The success of a dental implant treatment requires hard and soft tissue integration and osseointegration, mechanisms that entail a direct anchorage of the implant in the bone without interposition of soft tissue. Peri-implantitis is defined as an inflammatory reaction of the tissues surrounding a functioning dental implant. During inflammation, a high incidence of autoantibodies has been reported. The hypothesis of the present study is that the occurrence of autoantibodies to self-antigens including extracellular matrix (ECM) molecules and heat shock proteins (HSPs) might affect the dental implant outcome. Therefore, we evaluated the occurrence of antibodies to ECM molecules (Collagen (C) I, III, IV, V, fibronectin, laminin) and HSPs (HSP 27, HSP 65, HSP 90) in subjects with a healthy peri-implant microenvironment (n=29) as compared to patients with peri-implantitis (n=13). We also evaluated the HSP 27 expression in gingival fibroblasts grown in an inflammatory microenvironment. Antibodies to conformational ECM epitopes of CI, CIII and laminin were observed both in subjects with healthy peri-implant conditions and peri-implantitis. Antibodies to more than one HSP linear epitope were found in patients with peri-implantitis but not with healthy peri-implant conditions (p=0.024). Gingival fibroblasts grown in an inflammatory microenvironment showed increased HSP 27 cytoplasmic and plasma membrane expression as compared to fibroblasts grown in normal conditions. Immunity to multiple linear HSPs epitopes in patients with peri-implantitis and not in patients with a healthy peri-implant microenvironment might be relevant for monitoring the implant outcome and help to understand the role of subsets of autoantibodies in implant osseointegration.

The possibility to insert immediately-loaded implants in post-extraction sites where previously inserted implants had failed and had never received a prosthesis has not been sufficiently studied to the present day. Only few articles in the literature address this problem. The aim of the present study was to evaluate crestal bone remodeling around implants with a platform-switched design inserted and loaded immediately after the failure ofthe previous implants. This study has a follow-up of 36 months. Failed implants that had never received a prosthesis have been removed in 68 patients. In the present study 10 patients, whose bone crest measured at least 8 mm in width, were selected and 16 immediately loaded implants with a platform-switched design and a sandblasted and acid etched SLA surface, (Winsix®, Biosaf sri, Italy) were placed. Statistically significant differences were observed in crestal bone remodeling between 12 and 36 months (p<0.05) and between 24 and 36 months (p<0.001), although no statistically significant differences were found between 12 and 24 months (p>0.05). The values of periodontal indices have sometimes been borderline, although they returned normal later on. The cumulative success-rate of all the 16 implants inserted was of 93.75%, while the survival rate was 100%. Results show that immediately loaded platform-switched implants are a practicable solution for the rehabilitation of sites of early failed implants.Many studies describe the success of implants in time (1-4), but only a small number investigate the causes of implant failure, while studies describing the possibility to insert new implants used for a fixed prosthetic rehabilitation in the site of implants previously failed, (for various reasons) are even fewer (5-6). Very often in the past, patients who had suffered implant failure were treated with an overdenture to avoid additional implant surgery which was not predictable at that time. Only one article treated the insertion of implants in sites where previously inserted implants had failed, but the surgery was performed after 9 to 12 months after the removal of the failed implants (7). Today clinicians may choose between various implant designs, such as macro-implants, short implants, which allow implant insertion where bone volume is insufficient. It has been proven that in conventional dental implants, consisting in a fixture and an abutment, the peri-implant bone resorbs between 1 to 2 mm after -prosthetic loading, when the implant platform is positioned at a crestal level(8). Some investigators have demonstrated that when the implant platform is positioned at a sub-crestallevel, bone resorption increases (9). According to certain authors, crestal bone remodeling is caused by masticatory stress (10). Another hypothesis suggests that soft tissue inflammation may cause the crestal bone to resorb (11). Some researchers have demonstrated that in all two-piece implant systems there is a gap between the implant and the abutment. The gap measures approximately 10 urn and is respo...

The aim of the present study is to evaluate the peri-implant soft tissues and the amount of inflammatory cells around two different implant-abutment connections (self-locking conical connection with platform switching and screwed connection with standard abutment and internal anti-rotational system). Histological analysis was made of 14 implants, 7 with self-locking Morse tapered connection (experimental group A) and 7 with screw-retained anti-rotational connection (control group B). Sixty days after non-functional immediate loading, peri-implant tissue biopsies were performed. In the samples taken from the experimental group the peri-implant connective tissue consisted of a greater density of collagen and fibroblasts compared to the connective tissue of the control group. The experimental group specimens showed less inflammatory infiltrate close to the self-locking tapered connection compared to the tissues around the screw-retained connection. The SEM observations showed less microgap in the self-locking conical connection than in the screw connections with standard abutment and internal anti-rotational system. The presence of connective tissue with few inflammatory cells and the absence of inflammatory infiltrate, in self-locking conical connection implants is due to the minimal size of the implant-abutment microgap that does not allow the passage of fluids and bacteria from the oral cavity to the implant thus preventing tissue inflammation.

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