**1.1 Implant-based and implant-related factors in peri-implantitis**

## *1.1.1 Implant macro-design associated with peri-implantitis*

Specific implant topography, i.e., its macro-design such as body shape, threads number, and collar design as well as micro-design aimed to speed the process of osseointegration enabling a rapid implant loading [19]. However, these dental implant components themselves could be addressed as one of the implant-based risk factors associated with peri-implantitis onset.

A variety of commercially available implants with cylindrical or conical body shape, one-, double- or triple-threads number and different thread shapes are constructed not only to accelerate the osseointegration process but also to minimize a hazard shear force acting instantaneously. Moreover, the implant macro-design aimed to prevent additional further marginal bone loss that could jeopardize implant long-term stability after prosthetic rehabilitation. In contrast, cylindric implants and implants with triple-threads demonstrated the production of greater detrimental shear forces [19] resulting in higher bone loss with implant failure, respectively.

To speed up and shorten implant placement by increasing the threads number on the implant body (double- and triple-thread) could, unfortunately, induce more pressure forces [2]. This resulted in increased bone loss, especially at triple-threads compared to single-thread [19]. In a laboratory model, using finite element analysis (FEA), threads shape was used to stimulate and estimate stress distribution between implants and cortical or cancellous bone [20] indicating that "V" shape and a broader-square shape generated less stress in cancellous bone than other examined threads. In contrast, implants with "V" and butter thread shapes generated higher

#### *The Effect of Implant Surface Design and Their Decontamination Methods in Peri-Implantitis… DOI: http://dx.doi.org/10.5772/intechopen.99753*

forces that induced bone defect formation [20, 21], and may consequently contribute to peri-implantits. Although these facts arising from *in vitro* and *in vivo* conditions, localisation and bone quality could affect the success of implant therapy associated with implant macro-design. However, a significant incidence of peri-implantitis has been reported in the posterior region of the mandible [22–25] suggesting that the location and region of implant placement might be associated with peri-implantitis development.

Implant macro-design could also cause excess cement retention that could act as rough surface facilitating an adherence of microorganism and inflammation around peri-implant mucosa with subsequent bone loss. Moreover, other implant-based factors such as implant-abutment connection type, prosthetic rehabilitation, and occlusal overload, could also be taken into consideration as risks for peri-implantitis onset [8, 18, 26–28].

Since the current literature are insufficient in providing evidence whether the implant macrodesign parameters such as implant body shape and dimension, and threads number could be the possible risk factors associated with the initiation and progression of peri-implantitis, further studies are required.

#### *1.1.2 Implant micro-design in correlation with peri-implantitis onset*

Over the last few decades, implant surfaces topography has been modified to enhance BIC rates, primary implant stability as well as positive host-to-implant response aiming to attain long-term implant treatment success rates. Bone response to implant topography modification has been specifically related to surface roughness, surface free energy and surface chemistry.

The implant's surface could be "smooth" (machined) or rough. Roughness Average (Ra) or Arithmetical Mean Height (Sa) parameters are used to describe the roughness of dental implant surfaces referring to the height of the surface structure in two or three dimensions. Mostly, implant surface roughness could be divided into four groups: smooth implant surface with Sa roughness value less than 0.5 μm, minimally rough surface (Sa value 0.5–1.0 μm), moderately rough surface (Sa value 1.0–2.0 μm), and rough surface (Sa value more than 2.0 μm). Several methods are reported in the literature to create implant roughness including acid etching, sandblasting, titanium plasma spraying, and hydroxyapatite (HA) coating, contributing to changes in implant physicochemical properties [5, 29, 30]. Currently available dental implant systems could have either moderately rough surfaces such as SLA, TiUnite, OsseoSpeed, and TiOblast implants or a rough surface such as Ankylos, IMZ or TPS implants [29]. Nevertheless, these implant topography features may play a role in peri-implantitis onset [5, 29, 31].

A study by Polizzi and al. demonstrated that peri-implantitis was more commonly detected at implants with a rough TiUnite surface compared with the minimally rough machined surface [32]. Furthermore, the spontaneous and greater bone loss occurred at the implants with a TiUnite surface compared to Turned, SLA or TiOblast surfaces [33–35]. The hazardous effect of TiUnite surface could be explained by its microdesign and the presence of grooves and pits that might encourage bacterial adhesion [35]. Although microbial plaque accumulation had been detected on novel modified anodized surfaces (TiUltra), this surface affected minimal bone loss and inflammation resulting in marginal bone stability [36]. Additionally, zirconium surface promoted plaque reduction *in vitro* conditions compared to Ti-machined, sandblasted and acid-etched surfaces.

Implant roughness and surface free energy influenced the dental plaque accumulation and biofilm formation inducing peri-implantitis [37, 38]. According to a literature review by Teughels et al. [37] increasing surface roughness above 0.2 μm resulted in biofilm formation and bacteria adhesion. Despite differences in surface roughness, another *in vivo* study recorded plaque accumulation on three different titanium disk surfaces (machined, RBM sandblasted and Xpeed) [39]. Additionally, some periodontal bacteria such as *P. gingivalis* could have the ability and greater bacterial viability on titanium compared with zirconium abutments [40]. *S. aureus*, which is introduced as one of the main harmful bacteria in peri-implantitis development, has an immense affinity to colonize on titanium implant surfaces [41, 42]. Even though the role of *C. albicans* in peri-implantitis disease is still being investigated, this species has also been isolated around implants with diagnosed peri-implantitis. In combination with *Streptococcus* species, *C. albicans* has the ability to grow on titanium surfaces forming a robust mixed biofilm that could cause inflammatory tissue reactions with potential tissue damage [43–45].

The development of bioactive titanium surface coatings with antibacterial properties has been considered as an additional strategy for controlling biofilm formation [46]. Different antimicrobials, active molecules, compounds, and ions were incorporated into implant surface to stimulate bactericidal or/and bacteriostatic effect on surrounding tissue decreasing in this way bacterial adhesion on implant surface. Unfortunately, this strategy has a short-term effect since the remains of dead cells on the uncleaned surfaces may act as bridges for bacteria coaggregation and colonization [47] leading to possible peri-implantitis onset.

#### **1.2 Other peri-implantitis risk factors**

Other risk factors such as smoking, diabetes, medications used in the treatment of chronic diseases may influence bone metabolism supporting plaque accumulation and adversely impacting the periimplant-tissue response. Despite limited evidence, survival of implants in patients with diabetes could be disturbed by high blood glucose level, that affects the immune system impairing tissue repair and host defenses against dental plaque [48], therefore accelerating peri-implantitis development or progression. Special caution in the peri-implantitis treatment should be advised in patients with chronic disorders/ diseases.
