Morphological and Molecular-Biological Features of Inflammatory and Regeneratory Processes in Peridont Tissues with Periimplantitis and Periodontitis.

A morphological and immunohistochemical study of periodontal tissues was performed in patients with chronic generalized periodontitis who underwent dental implantation. We studied 44 biopsy specimens from 21 patients (13 women and 8 men) aged 35-60 years with a diagnosis of periimplantation mucositis (7 patients), periimplantitis (8 patients), and severe chronic generalized periodontitis (6 patients). It was established that periimplantitis differs from periimplantation mucositis by a more pronounced inflammatory reaction with a clear predominance of plasma cells in the infiltrate, which captures the fibrous capsule around the implant, destroys it and further spreads to the bone tissue. Based on the immunohistochemical differences in SMA, VEGF, and Ki-67, it is concluded that periimplantation mucositis and periimplantitis are successive stages of progression of the same process. When comparing chronic generalized periodontitis and periimplantitis, the latter shows much more pronounced inflammatory and destructive processes in the area of the implant, due to the addition of immune inflammation, impaired regeneration processes, and destruction of bone tissue.

Biology of teeth and implants: Host factors - pathology, regeneration, and the role of stem cells.

In chronic periodontitis and peri-implantitis, cells of the innate and adaptive immune systems are involved directly in the lesions within the tissues of the patient. Absence of a periodontal ligament around implants does not prevent a biologic process similar to that of periodontitis from affecting osseointegration. Our first focus is on factors in the biology of individuals that are responsible for the susceptibility of such individuals to chronic periodontitis and to peri-implantitis. Genetic factors are of significant importance in susceptibility to these diseases. Genetic factors of the host affect the composition of the oral microbiome in the same manner that they influence other microbiomes, such as those of the intestines and of the lungs. Our second focus is on the central role of stem cells in tissue regeneration, in the functioning of innate and adaptive immune systems, and in metabolism of bone. Epithelial cell rests of Malassez (ERM) are stem cells of epithelial origin that maintain the periodontal ligament as well as the cementum and alveolar bone associated with the ligament. The tissue niche within which ERM are found extends into the supracrestal areas of collagen fiber-containing tissues of the gingivae above the bony alveolar crest. Maintenance and regeneration of all periodontal tissues involves the activity of a variety of stem cells. The success of dental implants indicates that important groups of stem cells in the periodontium are active to enable that biologic success. Successful replantation of avulsed teeth and auto-transplantation of teeth is comparable to placing dental implants, and so must also involve periodontal stem cells. Biology of teeth and biology of implants represents the biology of the various stem cells that inhabit specialized niches within the periodontal tissues. Diverse biologic processes must function together successfully to maintain periodontal health. Osseointegration of dental implants does not involve formation of cementum or collagen fibers inserted into cementum - indicating that some stem cells are not active around dental implants or their niches are not available. Investigation of these similarities and differences between teeth and implants will help to develop a better understanding of the biology and physiologic functioning of the periodontium.

Onset, progression and resolution of experimental peri-implant mucositis at different abutment surfaces: A randomized controlled two-centre study.

OBJECTIVES: To assess the onset, progression and resolution of experimentally induced peri-implant mucositis lesions at abutments with different microstructures in humans. MATERIAL & METHODS: In a randomized, controlled, interventional two-centre study, a total of 28 patients had received 28 target implants and were randomly allocated to either partially microgrooved (test) or machined (control) healing abutments. The study was accomplished in three phases, including a wound healing period (WH) following implant placement (12 weeks), a plaque exposure phase (EP-21 days) and a resolution phase (RP-16 weeks). Clinical (e.g. bleeding on probing-BOP), immunological (MMP-8) and microbiological (DNA counts for 11 species) parameters were evaluated. RESULTS: The incidence of peri-implant mucositis at EPd21 was comparable in both test and control groups (60.0% versus 61.5%), but markedly lower at control abutments after a nonsurgical treatment and reconstitution of oral hygiene measures at RPw16 (46.7% versus 15.4%). At any follow-up visit (i.e. EP and RP), clinical parameters, MMP-8 levels and DNA counts of major bacterial species were not significantly different between both groups. CONCLUSION: The onset, progression and resolution of experimental peri-implant mucositis lesions were comparable in both groups.

Prevalence and Mechanisms of Peri-implant Diseases.

