The Pathology of Bone Tissue during Peri-Implantitis

Abstract

Dental implants are one of the most frequently used treatment options for tooth replacement. Approximately 30% of patients with dental implants develop peri-implantitis, which is an oral inflammatory disease that leads to loss of the supporting tissues, predominately the bone. For the development of future therapeutic strategies, it is essential to understand the molecular pathophysiology of human dental peri-implant infections. Here, we describe the gene and protein expression patterns of peri-implantitis bone tissue compared with healthy peri-implant bone tissue. Furthermore, cells from the osteoblastic lineage derived from peri-implantitis samples were immortalized and characterized. We applied microarray, quantitative reverse transcription polymerase chain reaction, fluorescence-activated cell sorting, and Western blot analyses. The levels of typical bone matrix molecules, including SPP1, BGLAP, and COL9A1, in patients with periimplantitis were reduced, while the inflammation marker interleukin 8 (IL8) was highly expressed. RUNX2, one of the transcription factors of mature osteoblasts, was also decreased in peri-implantitis. Finally, the human telomerase reverse transcriptase immortalized cell line from peri-implantitis exhibited a more fibro-osteoblastic character than did the healthy control.

Bone Cells Dynamics during Peri-Implantitis: a Theoretical Analysis

“…Additionally, osteocytes are key players in maintaining implant stability, due to their role in assuring the proper physiological turnover of the osseointegrated implant by modulating the bone cells activity in response to mechanical stress, i.e. by occlusal load of the implant, and in response to systemic and local factors interacting in the local microenvironment [7,43]. …”

“…Analysis of the peri-implant crevicular fluid (PICF) composition from diseased and healthy implants concerning pro- and anti-inflammatory cytokines, matrix metalloproteinases, matrix proteins and bone turnover markers have been providing relevant information on the activity of local bone cells in an attempt to understand the mechanisms leading to the induced alveolar bone loss in peri-implantitis [43,51]. Although a number of methodological limitations arises, a variety of studies shows increased levels of the pro-inflammatory cytokines IL-1β, IL-6, IL-17, TNF-α, IL-12, but especially IL-1β, in the PICF of implants with peri-implantitis, when compared with healthy implants [52-62].…”

“…It has been reported [43] that expression gene and protein levels of typical bone matrix molecules, namely osteopontin, osteocalcin, COL9A1 were downregulated in peri-implantitis bone tissue, as compared to healthy samples. Also, expression of the osteogenic transcription factor Runx-2 and BMP-7 were decreased in peri-implantitis samples.…”

“…In addition, reduced FGF-18 was also noted; this factor is known to play a role in bone development and disease [69]. Meanwhile, expression of matrix metalloproteinases, such as MMP-7 and MMP-8 were upregulated [43], in line with previous results [70]. It was also shown that the osteoblastic lineage cells derived from peri-implantitis bone samples exhibited a fibro-osteoblastic phenotype, with enhanced expression of fibrocytic markers and lower expression of Runx-2 [43].…”

Fatigue induced changes in conical implant–abutment connections

“…Besides technical complications a variety of biological complications occur among which are periimplant mucositis and periimplantitis with a prevalence of 43% and 22% respectively [18,19]. The etiopathogenesis of periimplantitis is not yet fully understood [20]. Besides bacterial contamination wear at the implant-abutment interface with discharge of wear debris is currently discussed [21][22][23].…”