implants and teeth in the same segment of the dentition in partially dentate subjects. Clin Oral Implants Res. 2017 May;28(5):626–630. doi: 10.1111/clr.12847. Epub 2016 Mar 27
Coli P, Christiaens V, Sennerby L, Bruyn H. Reliability of periodontal diagnostic tools for monitoring peri-implant health and disease. Periodontol 2000. 2017 Feb;73(1):203–217. doi: 10.1111/prd.12162.
De Bruyn H, Christiaens V, Doornewaard R, Jacobsson M, Cosyn J, Jacquet W, Vervaeke S. Implant surface roughness and patient factors on long‐term peri‐implant bone loss. Periodontol 2000. 2017 Feb;73(1):218–227. doi: 10.1111/prd.12177.
Fransson C, Wennström J, Berglundh T. Clinical characteristics at implants with a history of progressive bone loss. Clin Oral Implants Res. 2008 Feb;19(2):142–7. doi: 10.1111/j.1600-0501.2007.01448.x.
Jemt T, Gyzander V, Britse AÖ. Incidence of surgery related to problems with peri-implantitis: a retrospective study on patients followed up between 2003 and 2010 at one specialist clinic. Clin Implant Dent Relat Res. 2015 Apr;17(2):209–20. doi: 10.1111/cid.12097. Epub 2013 Jun 10.
Takanayagi H. Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems. Nat Rev Immunol. 2007 Apr;7(4):292–304.
Takanayagi H. New developments in osteoimmunology. Nat Rev Rheumatol. 2012 Nov;8(11):684–9. doi: 10.1038/nrrheum.2012.167. Epub 2012 Oct 16.
Trindade R, Albrektsson T, Tengvall P, Wennerberg A. Foreign Body Reaction to Biomaterials: On Mechanisms for Buildup and Breakdown of Osseointegration. Clin Implant Dent Relat Res. 2016 Feb;18(1):192–203. doi: 10.1111/cid.12274. Epub 2014 Sep 25.
This summary was prepared by the EAO Congress Scientific Report rapporteurs and approved by the speaker.
View the full publication at: www.eao.org
This session was devoted to recent advances in bone biology and how they can be applied to osseointegration. The first presentation focused on implant concepts influenced by recent bone research; the second provided new insights into the bone-implant interface; the third painted a modern vision of osseointegration and discussed peri-implantitis.
What is osseointegration in 2016 and why are we losing bone around dental implants?
'Peri-implantitis' – a foreign body reaction or a man-made 'disease' (Albrektsson et al. 2016)
Peri-implantitis is a controversial topic, with a discrepancy between the high reported rates in recent publications and the experience of clinicians. The definition of peri-implantitis as a common infectious disease similar to periodontitis is problematic in several ways.
Fundamental differences between the interface of teeth and implants with bone make them react differently. A study by Becker et al. on the transcriptomic profiling of both concludes that periodontitis and peri-implantitis exhibit different mRNA signatures:
While in peri-implantitis tissue the regulation of transcripts related to innate immune responses and defence responses were dominating, in periodontitis tissues bacterial response systems prevailed (Becker et al. 2014)
A recent clinical study of marginal bone loss in areas surrounding implants and teeth also seems to illustrate this, finding that bone loss in both areas behaved differently (Cecchinato et al. 2016). The authors conclude: 'marginal bone loss at implants and teeth … might be independent phenomena'. It has been shown that periodontal markers such as bleeding on probing (BoP) and periodontal disease (PD) are not reliable tools for diagnosing implant disease (Coli et al. 2016; De Bruyn et al. 2016).
In contrast to periodontitis, the onset of marginal bone resorption around oral implants is unrelated to bacteria or plaque. Rather, it is an aseptic reaction which arises as a complication of treatment. Sometimes it progresses and becomes problematic, and sometimes it remains in equilibrium, dormant for decades (Figure 1).
There is also evidence that contradicts the allegedly high incidence of peri-implantitis. Jemt et al. documented marginal bone levels around implants in the cohort of 182 patients evaluated by Fransson and co-workers 9 years earlier (Jemt et al. 2013; Fransson et al. 2008). They found that 91.4% of the allegedly affected implants had suffered no further significant bone loss than was initially reported, and that 95.3% still survived. The authors offered another intriguing conclusion: 'Treated patients did not perform better than untreated patients with regard to bone loss or implant failure'. To better understand these issues, we must go back to osseointegration as it was originally conceptualised.
