Periodontal Pocket Formation Research Articles

Tobacco Use as a Risk Factor.

Tobacco, particularly tobacco smoking, has a substantial influence on periodontal health and disease. It is associated with an increased disease rate in terms of periodontal bone loss, periodontal attachment loss, as well as periodontal pocket formation. In addition, it exerts a masking effect on gingival symptoms of inflammation. Risk assessment based on an increasing body of investigations over the past few years suggests that the tobacco attributable risk is considerable, estimated odds ratios being of the order 2.5 to 6.0 or even greater. Although the mechanisms by which tobacco exerts its influence are obscure, information available to date does not support the view that its action simply relates to other environmental factors such as the dental plaque or some specific microflora. It seems more likely that it primarily has a systemic influence affecting host response or susceptibility. The chief novelty of the present report is that current data suggest that, although the overall disease prevalence is decreasing, the proportion of periodontal disease attributed to tobacco is stable or even increasing. This seems to be analogous to what has been observed for other smoking-associated chronic diseases. This, in turn, indicates that periodontal disease behaves like several other chronic diseases and, further, that tobacco should be considered a major risk factor for chronic periodontal disease. J Petiodontol 1994;65:545-550.

Tobacco use as a risk factor.

Tobacco, particularly tobacco smoking, has a substantial influence on periodontal health and disease. It is associated with an increased disease rate in terms of periodontal bone loss, periodontal attachment loss, as well as periodontal pocket formation. In addition, it exerts a masking effect on gingival symptoms of inflammation. Risk assessment based on an increasing body of investigations over the past few years suggests that the tobacco attributable risk is considerable, estimated odds ratios being of the order 2.5 to 6.0 or even greater. Although the mechanisms by which tobacco exerts its influence are obscure, information available to date does not support the view that its action simply relates to other environmental factors such as the dental plaque or some specific microflora. It seems more likely that it primarily has a systemic influence affecting host response or susceptibility. The chief novelty of the present report is that current data suggest that, although the overall disease prevalence is decreasing, the proportion of periodontal disease attributed to tobacco is stable or even increasing. This seems to be analogous to what has been observed for other smoking-associated chronic diseases. This, in turn, indicates that periodontal disease behaves like several other chronic diseases and, further, that tobacco should be considered a major risk factor for chronic periodontal disease.

Oral conditions in individuals with selective immunoglobulin A deficiency and common variable immunodeficiency.

Saliva and serum samples were collected from 36 individuals with selective immunoglobulin A deficiency (IgAd) and 23 patients with common variable immunodeficiency (CVI). The oral examination included registration of the teeth, Russell's periodontal index (PI), pocket formation, and salivary flow rate in both unstimulated and stimulated saliva. No differences were found in salivary flow rate, number of teeth, or pocket depth when donors with IgAd or CVI were compared to age and sex matched controls. However, mucosal manifestations of lichenoid type were more frequent in both types of immunoglobulin deficient individuals. An increased PI was also seen in CVI patients. Increased serum IgG and salivary IgM levels were found in the IgAd population.

Chronic adult periodontitis and burst progression may reflect local neutrophil defects due to perivascular hyaline deposits

Chronic adult periodontitis (CAP) is a common disease of the supporting tissues of teeth, and is a major cause of tooth loss. This disease is distinguished from more rare rapidly progressing forms of periodontitis, in which a variety of neutrophilic polymorphonuclear leukocyte (PMN) defects have been identified. PMN dysfunctions have, however, not been observed in CAP. In CAP, destructive episodes of the disease occur sporadically and independently in different parts of the mouth. In this paper, it is proposed that CAP is due to highly localized defects in PMN function. Impaired PMN function is suggested as resulting in the formation of a virulent bacterial plaque, which is capable of initiating periodontal pocket formation. A previously reported perivascular hyaline material may account for localized PMN defects, by reducing the number of PMNs entering affected sites. The proposed model may explain both the presence of CAP in otherwise normal patients, and the sporadic pattern of tissue destruction seen in this disease.

The potential of periodontal pocket formation associated with untreated accessory root canals

Teeth that were to be extracted because of periodontic-endodontic involvement in six patients, were treated by hemisection or root amputation. The roots were processed histologically. All cases showed the presence of accessory root canals with remnants of pulpal tissue, bacteria, and necrotic debris. It was demonstrated in the cases studied that residual necrotic tissue in untreated root canals can result in periradicular pathosis. We may speculate that if the inflammatory process persists and drainage results via the sulcus, in time, plaque and then concentrations may develop.

