The use of barrier membranes and enamel matrix proteins in the treatment of angular bone defects. A prospective controlled clinical study.

UNLABELLED: In the present prospective clinical trial, the effect of various regenerative procedures performed at sites with angular bone defects were evaluated. The main outcome variable was probing attachment alteration. MATERIAL AND METHODS: 40 subjects, aged 32-61 years participated. They met the following inclusion criteria: (i) presence of generalized, advanced periodontal tissue destruction; (ii) presence of 2 similar, contralateral, angular bone defects (experimental sites) located in either the maxilla or the mandible; (iii) the defect site must exhibit a probing pocket depth (PPD) of > or = 6 mm, a probing attachment level (PAL) of > or = 7 mm, and a depth of the intrabony component of > or = 3 mm. All subjects had a good oral hygiene standard, were in good general health and did not use any medication. Prior to the start of the study, all subjects received non-surgical treatment for periodontal disease. Baseline clinical measurements (plaque, gingivitis, PPD, PAL and soft tissue recession) of the selected experimental sites were obtained 6 months after the completion of basic therapy. The 40 subjects were randomly divided into 4 treatment groups including 10 subjects each: 3 membrane groups and one Emdogain group. 1 h before surgery, the patients were given 3 g of Amoxicillin. No other antibiotics were prescribed. The test and control sites were treated during the same surgical session. Full thickness flaps were elevated and the exposed root surfaces were planed. Membrane placement: The root surface was rinsed with saline. A barrier membrane (Guidor or Resolut or Periodontal (e-PTFE) material) was positioned to cover the defect and the adjacent 2-3 mm of bone tissue. The control treatment was identical to the test treatment with the exception of barrier placement. Emdogain placement: The exposed root surfaces at both the test and control sites were, during a 2-min period, conditioned with a 24% EDTA gel. Emdogain was applied to the exposed root surface of the test site. In the control site, the vehicle, the PGA gel, was used as placebo control. The flaps were closed and sutured to obtain a complete coverage of the intrabony defect. RESULTS: Re-examinations, which were performed 12 months after surgery, disclosed that regenerative therapy, including either the use of barrier membranes or application of enamel matrix proteins to an instrumented root surface in an angular, intrabony defect, enhanced outcome variables such as probing pocket depth and probing attachment gain. It was furthermore demonstrated that clinical improvements were better at sites with deep, than at sites with shallow, intrabony defects. CONCLUSION: The 4 regenerative modalities tested appeared to be equally effective in terms of PPD reduction and PAL gain, and superior to open flap curettage alone.

Periodontal tissue alterations following Emdogain treatment of periodontal sites with angular bone defects. A series of case reports.

UNLABELLED: The aim of the present study was to assess the predictability of probing attachment gain and probing pocket depth reduction following Emdogain treatment at sites with deep angular bone defects. MATERIAL AND METHODS: 108 consecutively-treated periodontal patients (mean age 55.8 years) were included. Each subject exhibited at least 1 deep interproximal intrabony defect that could be identified as an experimental site based on the inclusion criteria: (i) probing pocket depth > or = 5 mm, (ii) probing attachment loss > or = 6 mm, (iii) radiographic evidence of an interproximal bone defect with a > or = 3 mm intrabony component. A total of 145 defects met the criteria for inclusion. All subjects received non-surgical periodontal therapy. This included subgingival instrumentation in all parts of the dentition. At least 6 months after the completion of this treatment, a baseline examination was performed to characterise the experimental site. Reconstructive therapy was subsequently performed. Full-thickness periodontal flaps were elevated, and the root surface scaled and planed. No bone recontouring was performed. A gel containing 24% EDTA was applied on the exposed root and was kept in place for 2 min. A preparation of enamel matrix proteins was applied to the root surface and adjacent defect space. The flaps were replaced and closed with sutures. The experimental sites were re-examined 12 months after reconstructive surgery. RESULTS: The re-examination demonstrated that a treatment including the application of enamel matrix proteins at periodontal sites with angular defects resulted in a mean probing attachment level gain of 4.6 mm and a probing pocket depth reduction of 5.2 mm. 87% of all sites treated exhibited a probing attachment gain of > 2 mm. One site suffered probing attachment loss. The radiographic assessments revealed that the bone defect had been reduced in depth by 2.9 mm on average. The reduction in defect size corresponded to an average bone fill of 69% of the original defect. In 43% of the defects, the bone fill amounted to > or = 80%. CONCLUSION: The overall probing pocket depth reduction, probing attachment level gain, and soft tissue recession, that results following Emdogain therapy, is similar to the corresponding outcome variables following GTR.