Osseointegration revisited
Body defence mechanisms can respond to the insertion of an implant in two ways: the implant fails and is expelled (primary failure), as happens in 1–2% of cases, or the implant is accepted and becomes encapsulated by a bone envelope. Secondary marginal bone loss depends on immunological phenomena, resulting in a delayed expulsion of the implant or late failure. This remodelling response may result in:
- minor bone resorption taking place over decades
- later complications, potentially resulting in infections
- aseptic loosening (Figure 2)
The balance of osteoblasts and osteoclasts is not only an expression of bone homeostasis, but the cells themselves are also part of the immune system (Takanayagi H. 2007; Takanayagi H. 2012). Marginal bone loss may be the result of multiple factors that cumulatively activate the immune system (with complement, macrophages, B- and T-cells), tilting the delicate balance between osteoblasts and osteoclasts towards resorption (Figure 3). However, even if immunological reactions result in bone resorption, we cannot ignore the fact that bacteria may plan an additional role in this process (Trindade et al. 2016).
References
Albrektsson T, Canullo L, Cochran D, De Bruyn H. “Peri-Implantitis”: A Complication of a Foreign Body or a Man-Made “Disease”. Facts and Fiction. Clin Implant Dent Relat Res. 2016 Aug;18(4):840–9. doi: 10.1111/cid.12427. Epub 2016 May 30.
Becker ST, Beck-Broichsitter BE, Graetz C, Dörfer CE, Wiltfang J, Häsler R. Peri-implantitis versus periodontitis: functional differences indicated by transcriptome profiling. Clin Implant Dent Relat Res. 2014 Jun;16(3):401–11. doi: 10.1111/cid.12001. Epub 2012 Sep 11.
Cecchinato D, Marino M, Lindhe J. Bone loss at implants and teeth in the same segment of the dentition in partially dentate subjects. Clin Oral Implants Res. 2017 May;28(5):626–630. doi: 10.1111/clr.12847. Epub 2016 Mar 27
Coli P, Christiaens V, Sennerby L, Bruyn H. Reliability of periodontal diagnostic tools for monitoring peri-implant health and disease. Periodontol 2000. 2017 Feb;73(1):203–217. doi: 10.1111/prd.12162.
De Bruyn H, Christiaens V, Doornewaard R, Jacobsson M, Cosyn J, Jacquet W, Vervaeke S. Implant surface roughness and patient factors on long‐term peri‐implant bone loss. Periodontol 2000. 2017 Feb;73(1):218–227. doi: 10.1111/prd.12177.
Fransson C, Wennström J, Berglundh T. Clinical characteristics at implants with a history of progressive bone loss. Clin Oral Implants Res. 2008 Feb;19(2):142–7. doi: 10.1111/j.1600-0501.2007.01448.x.
Jemt T, Gyzander V, Britse AÖ. Incidence of surgery related to problems with peri-implantitis: a retrospective study on patients followed up between 2003 and 2010 at one specialist clinic. Clin Implant Dent Relat Res. 2015 Apr;17(2):209–20. doi: 10.1111/cid.12097. Epub 2013 Jun 10.
Takanayagi H. Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems. Nat Rev Immunol. 2007 Apr;7(4):292–304.
Takanayagi H. New developments in osteoimmunology. Nat Rev Rheumatol. 2012 Nov;8(11):684–9. doi: 10.1038/nrrheum.2012.167. Epub 2012 Oct 16.
Trindade R, Albrektsson T, Tengvall P, Wennerberg A. Foreign Body Reaction to Biomaterials: On Mechanisms for Buildup and Breakdown of Osseointegration. Clin Implant Dent Relat Res. 2016 Feb;18(1):192–203. doi: 10.1111/cid.12274. Epub 2014 Sep 25.
This summary was prepared by the EAO Congress Scientific Report rapporteurs and approved by the speaker.