The aim of the present critical review is to summarize recent evidence on the prevalence of peri-implant diseases and their similarities and differences with periodontal diseases with a focus on their pathogenetic mechanisms. Reports on the extent and severity of peri-implant diseases are influenced by different case definitions. The prevalence of peri-implant diseases is reported at the subject or implant level and affected by the type of population samples analyzed (e.g., randomly selected population samples or convenience samples). The outcomes of studies on animals and humans indicate that experimental biofilm accumulation leads to a higher frequency of bleeding sites around implants as compared with teeth. Despite the proof of principle that experimentally induced mucositis may be reversible, early diagnosis and management of naturally occurring peri-implant mucositis are clinically relevant. Tissue destruction at experimental peri-implantitis sites is faster and more extensive when compared with that at experimental periodontitis sites. Although human periodontitis and peri-implantitis lesions share similarities with respect to etiology and clinical features, they represent distinct entities from a histopathologic point of view. To avoid implant loss, patients diagnosed with peri-implantitis should be treated without delay.

Nerve Growth Factor Expression and Its Receptors TrkA and p75NTR in Peri-Implantitis Lesions.

BACKGROUND: Nerve growth factor (NGF) can, through its receptors TrkA and p75NTR, convey signals for cell survival or cell differentiation. These proteins are also involved in inflammation and in bone resorption. The aim of this study is to evaluate, for the first time, the expression of NGF and its receptors TrkA and p75NTR in peri-implantitis lesions. MATERIALS AND METHODS: Fifteen biopsy specimens from patients with chronic peri-implantitis and 4 of healthy oral mucosa were immunostained with antibodies against NGF, TrkA, and p75NTR. The staining intensity and percentage of stained cells were semi-quantitatively evaluated and results were compared between the 2 groups. RESULTS: In the peri-implant pocket epithelium and gingival epithelium, NGF and TrkA expressions were similar to the healthy oral mucosa, however, a decreased expression of p75NTR was observed. In all cases, more than 75% of the inflammatory cells stained positively for NGF and TrkA, and p75NTR was negatively expressed. CONCLUSION: The intense expression of NGF and TrkA in the inflammatory cell infiltrate associated with decreased expression of p75NTR in both gingival and pocket epithelium suggests that these proteins may have a role in peri-implantitis lesions.

Can Periimplantitis Be Treated?

Over the past few decades, dental implants have been found to have high predictability and survival rates because of improvements in knowledge, clinical expertise, and implant designs. As such, dental implants are frequently integrated in the clinical management of fully or partially edentulous patients. It is prudent to realize that despite the high early survival rates, dental implants do have their fair share of long-term esthetic, biological, and mechanical complications. Therefore, this paper aims to review the current evidence on the management of peri-implant diseases in an attempt to answer the following question: Can periimplantitis be treated?

Group D. Initiator paper. Implants--peri-implant (hard and soft tissue) interactions in health and disease: the impact of explosion of implant manufacturers.

1. The best-documented implants have a threaded solid screw-type design and are manufactured from commercially pure (grade IV) titanium. There is good evidence to support implants ≥ 6 mm in length, and ≥ 3 mm in diameter. 2. Integrity of the seal between the abutment and the implant is important for several reasons, including minimization of mechanical and biological complications and maintaining marginal bone levels. Although the ideal design features of the implant-abutment connection have not been determined, an internal connection, micro-grooves at the implant collar, and horizontal offset of the implant-abutment junction (platform switch) appear to impart favorable properties. 3. Implants with moderately rough implant surfaces provide advantages over machined surfaces in terms of the speed and extent of osseointegration. While the favorable performances of both minimally and moderately rough surfaces are supported by long-term data, moderately rough surfaces provide superior outcomes in compromised sites, such as the posterior maxilla. 4. Although plaque is critical in the progression of peri-implantitis, the disease has a multi-factorial aetiology, and may be influenced by poor integrity of the abutment/implant connection. Iatrogenic factors, such as the introduction of a foreign body. (e.g., cement) below the mucosal margin, can be important contributors. 5. Clinicians should exercise caution when using a particular implant system, ensuring that the implant design is appropriate and supported by scientific evidence. Central to this is access to and participation in quality education on the impact that implant characteristics can have on clinical outcomes. Caution should be exercised in utilizing non-genuine restorative componentry that may lead to a poor implant-abutment fit and subsequent technical and biological complications.

Peri-implantitis. Part 2: Prevention and maintenance of peri-implant health.

The prevention of any disease process should be the cornerstone of any healthcare provision. This ethos is well established in dentistry with plaque associated disease such as periodontitis and caries but is at the current time less developed for peri-implantitis. The current review identities potential modifiable and non-modifiable risk factors for per-implantitis development and details strategies for the prevention of the disease. These include poor oral hygiene, previous history of periodontitis, smoking, genetic factors, occlusal overload and foreign body reactions. Local factors include soft tissue and bone quality, implant positioning, restoration design and the implant-abutment interface. An implant maintenance protocol is proposed and a schematic for maintenance visits is also detailed.

