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Notes: Background, aims: Little clinical data exist on the incidence and severity by which root dentin sensitivity (RDS) results from periodontal therapy. The aim of the present clinical trial was to study the degree to which a sample of patients requiring non-surgical periodontal treatment develops RDS.〈section xml:id="abs1-2"〉〈title type="main"〉Material and methods:Alterations in RDS was followed in 35 patients (29–65 years of age) requiring non-surgical treatment for moderate to advanced periodontal disease. Inclusion criteria for participation were need for periodontal treatment in at least 2 quadrants comprising a minimum of 4 teeth with vital pulps, no open caries lesions, no dental treatment in the last 3 months and no ongoing treatment for RDS. Baseline and follow-up recordings included responses of teeth to pain stimuli (directed compressed air) at buccal surfaces as graded by the patient on a 10-cm visual analogue scale (VAS). Periodontal therapy consisted of oral hygiene instruction (OH) followed by supra- and subgingival scaling/root planing by hand and ultrasonic instrumentation of one quadrant per each of the subsequent weeks. Thus, follow-up data included pain assessment after 1–3 weeks of OH alone, and 1–4 weeks post-instrumentation.Results: There was a statistically significant reduction in mean VAS-scoring over time in quadrants where only meticulous plaque control had been maintained, while VAS mean values increased significantly after instrumentation (p〈0.001). Also the % of subjects reporting higher mean VAS values increased after instrumentation. Changes in mean VAS scores were generally moderate and only 9 patients gave an increase on VAS of 〉2 cm for 3 or more teeth. A statistically significantly higher increase of RDS was observed for initially sensitive teeth (VAS〉0) than for teeth not responding at baseline (p〈0.001). Although a reduction in the intensity of RDS could be noticed during the later phase of the 4-week follow-up period after scaling and root planing, the percentage of sensitive teeth remained unchanged.Conclusion: The data confirm that meticulous plaque control will diminish RDS problems and that scaling and root planing procedures in periodontal therapy result in an increase of teeth that respond to painful stimuli. However, pain experiences in general appeared minor and only a few teeth in a few patients developed highly sensitive root surfaces following instrumentation.

Notes: Abstract Intra- and extracellular products from oral bacteria were placed in Class V cavities prepared in dentin of human and monkey teeth to compare initial and late pulp tissue reactions. In one set of teeth, the bacterial material was left in the cavities for the entire experimental period (4, 10, 30 d in monkeys, 30 d in humans). In other teeth the challenge was stopped after 32 h and the bacterial material was removed and substituted with zinc-oxide eugenol cement. The subsequent pulp tissue responses were observed histologically after 4, 10 (monkeys) and 30 d (humans and monkeys). Thirty-two hours of bacterial challenge to human teeth induced intense acute inflammatory lesions. Four days of challenge in monkeys resulted in severe inflammatory cell involvement and pulpal necroses in a few teeth. At extended periods of observation severe inflammatory lesions were less frequent and the majority of the pulps showed tissue repair and healing at 30 d. This occurred irrespective of experimental protocol. Fourteen of 84 monkey teeth and none of 17 human teeth presented pulp tissue necrosis at follow-up. Data showed that the-dental pulp of both young human and monkey teeth can recuperate from a state of suppurative inflammatory involvement. Healing occurred irrespective of whether the bacterial challenge was removed or left in place. Findings also indicated that an acute inflammatory lesion rapidly could result in total pulp tissue necrosis.

Notes: The aim of this experiment was to achieve support for the hypothesis that bone resorption, induced by jiggling forces, leaves a component within the supracrestal soft tissue with a capacity of reforming bone. The maxillary lateral incisors and first premolars and the mandibular second premolars in two monkeys were used in the study. Using metal pins inserted into the neighboring teeth as retainers, orthodontic elastics were stretched and placed alternately around the buccal and lingual surfaces of each experimental tooth in order to produce jiggling forces. After 5 months of continuous jiggling, when bone dehiscences were produced on the buccal aspect of the teeth, the elastics were removed. After repositioning of the teeth a split thickness flap was raised. On one side of the jaw the soft tissue within the bone dehiscences was removed. At the contralateral teeth a sham operation was performed maintaining the soft tissue within the bone dehiscences. The monkeys were sacrificed 6 months after surgery. Tissue blocks containing test and control specimens were dissected free and prepared for microscopic analysis. The length of the supracrestal connective tissue attachment and the amount of coronal bone regeneration were assessed in the histological sections. It was found that buccal alveolar bone, reduced in height by jiggling forces, regenerated after discontinuation of the forces. When the soft tissue within the buccal bone dehiscences produced by the jiggling forces was surgically removed, the coronal regeneration of the alveolar bone was markedly reduced. These observations suggest that bone resorption, induced by jiggling forces, leaves a soft tissue component with a capacity of forming bone.

Notes: The healing capacity of mechanically exposed and bacterially contaminated dental pulps was assessed in monkeys after capping with 2 commercial Ca(OH)2 containing compounds. One hundred eighty teeth in 7 monkeys were employed, 45 as untreated controls and 135 as treated exposures. Class V buccal cavity preparations resulting in pulpal exposure were prepared, left open to the oral cavity for 0, 1, 24 h or 7 days and employed as controls, or debrided, capped, restored with amalgam and left undisturbed for 5 weeks as treated exposures. Zero and 1 h untreated exposures presented damage from the mechanical trauma only, whereas 24 h and 7 day pulp wounds exhibited pronounced infiltrations of polymorphonuclear and mononuclear leukocytes. In addition, the 7 day exposures demonstrated several teeth with partial and total necrosis. Treated 0, 1 and 24 h exposures demonstrated wound healing, minimal pulp tissue inflammation, reorganization of soft tissue and formation of new hard tissue at the exposure site in 86 of 99 teeth. Treated 7 day exposures healed less frequently, showing signs of dentin bridging in 15 of 27 teeth. This study indicated that mechanically exposed and orally contaminated dental pulps in monkeys have a high capacity to resolve inflammation and initiate healing with new dentin formation at the exposure site when treated as described.

Notes: Abstract Experimental breakdown of the periodontal attachment apparatus was produced in six young adult monkeys to study the effect on the tissue of the dental pulp by (1) periodontitis, (2) scaling and plaque accumulation on exposed root dentin. Periodontal tissue breakdown was induced by the placement of ligatures around the neck of 92 permanent teeth. Subsequent plaque formation caused marked loss of periodontal tissue support, which after a period of 5–7 months amounted to 30-40% of the roof length. One group of teeth received no further treatment. Other teeth were subjected to scaling and root planning. Following treatment, plaque was allowed to accumulate for 2, 10, and 30 days on the freshly planed root dentin surfaces. Histoiogic examination revealed that in comparison to teeth with normal periodontal conditions, 57% of the teeth exposed to periodontitis exhibited pathologic pulp tissue alterations. Secondary dentin formation and/or inflammatory cell infiltrates were observed within localized areas of the pulp subjacent to root surfaces exposed to periodontal tissue destruction. The changes within the pulp were of “mild” nature and only one tooth displayed signs of total pulp necrosis. Lateral canals communicating with both the pulp cavity and the exposed root surface were never detected. Teeth subjected to seating and subsequent plaque accumulation in comparison with teeth with periodontitis alone exhibited no obvious aggravation or increased incidence of pathologic pulp reactions. The findings show that in the monkey (1) periodontal destruction limited to the cervical half of the root and (2) plaque accumulation on exposed root dentin does not cause severe alteration in the pulp of the roots involved.