Periodontal status of secondary crowded mandibular incisors. Long-term results after orthodontic treatment.

The present study was undertaken to examine whether secondary crowded mandibular incisors experience more periodontal breakdown than aligned lower incisors long-term after orthodontic treatment. Patients from 19 to 35 years after active treatment were selected. 2 groups were established: 1 with crowded mandibular incisors and 1 with aligned incisors. The groups were matched according to age, time after treatment, gender and periodontal disease classification. A separate group with crowded and aligned incisors within the same individual was established. Accumulation of plaque, gingival inflammation, probing pocket depth and probing attachment level were registered at 6 locations around each incisor. Among the patients studied, the oral hygiene level was high. In both groups, the loss of connective tissue attachment was largely due to periodontal pocket formation in interproximal areas and gingival retraction in buccal and lingual areas. A small but statistically significant difference in probing attachment level was found between crowded and aligned interproximal areas within the same individual (P less than 0.05). No differences in accumulation of plaque or in gingival inflammation were found. No differences were found for any of the dependent variables between the groups with crowded and aligned incisors.

Endodontic treatment of experimental root perforations in dog teeth.

Abstract Experimental root perforations were made in 131 teeth of 5 mongrel dogs. The perforations were treated according lo five different endodontic techniques and the results were observed after 3 weeks, 3 months and 1 year. The histologic reaction was dominated by inflammation and downgrowth of gingival epithelial tissue, regardless of observation time, technique or material Used. The epithelial downgrowth resulted in the formation of periodontal pockets with the epithelial attachment apical to the perforation. The frequency of the periodontal pockets increased with increasing observation time and after 1 year 75% of the perforations were lined with epithelium. The inflammation at the perforation site apparently was maintained by irritants from the periodontal pockets.

Long‐term calcium hydroxide treatment of a tooth with iatrogenic root perforation and lateral periodontitis

Abstract This case report describes the treatment of a lower right canine with a periapical radiolucency and a radiolucency associated with a lateral perforation that was made 10 years previously, during an apicoectomy procedure on the adjacent lateral incisor. Long‐term calcium hydroxide treatment was carried out. After 3 months the apical radiolucency was greatly reduced and after 1 year was completely resolved. After 3 years a hard tissue barrier had formed across the lateral perforation defect, but at no time during the treatment period did the inflammatory lesion adjacent to the perforation improve. It is suggested that epithelial downgrowth and possibly periodontal pocket formation had occurred, allowing irritants from the gingival sulcus to sustain the inflammatory reaction in the perforation area.

歯周ポケット滲出液中の燐脂質量の変動に関する研究

The formation of periodontal pockets is generally accepted as one of the three symptoms of a chronic marginal periodontitis. The exudation which flows itself into these periodontal pockets increases proportionately to the aggravation of a disease.There have been published many research reports on the composition of this periodontal pocket exudate to date, including those by Brill. As for lipid substance in the exudate, however, the published literature is scanty except for that of Watanabe among the domestic investigators. Further, concerning the phospholipids there seems to be a qualitative report by the present author and his collaborators alone.For this reason, the present study was concerned with the classification of the degrees of oral hygiene, gingival inflammation and depth of periodontal pockets on the part of patients suffering from chronic marginal periodontitis, efforts being made to measure quantitatively the values of phosphatidylcholin, phosphatidylethanolamine and sphingomyelin for the purpose of comparative analysis with the clinical findings.By way of study material, a total of 54 patients (26 males and 28 females) who visited the Department of Periodontology, Nihon University Dental Hospital, were selectively used. The subjects, who ranged from 18 to 74 years in age, were free from any systemic disease except for some kind of periodontal complaint. Of the female subjects, collection of their exudate was avoided for one week both before and after the menstruation in consideration of possible changes in the gingival state, its tone and systemic conditions.The areas of exudate collection, 3+3 and 3+3, were labially studied relative to the oral hygiene index (OHI), propounded by Greene and Vermillion, gingival index (GI) by Loe and Sillness and depths of the periodontal pockets.Upon examination, the means per tooth were classified into 3 groups. That is to say, in OHI the values below 1.5, those between 1.6 to 3.0 and those above 3.1 were designated as OHI group 1, OHI group 2 and OHI group 3 respectively.As for GI, on the other hand, the values below 1.10, those from 1.11 to 1.50 and those above 1.51 were similarly established as GI group 1, GI gronp 2 and GI group 3.Finally, concerning the mean values of pocket depth (PD), a threefold system was also adopted: those below 2.50mm was PD group 1, those between 2.51mm and 3.50mm was PD group 2 and those above 3.51mm constituted PD group 3.In collecting the exudate from the periodontal pockets, use was made of filter paper method (Whatman Co., No. 2, 1×10mm).An extraction of the phospholipids from the filter paper was carried out in accordance with the method by Folch et al.The extracted matter was evaporated to dryness under nitrogen at 45°C and was dissolved in a 0.05ml solution of chloroform/methanol (2:1v/v) to render it available for the purpose of Thinchrography. For the quantitative measurement of phospholipids, the Iatroscan TH-10 (Iatron Inc., TLC-FID) was employed, in which phosphatidyl-N, N-dimethylethanolamine was housed to serve the function of a internal standard.The three phospholipids to be examined were mixed with this internal standard, so that it was possible to establish the proportional relationship within a range of 1μg to 15μg for a given substance in terms of its area as compared to the internal standard matter.Subsequently, the calibration curves were prepared for the quantitative measurement and correction between each phospholipid and clinical findings were analyzed.As a result of the study, the author arrived at the following conclusions:1. The phospholipids existing inside periodontal pockets were identified as phosphatidylcholin, phosphatidylethanolamine and sphingomyelin by use of the Thinchrography.2. The values of phosphatidylcholin, phosphatidylethanolamine and sphingomyelin were reduced in proportion to the aggravation of the condition of oral hygiene and