View the full publication at: www.eao.org
What is osseointegration in 2016 and why are we losing bone around dental implants?
Prof. Tomas Albrektsson
Abstract
Discussion Forum (0)
The following report summarises the third paper presented during the Bone biology: where do we stand? session, at the EAO's 25th annual Scientific Meeting in Paris, 2016.
This session was devoted to recent advances in bone biology and how they can be applied to osseointegration. The first presentation focused on implant concepts influenced by recent bone research; the second provided new insights into the bone-implant interface; the third painted a modern vision of osseointegration and discussed peri-implantitis.
Peri-implantitis is a controversial topic, with a discrepancy between the high reported rates in recent publications and the experience of clinicians. The definition of peri-implantitis as a common infectious disease similar to periodontitis is problematic in several ways.
Fundamental differences between the interface of teeth and implants with bone make them react differently. A study by Becker et al. on the transcriptomic profiling of both concludes that periodontitis and peri-implantitis exhibit different mRNA signatures:
While in peri-implantitis tissue the regulation of transcripts related to innate immune responses and defence responses were dominating, in periodontitis tissues bacterial response systems prevailed (Becker et al. 2014)
A recent clinical study of marginal bone loss in areas surrounding implants and teeth also seems to illustrate this, finding that bone loss in both areas behaved differently (Cecchinato et al. 2016). The authors conclude: 'marginal bone loss at implants and teeth … might be independent phenomena'. It has been shown that periodontal markers such as bleeding on probing (BoP) and periodontal disease (PD) are not reliable tools for diagnosing implant disease (Coli et al. 2016; De Bruyn et al. 2016).
In contrast to periodontitis, the onset of marginal bone resorption around oral implants is unrelated to bacteria or plaque. Rather, it is an aseptic reaction which arises as a complication of treatment. Sometimes it progresses and becomes problematic, and sometimes it remains in equilibrium, dormant for decades (Figure 1).
Figure 1
There is also evidence that contradicts the allegedly high incidence of peri-implantitis. Jemt et al. documented marginal bone levels around implants in the cohort of 182 patients evaluated by Fransson and co-workers 9 years earlier (Jemt et al. 2013; Fransson et al. 2008). They found that 91.4% of the allegedly affected implants had suffered no further significant bone loss than was initially reported, and that 95.3% still survived. The authors offered another intriguing conclusion: 'Treated patients did not perform better than untreated patients with regard to bone loss or implant failure'. To better understand these issues, we must go back to osseointegration as it was originally conceptualised.
Body defence mechanisms can respond to the insertion of an implant in two ways: the implant fails and is expelled (primary failure), as happens in 1–2% of cases, or the implant is accepted and becomes encapsulated by a bone envelope. Secondary marginal bone loss depends on immunological phenomena, resulting in a delayed expulsion of the implant or late failure. This remodelling response may result in:
- minor bone resorption taking place over decades
- later complications, potentially resulting in infections
- aseptic loosening (Figure 2)
Figure 2
The balance of osteoblasts and osteoclasts is not only an expression of bone homeostasis, but the cells themselves are also part of the immune system (Takanayagi H. 2007; Takanayagi H. 2012). Marginal bone loss may be the result of multiple factors that cumulatively activate the immune system (with complement, macrophages, B- and T-cells), tilting the delicate balance between osteoblasts and osteoclasts towards resorption (Figure 3). However, even if immunological reactions result in bone resorption, we cannot ignore the fact that bacteria may plan an additional role in this process (Trindade et al. 2016).
Figure 3
Albrektsson T, Canullo L, Cochran D, De Bruyn H. “Peri-Implantitis”: A Complication of a Foreign Body or a Man-Made “Disease”. Facts and Fiction. Clin Implant Dent Relat Res. 2016 Aug;18(4):840–9. doi: 10.1111/cid.12427. Epub 2016 May 30.
Becker ST, Beck-Broichsitter BE, Graetz C, Dörfer CE, Wiltfang J, Häsler R. Peri-implantitis versus periodontitis: functional differences indicated by transcriptome profiling. Clin Implant Dent Relat Res. 2014 Jun;16(3):401–11. doi: 10.1111/cid.12001. Epub 2012 Sep 11.
