Variables that influence the relationship between osseointegration and bone adjacent to an implant.

It is often assumed that there is a direct relationship between the bone density adjacent to an implant, as revealed by radiographs, and the percent histologic osseointegration. Moreover, the lack of standardized methods for evaluation of histologic preparations makes it difficult to compare published studies, especially as little is known about the variables that influence these measurements. In this animal study, computer-assisted lineal analysis was used to evaluate the effects of subject, tooth position, and implant surface site on measured bone density and osseointegration in a bone augmentation experiment. Three sites--coronal lingual, apical lingual, and apical facial--were analyzed around each of 6 (3.75 x 8 mm) threaded machined titanium implants, as well as the apical facial site of 21 other implants placed in the mandibular premolar area of 5 dogs. In all sites, a progressive decrease in bone density was observed from bone adjacent to the implant to that at the titanium implant surface. There was an animal effect on osseointegration, but there were no differences between the mandibular premolar locations (second, third, and fourth). Most importantly, there were significant measurable effects attributable to the surface site examined. The need for carefully standardized histologic evaluations is established.

Evaluation of bone-implant integration: efficiency and precision of 3 methods.

Computer-assisted planimetry, computer-assisted lineal analysis, and point-counting stereology have been compared with respect to their reproducibility and the time required to analyze bone-implant integration. Sections of 6 threaded dental implants selected from a bone augmentation experiment for their wide range of new bone formation were analyzed by each method 3 times. The bone density and percentage of osseous integration were evaluated at 4 sites around each implant section. It was found that computer-assisted planimetry demonstrated a modest but significantly greater variance (P < .05) in bone density estimates when compared to the computer-assisted lineal analysis and point-counting methods. Computer-assisted planimetry requires a different method of measuring each parameter and separate fields of view to evaluate fields distant from the implant. However, this can all be accomplished with line probes, as in computer-assisted lineal analysis, which extend from the implant surface into the surrounding alveolar bone. Whereas computer-assisted planimetry requires a separate identification of the perimeter of each field to be analyzed (next to and distant from the implant), computer-assisted lineal analysis allows expansion of the field to be evaluated without creating a new field of view. Also, following a limited learning curve, both point-counting and computer-assisted lineal analysis required less time to complete than did computer-assisted planimetry.

Repair following treatment of circumferential periodontal defects in dogs with collagen and expanded polytetrafluoroethylene barrier membranes.

This study was designed to evaluate healing following treatment of periodontal defects using 2 collagen barrier membranes with different degrees of cross-linking, and to compare the results to those following use of an expanded polytetrafluoroethylene (ePTFE) membrane. Horizontal, circumferential defects were created in mandibular premolar teeth of 6 beagle dogs, followed by placement of membranes and wound closure. Postoperative healing was monitored clinically for 6 months, at which time the animals were sacrificed and specimens were taken for histological examination. Clinical observations indicated that the highly cross-linked, slow-resorbing collagen membrane did not integrate with the tissues the way the less crosslinked, rapid-resorbing collagen did. Membrane exposure was typical for the slow-resorbing membrane in contrast to the rapid-resorbing membrane which remained covered. The inferiority of the slow-resorbing membrane was evident by the extensive clinical recession and the attachment level measurements taken at 6 months, and it was decided to omit this membrane from histometric analysis. Histological examination of root surfaces treated with rapid-resorbing collagen or ePTFE membranes revealed substantial reparative healing. The connective tissue repair amounted to 84% of the treated root surface height for the rapid-resorbing collagen and 53% for the ePTFE membrane (difference not statistically significant). However, the connective tissue repair to the rapid-resorbing collagen group root surfaces was often associated with a layer of ankylosis (44%, versus 8% of the ePTFE group). It appeared that much of the ankylotic response was initiated from the furcation area and extended around to the buccal and lingual surfaces. In addition, this study provided histological evidence that granulation tissue forming under clinically exposed and plaque contaminated ePTFE membranes can still result in connective tissue repair. It was concluded that the rapid-resorbing collagen membranes and the ePTFE membranes seem capable of stimulating periodontal connective tissue repair, whereas the slow-resorbing collagen membranes were unsuccessful in this effort, as seen in this dog model.

Early healing events at the dentin-connective tissue interface. Light and transmission electron microscopy observations.

