Implications of considering peri-implant bone loss a disease, a narrative review

Abstract

Background: Peri-implantitis has been suggested to cause significant increasing proportions of implant failure with increasing time.

Purpose: To assess whether implant failure rates in long term studies are matching the supposed high prevalence of peri-implantitis.

Material and methods: This paper is written as a narrative review of the long-term clinical investigations available in the literature.

Results: Some implant systems have seen unacceptable marginal bone loss figures with time coupled to increased implant failure rates, resulting in the withdrawal of these systems. The reasons for such mishap are generally unknown, with the exception of one system failure that was found to be due to improper clinical handling. Modern, moderately rough implant systems have functioned excellently over 10-15 years of follow up with minor problems with marginal bone loss and implant failure rates within a few per cent. Machined implants have functioned adequately over 20-30 years of follow up. Implant failures occur predominantly during the first few years after implant placement. No significant increase of implant failures has been observed thereafter over 20-30 years of follow up. Over the years of our new millennium, scientific and technical advances have allowed the discovery of numerous molecular pathways and cellular interactions between the skeletal and immune system promoting the development of the interdisciplinary field called osteoimmunology. Nowadays, this knowledge has not only allowed the emergence of new etiologic paradigms for bone disease but also a new dynamic approach on the concept of osseointegration and MBL around oral implants, re-evaluating our older disease oriented outlook. This facilitates at the same time the emergence of translational applications with immunological perspectives, scientific approaches based on omics sciences, and the beginning of an era of personalized dental implant therapy to improve the prognosis of oral implant treatment.

Conclusions: Oral implant systems have been found to function with very good clinical outcome over follow-up times of 20-30 years. Registered implant failures have occurred predominantly during the first few years after implantation, and there has been no significant increase in late failures due to peri-implantitis.

Keywords: bone resorption; dental implants; immuno-modulation; peri-implantitis.

FIGURE 1

Abutment screw fracture with some marginal bone loss. Fracture of implants or implant components is one reason for loss of marginal bone. Courtesy of Dr Jacob Zellner, Texas, USA.

FIGURE 2

A clinical case 2 years after implant placement with MBL that was found dependent on the accidental presence of a ligature, of iatrogenic nature or patient caused(dental floss), around the implant. The ligature was removed and further MBL ceased immediately. Ligatures are known to cause significantly disturbed immune reactions that precede possible bacterial attacks. Had the ligature remained in situ in this case, it is likely that it would, with time, have caused a shift in the immune reaction from shield off to implant rejection in the same manner known for accidental cement remnants in the implant interface. Courtesy of Dr Örnhall Britse, Gothenburg, Sweden.

FIGURE 3

Marginal bone loss of a magnitude that may threaten the survival of the implant. Such cases occur, but have not been demonstrated to cause any significant increase of implant failure rates over long time. The great majority of implant failures occur during the first 1–2 years after implant placement. Courtesy of Dr. Kaleb Esplin. Texas, USA.

FIGURE 4

A clinical case with marginal bone loss. The implant was placed in an angle giving the restoration a mesial cantilever, but it is unknown whether this was the reason for the loss of bone. Courtesy of Dr Antonella Botto DDS, Texas, USA

FIGURE 5

Initially progressive Marginal bone loss which ended in a foreign body equilibrium. (a) Perfectly stable bone level after 4 years of function. (b). Three years later, bone loss was observed and considered dependent on a loose distal prosthetic screw and fractured mesial prosthetic screw. Patient chews only on the contralateral side of the jaw. (c) 10 years of function. Further bone loss assumed to be dependent on renewed loosening of distal prosthetic screw and fracture of mesial prosthetic screw 35. (patient is still only chewing on the left side). (d) 13 years of follow up. Bone level is now stable. Chewing ability in the right side has been re‐established. Note the thickening of the marginal bone around the re‐established “foreign body equilibrium.”

FIGURE 6

(A) In the complex peri‐implant osteoimmunology lies the biological mechanism behind osseointegration. (B) In turn, osseointegration is achieved after the generation of the FBE as a result of the immunomodulation capacity of the implant on the host. (C) Bone level can be maintained unchanged for years. (D) However, dental implants can display cumulative levels of ions, nano and microparticles at the implant–tissue interface activating an immune‐inflammatory response capable of triggering a FBR. (E) FBE susceptibility to implant close conditions could be represented by a transient imbalance in the local immune/inflammatory state, where MBL represents a clinical condition due to the special transmucosal arrangement. In some cases, if the inflammation is not resolved or reactive due to the stress signals and the immunogenicity of the elements present, persisting inflammation could impede tissue repair and favor bacterial overgrowth. Bac = bacteria; Cp = cement particle; i‐TiPs = Implant‐derived Titanium particles; DC = dendritic cell; F = fibroblast; HBMMSC = human mesenchymal stem cells derived from bone marrow; L = lymphocyte; M1 = macrophage; M2 = Macrophage; MNGCs = multinucleated giant cells; Ob = osteoblast; Oc = osteoclast; Ost = osteocyte.