Cecchinato D, Marino M, Lindhe J. Bone loss at implants and teeth in the same segment of the dentition in partially dentate subjects. Clin Oral Implants Res. 2017 May;28(5):626–630. doi: 10.1111/clr.12847. Epub 2016 Mar 27
Coli P, Christiaens V, Sennerby L, Bruyn H. Reliability of periodontal diagnostic tools for monitoring peri-implant health and disease. Periodontol 2000. 2017 Feb;73(1):203–217. doi: 10.1111/prd.12162.
De Bruyn H, Christiaens V, Doornewaard R, Jacobsson M, Cosyn J, Jacquet W, Vervaeke S. Implant surface roughness and patient factors on long‐term peri‐implant bone loss. Periodontol 2000. 2017 Feb;73(1):218–227. doi: 10.1111/prd.12177.
Fransson C, Wennström J, Berglundh T. Clinical characteristics at implants with a history of progressive bone loss. Clin Oral Implants Res. 2008 Feb;19(2):142–7. doi: 10.1111/j.1600-0501.2007.01448.x.
Jemt T, Gyzander V, Britse AÖ. Incidence of surgery related to problems with peri-implantitis: a retrospective study on patients followed up between 2003 and 2010 at one specialist clinic. Clin Implant Dent Relat Res. 2015 Apr;17(2):209–20. doi: 10.1111/cid.12097. Epub 2013 Jun 10.
Takanayagi H. Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems. Nat Rev Immunol. 2007 Apr;7(4):292–304.
Takanayagi H. New developments in osteoimmunology. Nat Rev Rheumatol. 2012 Nov;8(11):684–9. doi: 10.1038/nrrheum.2012.167. Epub 2012 Oct 16.
Trindade R, Albrektsson T, Tengvall P, Wennerberg A. Foreign Body Reaction to Biomaterials: On Mechanisms for Buildup and Breakdown of Osseointegration. Clin Implant Dent Relat Res. 2016 Feb;18(1):192–203. doi: 10.1111/cid.12274. Epub 2014 Sep 25.
This summary was prepared by the EAO Congress Scientific Report rapporteurs and approved by the speaker.
View the full publication at: www.eao.org
This session was devoted to recent advances in bone biology and how they can be applied to osseointegration. The first presentation focused on implant concepts influenced by recent bone research; the second provided new insights into the bone-implant interface; the third painted a modern vision of osseointegration and discussed peri-implantitis.
What is osseointegration in 2016 and why are we losing bone around dental implants?
'Peri-implantitis' – a foreign body reaction or a man-made 'disease' (Albrektsson et al. 2016)
Peri-implantitis is a controversial topic, with a discrepancy between the high reported rates in recent publications and the experience of clinicians. The definition of peri-implantitis as a common infectious disease similar to periodontitis is problematic in several ways.
Fundamental differences between the interface of teeth and implants with bone make them react differently. A study by Becker et al. on the transcriptomic profiling of both concludes that periodontitis and peri-implantitis exhibit different mRNA signatures:
While in peri-implantitis tissue the regulation of transcripts related to innate immune responses and defence responses were dominating, in periodontitis tissues bacterial response systems prevailed (Becker et al. 2014)
A recent clinical study of marginal bone loss in areas surrounding implants and teeth also seems to illustrate this, finding that bone loss in both areas behaved differently (Cecchinato et al. 2016). The authors conclude: 'marginal bone loss at implants and teeth … might be independent phenomena'. It has been shown that periodontal markers such as bleeding on probing (BoP) and periodontal disease (PD) are not reliable tools for diagnosing implant disease (Coli et al. 2016; De Bruyn et al. 2016).
In contrast to periodontitis, the onset of marginal bone resorption around oral implants is unrelated to bacteria or plaque. Rather, it is an aseptic reaction which arises as a complication of treatment. Sometimes it progresses and becomes problematic, and sometimes it remains in equilibrium, dormant for decades (Figure 1).