The objective of these studies was to follow early healing at the dentin-connective tissue interface. Small dentin blocks were surgically implanted in bone cavities under mucoperiosteal flaps in the edentulous alveolar ridges of five beagle dogs at various times. In two separate experiments, wound maturation on native dentin surfaces and on citric acid or heparin conditioned dentin surfaces was observed. Block specimens including bone, dentin, and surrounding soft tissues were obtained at 10 minutes, 1 and 6 hours, and 1, 3, and 7 days after flap closure and prepared for light and transmission electron microscopic examination of the interface. The very initial attachment to native dentin was mediated by a granular precipitate. At 1 and 6 hours, the intercellular matrix was more organized with fibrin formation around red blood cell aggregates and at the dentin surface. Polymorphonuclear leukocytes were observed throughout the interface. Red blood cells were undergoing degradation at day 1 and polymorphonuclear cells were prevalent at the dentin surface. The 3-day observation interval was characterized by further maturation of the fibrin clot. Macrophages were observed near the dentin surface and fibroblasts could be identified. The 7-day specimens exhibited areas of cell rich connective tissue attachment without inflammatory cells as well as areas showing the fibrin clot in various stages of decomposition. These observations suggest that connective tissue attachment to dentin surfaces is mediated by adsorption of plasma proteins to the surface and subsequent development and maturation of a fibrin clot. The sequence of healing events at dentin surfaces conditioned with citric acid or heparin was largely similar to healing at native dentin surfaces. However, at day 1 and later time points, clot adhesion to heparin-conditioned dentin appeared compromised, whereas the fibrin clot seemed to adhere to citric acid-conditioned dentin at all observation periods. These observations indicate that in the absence of mechanical trauma, epithelial proliferation, and infection, wound maturation at the dentin-connective tissue interface may not necessarily be affected by treatments that either enhance or inhibit clot adhesion to the dentin surface.

Subjective criteria and probing attachment loss to evaluate the effects of plaque control and root debridement.

11 adult patients with moderate to advanced periodontitis were treated with oral hygiene instruction and an initial, single episode of root debridement. Before therapy, 3 independent clinicians examined all patients and identified sites that in their opinion probably would not respond to the therapy and would continue to lose attachment. On 2 occasions, 3 and 12 months later, the clinicians re-examined and re-evaluated all patients and all sites. The results of therapy were also monitored by probing attachment level measurements performed every 3rd month. All 11 patients completed 24 months of follow-up, and 6 subjects were available until 36 months. Sites with probing attachment loss after 12, 24 and 36 months were identified using linear regression analysis and compared to the clinicians' prediction of probing attachment loss. The results demonstrated a limited agreement between probing attachment loss determined by linear regression and the clinicians' predictions of probing attachment loss. It appears that the traditional clinical signs and factors used to forecast and identify periodontal disease activity are only moderately associated with probing attachment loss. This suggests that attachment loss may be caused by several factors, at least following initial therapy. The progression of an inflammatory disease of microbial etiology may be only 1 of such causes. Further studies are needed to clarify the nature and cause of probing attachment loss.

Effects of oral hygiene measures on clinical and microbiological parameters of periodontal disease.

The effects of a 12-week period of oral hygiene alone on gingival conditions and subgingival microflora in 15 patients with severe periodontitis were investigated. Clinical measurements and plaque samples from selected sites were taken at week 0 (baseline), week 6, and week 12. Plaque samples were also taken at week 13, that is, 1 week following debridement. At week 0, the patients were instructed in supragingival plaque control and at week 6, the hygiene regimen was supplemented with the subgingival use of a toothpick device. At week 12, the patients received a full mouth supra- and subgingival debridement under local anesthesia. In those patients who complied with oral hygiene instructions (subgroup A), the gingival condition improved moderately while no improvement was found in less compliant patients (subgroup B). No significant changes were noted in the subgingival microflora in either subgroups A or B throughout the 12-week period of oral hygiene alone. However, significant reductions for all microbial parameters were found 1 week after debridement. Therefore, while moderate clinical improvements followed oral hygiene alone, no measurable changes in the subgingival microflora were observed concomitantly.

Subgingival spirochete and leukocyte counts as indicators of response to therapy.