The mucosal attachment at different abutments. An experimental study in dogs.

The present experiment was performed to examine if the material used in the abutment part of an implant system influenced the quality of the mucosal barrier that formed following implant installation. 5 beagle dogs were included in the study. The mandibular premolars and the 1st, 2nd and 3rd maxillary premolars were extracted. Three fixtures of the Brånemark System were installed in each mandibular quadrant (a total of 6 fixtures per animal). Abutment connection was performed after 3 months of healing. In each dog the following types of abutments were used: 2 "control abutments" (c.p. titanium), 2 "ceramic abutments" (highly sintered Al2O3), 1 "gold abutment", and 1 "short titanium abutment". This "short titanium abutment" was provided with an outer structure made of dental porcelain fused to gold. Following abutment connection a plaque control program was initiated and maintained for 6 months. The animals were sacrificed and perfused with a fixative. The mandibles were removed and each implant region was dissected, demineralized in EDTA and embedded in EPON. Semithin sections representing the mesial, distal, buccal and lingual aspects of the peri-implant tissues were produced and subjected to histological examination. The findings from the analysis demonstrated that the material used in the abutment portion of the implant influenced the location and the quality of the attachment that occurred between the periimplant mucosa and the implant. Abutments made of c.p. titanium or ceramic allowed the formation of a mucosal attachment which included one epithelial and one connective tissue portion that were about 2 mm and 1-1.5 mm high, respectively. At sites where abutments made of gold alloy or dental porcelain were used, no proper attachment formed at the abutment level, but the soft tissue margin receded and bone resorption occurred. The abutment fixture junction was hereby occasionally exposed and the mucosal barrier became established to the fixture portion of the implant. It was suggested that the observed differences were the result of varying adhesive properties of the materials studied or by variations in their resistance to corrosion.

GTR treatment of degree III furcation defects following application of enamel matrix proteins. An experimental study in dogs.

The aim of the present study was to evaluate the effect of enamel matrix proteins (EMD) on periodontal wound healing in degree III furcation defects in dogs. The experiment was performed in 5 foxhound dogs. 2 months prior to the start of the experiment, the 2nd and 4th lower premolars were extracted. Degree III furcation defects were created in the 3rd mandibular premolars (3P3). The furcation defects were subsequently exposed to reconstructive surgery. Buccal and lingual full thickness flaps were elevated in the lower premolar regions. The exposed root surfaces of the experimental teeth were planed. A notch was placed in the roots at the base of the defect. In one side of the mandible (Test group), phosphoric acid gel was applied over the root surfaces for 15 s. The acid was removed by flushing the root surfaces with sterile saline. Subsequently, a gel of EMD was applied to cover all instrumented root surfaces. Following gel application, a resorbable barrier membrane was adjusted to cover the buccal and lingual entrances of the furcation defect. The flaps were repositioned to cover the barrier and sutured. The contralateral premolar (Control group) received the same treatment, but acid etching was not performed and EMD was not applied prior to barrier installation. 4 months after reconstructive surgery, the animals were sacrificed and biopsies from the 3P3 regions harvested. The biopsies were placed in a fixative, demineralized in EDTA, dehydrated and embedded in paraffin. 3 mesiodistal sections, representing the central portion of the furcation site, were selected for histological analysis of the defect. The furcation defects of both the Test and Control groups were clinically closed and were found to harbor bone and periodontal ligament tissue which appeared to be in structural continuity with a newly formed root cementum. The relative amounts of mineralized bone, bone marrow and periodontal ligament tissue that had formed were similar in the Test and the Control group. In the Test group, however, the cementum that had formed in the apical portion of the furcation defect was different from the corresponding tissue in the coronal portion, and also different from the cementum observed in the Control group. In the apical portion of the test defect a thin (12 microm) acellular cementum had been laid down, while in the coronal portion a thick (32 microm) cellular cementum, similar to the cementum found in the Control group, could be observed. The current observation, hence, seems to confirm that EMD when applied onto an instrumented and acid etched dentine surface may create an environment conducive for the formation of acellular cementum.