There is also evidence that contradicts the allegedly high incidence of peri-implantitis. Jemt et al. documented marginal bone levels around implants in the cohort of 182 patients evaluated by Fransson and co-workers 9 years earlier (Jemt et al. 2013; Fransson et al. 2008). They found that 91.4% of the allegedly affected implants had suffered no further significant bone loss than was initially reported, and that 95.3% still survived. The authors offered another intriguing conclusion: 'Treated patients did not perform better than untreated patients with regard to bone loss or implant failure'. To better understand these issues, we must go back to osseointegration as it was originally conceptualised.
Osseointegration revisited
Body defence mechanisms can respond to the insertion of an implant in two ways: the implant fails and is expelled (primary failure), as happens in 1–2% of cases, or the implant is accepted and becomes encapsulated by a bone envelope. Secondary marginal bone loss depends on immunological phenomena, resulting in a delayed expulsion of the implant or late failure. This remodelling response may result in:
- minor bone resorption taking place over decades
- later complications, potentially resulting in infections
- aseptic loosening (Figure 2)
The balance of osteoblasts and osteoclasts is not only an expression of bone homeostasis, but the cells themselves are also part of the immune system (Takanayagi H. 2007; Takanayagi H. 2012). Marginal bone loss may be the result of multiple factors that cumulatively activate the immune system (with complement, macrophages, B- and T-cells), tilting the delicate balance between osteoblasts and osteoclasts towards resorption (Figure 3). However, even if immunological reactions result in bone resorption, we cannot ignore the fact that bacteria may plan an additional role in this process (Trindade et al. 2016).
References
Albrektsson T, Canullo L, Cochran D, De Bruyn H. “Peri-Implantitis”: A Complication of a Foreign Body or a Man-Made “Disease”. Facts and Fiction. Clin Implant Dent Relat Res. 2016 Aug;18(4):840–9. doi: 10.1111/cid.12427. Epub 2016 May 30.
Becker ST, Beck-Broichsitter BE, Graetz C, Dörfer CE, Wiltfang J, Häsler R. Peri-implantitis versus periodontitis: functional differences indicated by transcriptome profiling. Clin Implant Dent Relat Res. 2014 Jun;16(3):401–11. doi: 10.1111/cid.12001. Epub 2012 Sep 11.
Cecchinato D, Marino M, Lindhe J. Bone loss at implants and teeth in the same segment of the dentition in partially dentate subjects. Clin Oral Implants Res. 2017 May;28(5):626–630. doi: 10.1111/clr.12847. Epub 2016 Mar 27
Coli P, Christiaens V, Sennerby L, Bruyn H. Reliability of periodontal diagnostic tools for monitoring peri-implant health and disease. Periodontol 2000. 2017 Feb;73(1):203–217. doi: 10.1111/prd.12162.
De Bruyn H, Christiaens V, Doornewaard R, Jacobsson M, Cosyn J, Jacquet W, Vervaeke S. Implant surface roughness and patient factors on long‐term peri‐implant bone loss. Periodontol 2000. 2017 Feb;73(1):218–227. doi: 10.1111/prd.12177.
Fransson C, Wennström J, Berglundh T. Clinical characteristics at implants with a history of progressive bone loss. Clin Oral Implants Res. 2008 Feb;19(2):142–7. doi: 10.1111/j.1600-0501.2007.01448.x.
Jemt T, Gyzander V, Britse AÖ. Incidence of surgery related to problems with peri-implantitis: a retrospective study on patients followed up between 2003 and 2010 at one specialist clinic. Clin Implant Dent Relat Res. 2015 Apr;17(2):209–20. doi: 10.1111/cid.12097. Epub 2013 Jun 10.
Takanayagi H. Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems. Nat Rev Immunol. 2007 Apr;7(4):292–304.
Takanayagi H. New developments in osteoimmunology. Nat Rev Rheumatol. 2012 Nov;8(11):684–9. doi: 10.1038/nrrheum.2012.167. Epub 2012 Oct 16.
Trindade R, Albrektsson T, Tengvall P, Wennerberg A. Foreign Body Reaction to Biomaterials: On Mechanisms for Buildup and Breakdown of Osseointegration. Clin Implant Dent Relat Res. 2016 Feb;18(1):192–203. doi: 10.1111/cid.12274. Epub 2014 Sep 25.
This summary was prepared by the EAO Congress Scientific Report rapporteurs and approved by the speaker.