The aim of this study was to determine whether changes in probing attachment levels are related to subgingival spirochete or leukocyte counts in periodontal pockets. Following initial clinical recordings and therapy consisting of oral hygiene instruction and root debridement, the probing attachment levels of proximal sites of 120 single-rooted teeth in 7 patients were measured every 3 months for 12 months. The measurements of each site were subjected to regression analysis, which determined whether the site was deteriorating, improving, or non-changing. Subgingival washings were taken of 19 deteriorating, 22 improving, and 127 non-changing sites to determine the number and % of spirochetes and the number of leukocytes at each site. Improved probing attachment levels were associated with reduced numbers of spirochetes and leukocytes. However, the ranges of individual measurements of subgingival washing variables overlapped considerably between groups. Spirochete and leukocyte counts related better to the 12-month probing depths than to changes in probing attachment levels during the preceding 12 months. These findings suggest that none of the tested subgingival washing parameters are suitable indicators of changes in attachment levels on an individual site basis.

Antimicrobial irrigation of deep pockets to supplement oral hygiene instruction and root debridement. I. Bi-weekly irrigation.

64 sites with probing pocket depth greater than or equal to 6 mm from 11 patients were treated with plaque control instruction and one episode of root planning. Subsequently, selected sites in each patient were irrigated with either chlorhexidine, tetracycline, saline or served as non-irrigated control sites. Irrigation immediately followed instrumentation, and was repeated every 2 weeks for 24 weeks. Healing was monitored at 8, 16, and 24 weeks clinically and at 7, 15, and 23 weeks with subgingival washings for determination of % as well as total number of spirochetes. The following changes were apparent from comparing pooled site means at 24 weeks with pretreatment data: (1) bleeding sites decreased from 62 of 64 sites initially to 22 of 64 at 24 weeks; (2) spirochetes decreased from 34% to 2%; (3) probing pocket depths decreased from 7.6 to 4.7 mm; (4) probing attachment levels showed a gain of 1.2 mm. The improvement of the chlorhexidine and tetracycline irrigated sites was similar to that of the saline irrigated and non-irrigated control sites. Thus, biweekly chlorhexidine, tetracycline or saline irrigation of deep pockets did not appear to augment the effects of non-surgical periodontal therapy.

Histologic probe position in treated and untreated human periodontal tissues.

This study was designed to histologically determine the relationship of the periodontal probe tip to the periodontal tissues during probing of untreated periodontal pockets and periodontal pockets treated with oral hygiene and root planing. Human, condemned, single rooted teeth with buccal probing pocket depth at least 6 mm were used. Two groups of specimens were included: 12 untreated teeth from six patients and 15 treated teeth from 10 patients. In the treated group, the effects of therapy were monitored clinically every 2 weeks until maximum improvement had taken place. A periodontal probe tip was then inserted on the buccal aspect of the tooth using 0.50 N pressure, and block section biopsies were taken. The histologic examination of the untreated teeth showed that the probe tip penetrated beyond the apical termination of the junctional epithelium and into the subjacent connective tissue by a mean of 0.45 +/- 0.34 mm, whereas in the treated specimens the probe stopped coronally to this landmark by a mean of 0.73 +/- 0.80 mm. This study demonstrated that the probe tip most often does not reach the base of the junctional epithelium in pockets treated by plaque control and root planing, and that clinical measurements of attachment levels are not reliable in determining the true histologic level of connective tissue attachment.

Gingival condition in areas of minimal and appreciable width of keratinized gingiva.

Sixteen dental, dental hygiene, and dental assisting students and dental faculty members who had contralateral or unilateral areas of minimal (less than or equal to 1.0 mm) and appreciable (greater than or equal to 2.0 mm) widths of keratinized gingiva on mid-buccal plaque-free surfaces of mandibular bicuspids were examined. Gingival exudate amounts and clinical inflammation based on color change and/or swelling and bleeding on probing were evaluated. The results showed that gingiva with "appreciable" width as well as gingiva with "minimal" width of keratinized tissue exhibited only minute amounts of gingival exudate. Also, there were generally no clinical signs of inflammation for both types of tissue. From the groups of 16, six subjects were selected who had contralateral pairs of minimal and appreciable keratinized gingiva. They were instructed to cease oral hygiene in the lower bicuspid area for 25 days. At day 0, 4, 7, 11, 14, 18, 21, and 25, plaque, gingival exudate, and clinical gingival inflammation were evaluated. Results revealed increases in plaque, gingival exudate scores and clinical gingival inflammation over the 25-day period with no apparent difference between the areas with minimal and appreciable width of keratinized gingiva.