Experimental marginal periodontitis in rats produced by coprophagy (author's transl)

The purpose of the present study was investigated to the effects of the high carbohydrate diet (Keyes No. 2000) and coprophagy on the periodontal tissues of the normal and alloxan diabetic rats. The experimental animals were divided into four groups of normal rats (A, B, C, D) and four groups of alloxan diabetic rats (a, b, c, d). A and a groups received a powder diet (a normal laboratory diet), B and b groups a high carbohydrate diet, C and c groups a powder diet+feces, and D and d groups a high carbohydrate diet+feces. The experimental animals were killed at intervals of 1, 3, 5, 7 and 9 weeks, and the periodontal tissues between mandibular first and second molars of these animals were examined macroscopically and histpathologically. The results were as follows;1. Normal rats (A, B, C and D groups).During the entire experimental period, there were no apparent changes in the periodontal tissues of animals receiving a powder diet (A) or a high carbohydrate diet (B). At 3, 5 and 7 weeks, proliferation of the gingival epithelium and deposition of foreign materials in the gingival epithelium and connective tissue were observed in the periodontal tissues of animals receiving a powder diet+feces (C) or a high carbohydrate diet+feces (D). At 9 weeks, loss of the gingival epithelium and proliferation of the functional epithelium were observed in the periodontal tissues of animals receiving a powder diet+feces (C). In addition, at 7 and 9 weeks, a periodontal pocket formation was also observed in the animals receiving a high carbohydrate diet+feces (D). During the entire experimental period, however, the changes were not found in the periodontal ligament and alveolar bone of these grups (C and D).2. Alloxan diabetic rats (a, b, c and d groups).During the entire experimental period, there were no apparent changes in the periodontal tissues of animals receiving a powder diet (a) or a high carbohydrate diet (b). At 3 and 5 weeks, proliferation of the gingival epithelium and deposition of foreign materials in the gingival epithelium and connective tissue were observed in the periodontal tissues of animals receiving a powder diet+feces (c) or a high carbohydrate diet+feces (d). At 7 and 9 weeks, the destructive changes, such as a loss of gingival epithelium, ulceration, inflammatory cell infiltration in the connective tissue and alveolar bone resorption, were observed in the periodontal tissues of animals receiving a powder diet+feces (c). At 5, 7 and 9 weeks, the similar periodontal changes were also found in the animals receiving a high carbohydrate diet+feces (d). Moreover, at 9 weeks, severe hyaline degeneration of the gingival connective tissue and disorganization of the periodontal fibers were observed in this group (d).

Alveolar bone loss in a strain of mice.

Alveolar bone loss with increasing age was compared in strain STR/N and random‐bred Swiss‐Webster mice. All animals were fed pelleted laboratory chow and tap water and killed at 3 month intervals from 3–18 months of age. Alveolar bone loss was quantitated by measuring loss of alveolar crest height on the lingual aspect of the defleshed right hemimandible, and by planimetric measurement of the quantity of trabecular bone in a single undecalcified mesiodistal section of the same hemimandible. The left hemimandible was fixed in formalin and examined histologically. There was a progressive severe loss of alveolar bone with increasing age in strain STR/N mice, which was not observed in random‐bred Swiss‐Webster mice. Histologically, the bone loss was associated with progressive gingivitis and periodontal pocket formation. The bone loss was not related to hair or bedding impaction or to obvious dental morphological differences between the two strains. Systemic disturbances such as generalized osteoporosis or diabetes mellitus were not present. The occurrence of bone loss in STR/N mice in the absence of any applied stimulus suggests that this strain is suitable for studying mechanisms of alveolar bone loss and factors capable of modifying bone loss.