View the full publication at: www.eao.org
The following report summarises the third paper presented during the Bone biology: where do we stand? session, at the EAO's 25th annual Scientific Meeting in Paris, 2016.
This session was devoted to recent advances in bone biology and how they can be applied to osseointegration. The first presentation focused on implant concepts influenced by recent bone research; the second provided new insights into the bone-implant interface; the third painted a modern vision of osseointegration and discussed peri-implantitis.
Peri-implantitis is a controversial topic, with a discrepancy between the high reported rates in recent publications and the experience of clinicians. The definition of peri-implantitis as a common infectious disease similar to periodontitis is problematic in several ways.
Fundamental differences between the interface of teeth and implants with bone make them react differently. A study by Becker et al. on the transcriptomic profiling of both concludes that periodontitis and peri-implantitis exhibit different mRNA signatures:
While in peri-implantitis tissue the regulation of transcripts related to innate immune responses and defence responses were dominating, in periodontitis tissues bacterial response systems prevailed (Becker et al. 2014)
A recent clinical study of marginal bone loss in areas surrounding implants and teeth also seems to illustrate this, finding that bone loss in both areas behaved differently (Cecchinato et al. 2016). The authors conclude: 'marginal bone loss at implants and teeth … might be independent phenomena'. It has been shown that periodontal markers such as bleeding on probing (BoP) and periodontal disease (PD) are not reliable tools for diagnosing implant disease (Coli et al. 2016; De Bruyn et al. 2016).
In contrast to periodontitis, the onset of marginal bone resorption around oral implants is unrelated to bacteria or plaque. Rather, it is an aseptic reaction which arises as a complication of treatment. Sometimes it progresses and becomes problematic, and sometimes it remains in equilibrium, dormant for decades (Figure 1).
Figure 1
There is also evidence that contradicts the allegedly high incidence of peri-implantitis. Jemt et al. documented marginal bone levels around implants in the cohort of 182 patients evaluated by Fransson and co-workers 9 years earlier (Jemt et al. 2013; Fransson et al. 2008). They found that 91.4% of the allegedly affected implants had suffered no further significant bone loss than was initially reported, and that 95.3% still survived. The authors offered another intriguing conclusion: 'Treated patients did not perform better than untreated patients with regard to bone loss or implant failure'. To better understand these issues, we must go back to osseointegration as it was originally conceptualised.
Body defence mechanisms can respond to the insertion of an implant in two ways: the implant fails and is expelled (primary failure), as happens in 1–2% of cases, or the implant is accepted and becomes encapsulated by a bone envelope. Secondary marginal bone loss depends on immunological phenomena, resulting in a delayed expulsion of the implant or late failure. This remodelling response may result in:
- minor bone resorption taking place over decades
- later complications, potentially resulting in infections
- aseptic loosening (Figure 2)
Figure 2
The balance of osteoblasts and osteoclasts is not only an expression of bone homeostasis, but the cells themselves are also part of the immune system (Takanayagi H. 2007; Takanayagi H. 2012). Marginal bone loss may be the result of multiple factors that cumulatively activate the immune system (with complement, macrophages, B- and T-cells), tilting the delicate balance between osteoblasts and osteoclasts towards resorption (Figure 3). However, even if immunological reactions result in bone resorption, we cannot ignore the fact that bacteria may plan an additional role in this process (Trindade et al. 2016).
Figure 3
Albrektsson T, Canullo L, Cochran D, De Bruyn H. “Peri-Implantitis”: A Complication of a Foreign Body or a Man-Made “Disease”. Facts and Fiction. Clin Implant Dent Relat Res. 2016 Aug;18(4):840–9. doi: 10.1111/cid.12427. Epub 2016 May 30.
Becker ST, Beck-Broichsitter BE, Graetz C, Dörfer CE, Wiltfang J, Häsler R. Peri-implantitis versus periodontitis: functional differences indicated by transcriptome profiling. Clin Implant Dent Relat Res. 2014 Jun;16(3):401–11. doi: 10.1111/cid.12001. Epub 2012 Sep 11.