GTR treatment of degree III furcation defects with 2 different resorbable barriers. An experimental study in dogs.

The aim of the present study was to describe the periodontal tissue that formed after GTR when different resorbable barriers were applied to degree III furcation defects. The study was performed in 5 foxhound dogs. The 2nd and 4th premolars in both sides of the mandible were extracted. Degree III furcation defects were produced in the 3rd mandibular premolars. 5 weeks later, GTR therapy using a barrier composed by a polylactide-glycolide copolymer was performed on one quadrant (group A). In the contralateral quadrant, a barrier made of polylactide and citric acid ester (group B) was used. The dogs were sacrificed 6 months after reconstructive therapy. Tissue blocks containing the experimental teeth were excised, demineralised in EDTA and embedded in paraffin. Serial sections were cut in the mesio-distal plane and parallel with the long axis of the roots. The microtome was set at 7 microm. The sections were stained in hematoxyline and eosin. From each biopsy, 3 sections representing the central part of the furcation were selected for light microscopic examination. In the healed furcation sites, descriptive histological analysis and histomorphometric measurements of the newly formed tissues were performed. In both groups the root surface of the healed furcation defects was covered by a cellular, extrinsic-intrinsic fibers type cementum. The composition of the newly formed periodontal ligament was similar in both groups. The proportions of bone, bone marrow and periodontal ligament, however, were substantially larger in group A than in group B. In Group B, an area in the previous furcation defect was consistently occupied by a granuloma. It is suggested that the presence of the granuloma in the healed furcation defect prevented bone regrowth.

A model for studying the effects of mouthrinses on de novo plaque formation.

The aim of the present study was to describe a 4-day no oral hygiene model to assess the pattern of de novo plaque formation and to use this model to appraise the potential of some mouthwash preparations to retard or inhibit plaque formation in the human dentition. 10 subjects were recruited for the trial. During a preparatory period, the participants were exposed to repeated professional plaque control and given oral hygiene instruction to eliminate signs of gingivitis. At the end of the preparatory period, each participant received a final professional tooth cleaning and was subsequently told to abstain from mechanical plaque control efforts for the next 4 days. They were asked to rinse twice daily for 60 s with 10 ml varying test solutions. On Day 4, the volunteers were exposed to a new clinical examination and the presence and amount of plaque were examined by the use of the plaque index system (P1I). The participants were subsequently given a professional tooth cleaning and asked to exercise proper self performed plaque control during the next 10 days. A new test period was then initiated. 6 different mouthwash preparations were tested in each subject namely, (1) placebo (a negative control rinse), (2) Veadent mouthrinse, (3) Listerine mouthrinse, (4) 0.06% triclosan + polyvinyl phosphonic acid (PVPA), (5) 0.06% triclosan + phenolic flavor and (6) 0.12% chlorhexidine digluconate (a positive control rinse). The results from the study revealed that the mean P1I values for individuals, groups of teeth and tooth surfaces provide an adequate but gross overall estimation of the potential of a given mouthrinse to retard/inhibit plaque build up. More detailed information on the effects of the test rinses could be obtained by data describing the % distribution of different P1I score categories; a high frequency of score 0 describes the potential of a mouthrinse to maintain tooth surfaces free from plaque while a low frequency of score 2/3 describes the ability of a treatment to retard/prevent gross plaque formation. The plaque pattern displays finally allowed assessment of the magnitude of plaque prevention, in comparison to the positive and negative controls, that could be achieved by a given compound in various parts and surfaces of the dentition. In this model, all test rinses (i) were significantly more effective than the placebo rinse in retarding de novo plaque build up and (ii) had a minor effects on plaque build up in the maxillary molars and at the approximal surfaces.(ABSTRACT TRUNCATED AT 400 WORDS)

