Comparison of Bone Immunological Biomarkers and Microbiological Parameters of Extra Short Dental Implants and Standard Dental Implants Loaded in the Posterior Mandible

INTRODUCTION

Dental implants are usually considered an alternative treatment option to replace lost teeth in edentulous patients. The rate of implant placement in regions more difficult to rehabilitate has increased with the increase in the success of osseointegration and survival. However, besides implant placement in sites with insufficient crest width and height, treatment times and costs have also increased with the use of grafting procedures.1 Various surgical techniques, such as vertical bone augmentation, sinus floor elevation, and nerve transposition, have been developed for the treatment of these bone volume insufficiencies. However, these methods are technically sensitive and can cause significant postoperative complications. Short dental implants have been suggested as a simpler, cheaper, and faster alternative to prevent the disadvantages of surgical techniques and for the rehabilitation of toothless areas.2,3 A large number of randomized controlled clinical trials demonstrated that the long-term success and survival rates of short implants were similar to those of standard long implants.4-6 Accumulation of microbial dental plaque around the implant is the most important cause of implant loss. If the microbial attachment is not removed, diseases such as peri-implant mucositis and peri-implantitis may occur and result in implant loss in the long term. Peri-implant mucositis is a reversible inflammatory reaction in the soft tissue surrounding the implant in function. Peri-implantitis is a microbial inflammatory disease characterized by the resorption of the supportive bone surrounding the implant in function.7 Gram-negative anaerobic bacteria predominate around the implant sites affected by the disease. While they resemble chronic periodontal infections, they have a more complex microbiological character.8 Predominant species around a peri-implantitis implant are red complex (P. gingivalis, T. denticola, and T. forsythia) and orange complex bacteria (F. nucleatum and P. intermedia) described by Socransky.9 In 1989, Apse et al. reported a fluid around the peri-implant sulcus with properties similar to those of the gingival crevicular fluid, and they called this fluid peri-implant crevicular fluid (PICF).10 The PICF is an inflammatory exudate formed by osmotic pressure. Biochemical mediators in the PICF are highly important to determine the health of tissues around the implant.11 Prostaglandins, especially prostaglandin E2 (PGE2), are considered as a potent mediator of alveolar bone destruction in periodontitis. A large number of studies reported an increase in PGE2 levels from healthy state to periodontitis.12 Tumor necrosis factor α (TNF-α) is a proinflammatory cytokine regulating the Gram-negative bacterial response. The TNF-α concentration is an indicator of bacterial load and degree of inflammation.13 In areas where peri-implantitis is active, the presence and activity of osteoclasts are necessary for bone destruction to occur. The formation and activation of osteoclasts are regulated through the activation of three members of the TNF family: receptor activator of nuclear factor kappa B ligand (RANKL), receptor activator of nuclear factor kappa B (RANK), and osteoprotegerin (OPG). Osteoclast differentiation and activation occur with the binding of RANKL to RANK over the surface of osteoclasts and precursors. OPG, which is a soluble protein of TNF receptors, antagonizes RANK-RANKL interaction and increases bone formation by inhibiting osteoclastogenesis. The levels of proinflammatory cytokines, such as IL-1, IL-6, TNF-α, and PGE2, and RANKL/OPG rates, which allow the determination of osteoclastic activity, change in the case of peri-implantitis.14 The aim of this study was to evaluate the levels of TNF-α, PGE2, RANKL, RANK, and OPG in extra short and standard dental implants functioning in the posterior mandible. An additional aim was to investigate the levels of putative oral pathogens F. nucleatum, P. gingivalis, T. denticola, T. forsythia, P. intermedia, and S. oralis in submucosal biofilm samples from the studied sites.

MATERIALS AND METHODS This study was carried out by recalling individuals whose bilateral partial tooth losses were treated with implant-supported fixed restorations and whose implants had been functioning for at least 3 years after prosthetic rehabilitation. The study was conducted in accordance with the ethical guidelines from the World Medical Association Declaration of Helsinki (version 2013) (Clinical Researches Ethical Board with the 28. 09. 2016 and 2016/009 decision numbered approval).

A total of 31 patients met the inclusion criteria. One patient did not continue the study. Further, 60 implants were researched in 30 patients (16 female and 14 male). The bilateral regions of patients with a standard implant and an extra short implant were grouped into two.16 Control group: Standard implant, intra-bone length ≥8 mm (30 implants) Test group: Extra Short implant, intra-bone length ≤6 mm (30 implants)

Collection of clinical data A single calibrated examiner performed all (full-mouth and site-specific) clinical measurements (B.K.), including probing depth (PD), clinical attachment level (CAL), presence of bleeding on probing (BOP), 3-year survival rate (CSR), and bone loss (BL).