In the present animal experiment, analyses and comparisons were made between the structure and composition of clinically healthy supraalveolar soft tissues adjacent to implants and teeth. 5 beagle dogs were used. The right mandibular premolar region was selected in each dog for placement of titanium implants, while the left mandibular premolar region served as control. Extractions of the mandibular premolars were preformed, healing allowed, following which titanium fixtures were installed in the edentolous premolar region. Abutment connection was carried out 3 months later. After another 2 months of healing, plaque control was initiated and maintained for 8 weeks. At the end of the plaque control period, clinical examinations were performed and biopsies harvested from the implant site and the contralateral premolar tooth region. Following fixation and decalcification, all tissue samples were embedded in EPON and examined by histometric and morphometric means. The result from the analyses demonstrated that the periimplant mucosa which formed at titanium implants following abutment connection had many features in common with gingival tissue at teeth. Thus, like the gingiva, the peri-implant mucosa established a cuff-like barrier which adhered to the surface of the titanium abutment. Further, both the gingiva and the peri-implant mucosa had a well-keratinized oral epithelium which was continuous with a junctional epithelium that faced the enamel or the titanium surface. In the periimplant mucosa, the collagen fibers appeared to commence at the marginal bone and were parallel with the abutment surface. All gingival and periimplant units examined were free from infiltrates of inflammatory cells. It was suggested that under the conditions of study, both types of soft tissues, gingiva and periimplant mucosa, have a proper potential to prevent subgingival plaque formation.

The objective of the present experiment was to study lesions in the peri-implant and periodontal tissues resulting from ligature placement and subgingival plaque formation. The experiment was performed in 5 beagle dogs which at the start of the study were about 15 months old. They were given a diet which allowed gross plaque formation. The mandibular right premolars were extracted, 3 fixtures (a.m. Brånemark) installed and abutment connection performed. Towards the end of a 6-month plaque control period, a clinical and radiographic examination was performed. Ligatures were placed in a subgingival position at 2 of the implants and the contralateral premolars. Plaque was allowed to accumulate. After 6 weeks, the ligatures were removed. 1 month later, the clinical and radiographical examination was repeated and samples from the subgingival microbiota obtained. Biopsies from the teeth and implant sites were harvested and processed for histometric and morphometric analyses. The results from the clinical and histological examinations revealed that: (i) clinical and radiographic signs of tissue destruction were more pronounced at implants than at teeth; (ii) the size of the soft tissue lesion was larger at implants than at teeth; (iii) the lesion at implants but not at teeth extended into the bone marrow.

The present findings demonstrated that great variability exists in man with respect to hard tissue formation within extraction sockets. Thus, whereas a provisional connective tissue consistently forms within the first weeks of healing, the interval during which mineralized bone is laid down is much less predictable.

The aim of the present investigation was to assess the effect of de novo plaque formation on the gingiva and masticatory mucosa around teeth and implants. The study was performed in 5 beagle dogs which at the initiation of the experiment were 15 months old. During a preparatory period, the mandibular right premolars were extracted, 3 fixtures installed, abutment connection performed and a 4-month period of plaque control completed. A clinical examination was performed and biopsies of the second mandibular premolar (P2) and the contralateral implant site (2P) were sampled. The dogs were allowed to form plaque during a period of 3 weeks. The clinical examination was repeated and biopsies harvested from the 2 remaining implants and the contralateral tooth sites. The tissue samples were prepared for histometric and morphometric analysis. Both the masticatory mucosa at implants and the gingiva responded to de novo plaque formation with the development of an inflammatory lesion. The size as well as the composition of the lesions in the 2 tissues had many features in common. It was concluded that the mucosa around implants and the gingiva around teeth had a similar potential to respond to early plaque formation.

The present investigation was carried out to study some aspects of the recolonization of a subgingival microbiota following subgingival instrumentation in sites with deep pockets. 16 patients were recruited for the study. From each patient 4 inflamed gingival sites with deep pockets were selected. These sites were examined for plaque, overt gingivitis, bleeding on probing and probing depth. Samples of the subgingival microbiota were obtained and examined in the darkfield microscope and in a Neubauer chamber. Following the Baseline examination the teeth of all 4 jaw quadrants were carefully scaled and planed. Subgingival instrumentation was carried out under local anesthesia and required between 2-4 appointments. The patients were subsequently divided into 2 groups (Groups A and B) consisting of 9 and 7 subjects, respectively. During the first 16 weeks of maintenance the patients of Group A were not supervised regarding their self-performed plaque control measures and they accumulated supragingival plaque. The patients of Group B, however, were during these 16 weeks recalled once every 2 weeks for professional tooth cleaning. In addition they rinsed twice daily with a 0.2% solution of chlorhexidine digluconate. Reexaminations including assessments of the same parameters as those studied at Baseline were performed after 2, 4, 8, 12 and 16 weeks. After the 16-week examination the patients of Group A received a new sequence of subgingival scaling and root planing. During the subsequent 16 weeks the patients of Group A were also recalled for professional tooth cleaning. They were reexamined 18, 20, 24, 28 and 32 weeks after the Baseline examination. Subgingival scaling followed by carefully supervised oral hygiene measures resulted in a marked improvement of periodontal conditions. This improvement was accompanied by a pronounced and sustained reduction in the motile segments of the subgingival microbiota. In the presence of supragingival plaque (Group A), however, a subgingival microbiota containing large numbers of spirochetes and motile rods was soon (4-8 weeks) reestablished. A small number of sites with deep pockets (greater than or equal to 8 mm) was not substantially reduced in depth following subgingival instrumentation. In these sites which were kept free from supragingival deposits a subgingival microbiota with a large proportion of motile bacteria soon recurred.