Design of clinical trials of traditional therapies of periodontitis.

The present paper on the design of clinical trials of periodontal therapy first addresses the issue of the etiology of periodontal disease. It is suggested that most if not all forms of destructive periodontal disease are caused by microorganisms and that there are different forms of disease with different microbial etiologies. The progressive nature of destructive periodontal disease is subsequently discussed and it is emphasized that, in a given patient, periodontal sites which show signs of inflammation and attachment loss may not over a period of several months and years show further sign of attachment loss. The present methods of assessing periodontal disease do not allow us to discriminate between potentially active and inactive sites in untreated patients. The significance and variability of indicators of periodontal disease such as bleeding on probing, probing pocket depth and probing attachment level measurements are discussed. The errors inherent in the various measurements are analyzed and suggestions are presented describing how alterations in any of the above parameters could be identified and presented in a clinical trial. Of concern for the statistical analysis of clinical data of periodontal disease is the definition of the "experimental unit". For a number of years, the "experimental unit" in periodontal trials was the patient. It is clear, however, that different sites within the same individual show different patterns of disease progression and lesion morphology and often respond differently to periodontal therapy. Statistical analyses must consequently be designed which recognize differences in site-to-site infection and lesion morphology within a common host. Until such analyses are available, the investigator should be wary of pooling data within the same individual, since such pooling may obscure meaningful alternatives which may take place in individual periodontal sites. Some goals of periodontal therapy are subsequently identified. 4 goals are discussed more in detail, namely: to establish conditions which will allow the patient to maintain a dentition without further breakdown of the periodontium; to reduce pocket depth to establish an anatomy in the dentogingival region which with proper maintainance care will prevent the re-establishment of the subgingival infection; to gain attachment as a result of treatment; to assess the effect of a certain chemotherapeutic agent on periodontal disease.

Effect of selective antimicrobial therapy on plaque and gingivitis in the dog.

The present investigation was performed to assess the effect of selective antibiotic therapy on developing plaque and gingivitis in dogs, which at the start of the study had normal gingiva. Fifteen beagle dogs were used. Throughout the entire observation period the animals were fed a diet which favored plaque accumulation. A baseline examination involved assessments of plaque, gingivitis and gingival exudate. The subgingival bacterial flora was assessed by dark-field microscopy. Subsequently the teeth of the right jaws were allowed to accumulate plaque. A careful tooth-cleaning program was maintained in the left jaws. Plaque and gingivitis assessments were repeated and subgingival plaque sampled in the right jaws after 14 and 28 days. On experimental day 28 the second part of the study was initiated. The dogs were randomly distributed into three groups of five animals each. A new baseline examination was performed in the left jaws, after which all tooth cleanings were terminated. During the subsequent 28 days each group of dogs was treated with one of three antimicrobial compounds (vancomycin, metronidazole or clindamycin). Examinations were repeated after 14 and 28 days. The results demonstrated that systemic administration of antimicrobial substances can reduce the rate of plaque formation, change the composition of the developing subgingival microbiota and prevent (or retard) the onset of gingivitis. A comparison of the ability of the three compounds to prevent the formation of a "gingivitis-inducing" plaque revealed that metronidazole and clindamycin were markedly more effective than vancomycin. In fact, in dogs receiving metronidazole and clindamycin treatment, the initiation of gingivitis was almost entirely prevented during the 28 days of treatment.