Cecchinato D, Marino M, Lindhe J. Bone loss at implants and teeth in the same segment of the dentition in partially dentate subjects. Clin Oral Implants Res. 2017 May;28(5):626–630. doi: 10.1111/clr.12847. Epub 2016 Mar 27
Coli P, Christiaens V, Sennerby L, Bruyn H. Reliability of periodontal diagnostic tools for monitoring peri-implant health and disease. Periodontol 2000. 2017 Feb;73(1):203–217. doi: 10.1111/prd.12162.
De Bruyn H, Christiaens V, Doornewaard R, Jacobsson M, Cosyn J, Jacquet W, Vervaeke S. Implant surface roughness and patient factors on long‐term peri‐implant bone loss. Periodontol 2000. 2017 Feb;73(1):218–227. doi: 10.1111/prd.12177.
Fransson C, Wennström J, Berglundh T. Clinical characteristics at implants with a history of progressive bone loss. Clin Oral Implants Res. 2008 Feb;19(2):142–7. doi: 10.1111/j.1600-0501.2007.01448.x.
Jemt T, Gyzander V, Britse AÖ. Incidence of surgery related to problems with peri-implantitis: a retrospective study on patients followed up between 2003 and 2010 at one specialist clinic. Clin Implant Dent Relat Res. 2015 Apr;17(2):209–20. doi: 10.1111/cid.12097. Epub 2013 Jun 10.
Takanayagi H. Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems. Nat Rev Immunol. 2007 Apr;7(4):292–304.
Takanayagi H. New developments in osteoimmunology. Nat Rev Rheumatol. 2012 Nov;8(11):684–9. doi: 10.1038/nrrheum.2012.167. Epub 2012 Oct 16.
Trindade R, Albrektsson T, Tengvall P, Wennerberg A. Foreign Body Reaction to Biomaterials: On Mechanisms for Buildup and Breakdown of Osseointegration. Clin Implant Dent Relat Res. 2016 Feb;18(1):192–203. doi: 10.1111/cid.12274. Epub 2014 Sep 25.
This summary was prepared by the EAO Congress Scientific Report rapporteurs and approved by the speaker.
View the full publication at: www.eao.org
This session was devoted to recent advances in bone biology and how they can be applied to osseointegration. The first presentation focused on implant concepts influenced by recent bone research; the second provided new insights into the bone-implant interface; the third painted a modern vision of osseointegration and discussed peri-implantitis.
What is osseointegration in 2016 and why are we losing bone around dental implants?
'Peri-implantitis' – a foreign body reaction or a man-made 'disease' (Albrektsson et al. 2016)
Peri-implantitis is a controversial topic, with a discrepancy between the high reported rates in recent publications and the experience of clinicians. The definition of peri-implantitis as a common infectious disease similar to periodontitis is problematic in several ways.
Fundamental differences between the interface of teeth and implants with bone make them react differently. A study by Becker et al. on the transcriptomic profiling of both concludes that periodontitis and peri-implantitis exhibit different mRNA signatures:
While in peri-implantitis tissue the regulation of transcripts related to innate immune responses and defence responses were dominating, in periodontitis tissues bacterial response systems prevailed (Becker et al. 2014)
A recent clinical study of marginal bone loss in areas surrounding implants and teeth also seems to illustrate this, finding that bone loss in both areas behaved differently (Cecchinato et al. 2016). The authors conclude: 'marginal bone loss at implants and teeth … might be independent phenomena'. It has been shown that periodontal markers such as bleeding on probing (BoP) and periodontal disease (PD) are not reliable tools for diagnosing implant disease (Coli et al. 2016; De Bruyn et al. 2016).
In contrast to periodontitis, the onset of marginal bone resorption around oral implants is unrelated to bacteria or plaque. Rather, it is an aseptic reaction which arises as a complication of treatment. Sometimes it progresses and becomes problematic, and sometimes it remains in equilibrium, dormant for decades (Figure 1).
There is also evidence that contradicts the allegedly high incidence of peri-implantitis. Jemt et al. documented marginal bone levels around implants in the cohort of 182 patients evaluated by Fransson and co-workers 9 years earlier (Jemt et al. 2013; Fransson et al. 2008). They found that 91.4% of the allegedly affected implants had suffered no further significant bone loss than was initially reported, and that 95.3% still survived. The authors offered another intriguing conclusion: 'Treated patients did not perform better than untreated patients with regard to bone loss or implant failure'. To better understand these issues, we must go back to osseointegration as it was originally conceptualised.