Comparison of the levels of tumor necrosis factor-α and interleukin-17 in gingival crevicular fluid of patients with peri-implantitis and a control group with healthy implants.

Peri-implantitis is a multi-factorial disease involving peri-implant tissues and resulting in therapeutic failure. Inflammatory mediators and cytokines in the Gingival Crevicular Fluid (GCF) have pivotal roles in the disease pathogenesis and could be used for disease monitoring. Therefore, the present study was conducted to compare the GCF levels of TNF-α and IL-17 between patients with peri-implantitis and healthy implants.In this case-control study, 24 patients with peri-implantitis and 18 individuals with healthy implants referring to faculty of dentistry in Tehran University of Medical Sciences were selected. GCF was collected by paper cons number 30. Samples were preserved in PBS -70ºC. TNF-α and IL-17 levels in GCF were determined by ELISA method. Data were analyzed by SPSS software version 13, using descriptive indices and independent t tests.Mean probing depth in peri-implantitis and control groups were 6.2 ± 1.1 and 3.7 ± 1.6 mm respectively. Mean level of IL-17 in patients with peri-implantitis was significantly more than the control group (19.8 ± 16.0 versus 9.3 ± 8.4 pg per site in 40 seconds, p=0.016). Also, mean level of TNF-α in patients with peri-implantitis was more than control group (39.0 ± 3.9 versus 14.5 ± 9.0 pg per site in 40 seconds, p =0.000).The significant higher levels of TNF-α and IL-17 in patients with peri-implantitis compared to control group indicated the pivotal role of these cytokines in peri-implantitis and could be suggested as diagnostic markers and in future possibly for immunomodulatory treatments.

Extent and location of bone loss at dental implants in patients with peri-implantitis.

Peri-implantitis is an infectious disease, which leads to loss of supporting bone around dental implants. To evaluate the extent and location of bone loss, 43 patients with peri-implantitis were examined. The bone loss was clinically measured at the time of dental surgery. Data revealed that 25% of subjects had bone loss associated with all their implants although the majority of the subjects had fewer than 50% of their implants affected by bone loss. A total number of 264 implants were examined and 131 of those had peri-implantitis associated bone loss. The pattern of bone loss at implants varied between and within subjects and location in the jaws. The highest proportion of implants with peri-implantitis was found in the upper jaw and within this group, at implants located in the incisor area of the upper jaw; the lowest was the canine area of the lower jaw. The highest proportion of implants that lost ≥ 2/3 of their bone support was found in the incisor area of the maxilla. We concluded that in the presence of peri-implant inflammation, bone quantity and characteristics may influence the progression of peri-implantitis bone loss at dental implants. We hypothesize that the ability of the bone to withstand occlusal forces will be altered as consequence of the loss of bone at the neck of the implants. To achieve an understanding of the local degradation of bone due to peri-implantitis, we need to analyze the microstructure of the bone as well the cellular biology of the peri-implant inflammation.

Receptor activator of nuclear factor kappa B ligand (RANKL) levels in peri-implant crevicular fluid.

BACKGROUND: Receptor activator of nuclear factor kappa B ligand (RANKL) is one of the key cytokines in the induction of osteoclastogenesis both in vitro and in vivo. Several reports indicated the presence of sRANKL in gingival crevicular fluid of patients with periodontal diseases. OBJECTIVE: To determine the presence of RANKL in peri-implant crevicular fluid samples of implants with peri-implantitis, peri-implant mucositis and healthy controls. METHODS: In this study, 40 implants were categorized as clinically healthy, peri-implant mucositis and peri-implantitis according to the clinical and radiographic findings. Filter paper strips were used to collect peri-implant crevicular fluid for 30 seconds in the base of the crevice/pocket. Peri-implant crevicular fluid (PICF) samples were obtained from buccal and lingual aspects of implants. Plaque index, probing depth, gingival index and bleeding on probing were recorded at six sites per implant. Enzyme-linked immunosorbent assay (ELISA) was performed to determine the PICF levels of sRANKL. RESULTS: There were no statistically significant differences in sRANKL concentration between healthy group, peri-implant mucositis and periimplantitis (p=0.12). There were also no statistical correlation between the concentration of sRANKL and probing pocket depth (R=0.051, p=0.65), or any of the other clinical regarding (p>0.05). No differences between the mean sRANKL concentration in the buccal and lingual sites were found (p=0.693). CONCLUSION: Our results may suggest that peri-implant crevicular fluid analysis of sRANKL in conjunction with some other osteoclastogenic mediators could be further investigated in further well-designed prospective longitudinal studies on a larger-scale sample size in the evaluation of dental implants.