Conversion of stable established gingivitis in the dog into destructive periodontitis

A quantitative clinical and histopathological study of the conversion of chronic gingivitis into a destructive periodontitis was made in 3 Beagle-dogs 4-years of age. This conversion was induced by the placement of a cotton-floss ligature supragingivally around the crown of a tooth. This resulted in enhanced plaque accumulation, a pronounced increase in gingival exudation and rapid formation of periodontal pockets. There was also an overt loss of alveolar bone, attachment and tooth substance (resorption) and an apical displacement of the gingival tissue. The composition of the chronic inflammatory infiltrate was different around ligated and non-ligated teeth, in that the tissues around the former contained a plasma cell-dominated advanced lesion, and around the latter a lymphocyte and plasma cell-rich lesion intermediate between the early and established type.

The effect of toothbrushing and scaling in periodontal therapy (author's transl)

The efficacy and limitation of toothbrushing (rolling method) and scaling in the treatment of periodontal disease were examined in 14 patients, who were suffering from gingivitis and mild periodontitis not due to poor restoration and malocclusions. The periodontal status was measured with Gingival Index system (GI), periodontal pocket depth, purulent exudation and bone score. The oral hygiene was expressed as debris index (DI) and calculus index (CI).The results were summarized as follows:1. Brushing and scaling was effective in removing a dental plaque.2. Gingival inflammatory intensity was reduced by removing a dental plaque (DI=0), but gingival inflammation was not improved in about 15% of that group.3. Scaling was effective in the reduction of gingival inflammation. The deposition of a dental plaque was found in 49% of the group in which gingival inflammatory status was not improved by scaling.4. The effect of brushing and scaling on a periodontal pocket:1) The deeper the periodontal pocket, the lower the rate of healing of a periodontal pocket.2) Correlation between a periodontl pocket depth and a degree of a dental plaque deposit was not found.3) It was shown that the improvement of gingival inflammation followed by removing a dentalplaque deposit was necessary in the healing of a periodontal pocket.4) The improvement of gingival inflammation with removing a dental deposit was observed in about 25% of the group in which a periodontal pocket was not still diminished by brushing and scaling. It was assumed that many other factors except a dental deposit played an important role in the pathosis of a periodontal pocket formation.5) The percentage of purulent exudation was higher in the group in which a periodontal pocket was not diminished than in the group in which a pocket was healed. The periodontal pocket with purulent exudation was one of the criteria of the limitation of brushing and scaling.

Effects of soft dietary consistency and protein deprivation on the periodontium of the dog: A preliminary report

Manifestations of periodontal disease produced in dogs by a combined regimen of protein deprivation (with alternate repletion) and soft dietary consistency have been described. Clinical, roentgenographic, and histologic aspects of the observed lesions were presented. The noteworthy features of the oral tissue response were extensive calculus deposition, associated gingival inflammation and hyperplasia, periodontal pocket formation, and severe resorption of alveolar and supporting bone. The significance of the foregoing observations was discussed in relation to the ecology of human periodontal disease.

Role of Trauma from Occlusion in Initiation of Periodontal Pocket Formation in Experimental Animals

The Journal of PeriodontologyVolume 26, Issue 1 p. 14-20 Role of Trauma from Occlusion in Initiation of Periodontal Pocket Formation in Experimental Animals Irving Glickman, Irving Glickman Professor of Oral Pathology and Periodontology, Boston, Massachusetts.Search for more papers by this authorLeon A. Weiss, Leon A. Weiss Instructor in Oral Pathology and Periodontology, Boston, Massachusetts.Search for more papers by this author Irving Glickman, Irving Glickman Professor of Oral Pathology and Periodontology, Boston, Massachusetts.Search for more papers by this authorLeon A. Weiss, Leon A. Weiss Instructor in Oral Pathology and Periodontology, Boston, Massachusetts.Search for more papers by this author First published: 01 January 1955 https://doi.org/10.1902/jop.1955.26.1.14Citations: 42AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume26, Issue1January 1955Pages 14-20 RelatedInformation