Osseointegration revisited
Body defence mechanisms can respond to the insertion of an implant in two ways: the implant fails and is expelled (primary failure), as happens in 1–2% of cases, or the implant is accepted and becomes encapsulated by a bone envelope. Secondary marginal bone loss depends on immunological phenomena, resulting in a delayed expulsion of the implant or late failure. This remodelling response may result in:
- minor bone resorption taking place over decades
- later complications, potentially resulting in infections
- aseptic loosening (Figure 2)
The balance of osteoblasts and osteoclasts is not only an expression of bone homeostasis, but the cells themselves are also part of the immune system (Takanayagi H. 2007; Takanayagi H. 2012). Marginal bone loss may be the result of multiple factors that cumulatively activate the immune system (with complement, macrophages, B- and T-cells), tilting the delicate balance between osteoblasts and osteoclasts towards resorption (Figure 3). However, even if immunological reactions result in bone resorption, we cannot ignore the fact that bacteria may plan an additional role in this process (Trindade et al. 2016).
References
Albrektsson T, Canullo L, Cochran D, De Bruyn H. “Peri-Implantitis”: A Complication of a Foreign Body or a Man-Made “Disease”. Facts and Fiction. Clin Implant Dent Relat Res. 2016 Aug;18(4):840–9. doi: 10.1111/cid.12427. Epub 2016 May 30.
Becker ST, Beck-Broichsitter BE, Graetz C, Dörfer CE, Wiltfang J, Häsler R. Peri-implantitis versus periodontitis: functional differences indicated by transcriptome profiling. Clin Implant Dent Relat Res. 2014 Jun;16(3):401–11. doi: 10.1111/cid.12001. Epub 2012 Sep 11.
Cecchinato D, Marino M, Lindhe J. Bone loss at implants and teeth in the same segment of the dentition in partially dentate subjects. Clin Oral Implants Res. 2017 May;28(5):626–630. doi: 10.1111/clr.12847. Epub 2016 Mar 27
Coli P, Christiaens V, Sennerby L, Bruyn H. Reliability of periodontal diagnostic tools for monitoring peri-implant health and disease. Periodontol 2000. 2017 Feb;73(1):203–217. doi: 10.1111/prd.12162.
De Bruyn H, Christiaens V, Doornewaard R, Jacobsson M, Cosyn J, Jacquet W, Vervaeke S. Implant surface roughness and patient factors on long‐term peri‐implant bone loss. Periodontol 2000. 2017 Feb;73(1):218–227. doi: 10.1111/prd.12177.
Fransson C, Wennström J, Berglundh T. Clinical characteristics at implants with a history of progressive bone loss. Clin Oral Implants Res. 2008 Feb;19(2):142–7. doi: 10.1111/j.1600-0501.2007.01448.x.
Jemt T, Gyzander V, Britse AÖ. Incidence of surgery related to problems with peri-implantitis: a retrospective study on patients followed up between 2003 and 2010 at one specialist clinic. Clin Implant Dent Relat Res. 2015 Apr;17(2):209–20. doi: 10.1111/cid.12097. Epub 2013 Jun 10.
Takanayagi H. Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems. Nat Rev Immunol. 2007 Apr;7(4):292–304.
Takanayagi H. New developments in osteoimmunology. Nat Rev Rheumatol. 2012 Nov;8(11):684–9. doi: 10.1038/nrrheum.2012.167. Epub 2012 Oct 16.
Trindade R, Albrektsson T, Tengvall P, Wennerberg A. Foreign Body Reaction to Biomaterials: On Mechanisms for Buildup and Breakdown of Osseointegration. Clin Implant Dent Relat Res. 2016 Feb;18(1):192–203. doi: 10.1111/cid.12274. Epub 2014 Sep 25.
This summary was prepared by the EAO Congress Scientific Report rapporteurs and approved by the speaker.
View the full publication at: www.eao.org
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