A 15-year study of osseointegrated implants in the treatment of the edentulous jaw

Microbial etiological agents of destructive periodontal diseases

Recent evidence implicates Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis. This paper reviews the morphological, biochemical and serological charcteristics of A. actinomycetemcomitans, evidence incriminating it as a periodontopathogen, its importance in human nonoral infections, and virulence factors which may be involved in the pathogenesis of A. actinomycetemcomitans infections. A. actinomycetemcomitans is a non-motile, gram-negative, capnophilic, fermentative coccobacillus which closely resembles several Haemophilus species but which does not require X or V growth factors. The organism has been categorized into 10 biotypes based on the variable fermentation of dextrin, maltose, mannitol, and xylose and into 3 serotypes on the basis of heat stable, cell surface antigens. A. actinomycetemcomitans' primary human ecologic niche is the oral cavity. It is found in dental plaque, in periodontal pockets, and buccal mucosa in up to 36% of the normal population. The organism can apparently seed from these sites to cause severe infections throughout the human body such as brain abscesses and endocarditis. There is a large body of evidence which implicates A. actinomycetemcomitans as an important micro-organism in the etiology of localized juvenile periodontitis including: (1) an increased prevalence of the organism in almost all localized juvenile periodontitis patients and their families compared to other patient groups; (2) the observation that localized juvenile periodontitis patients exhibit elevated antibody levels to A. actinomycetemcomitans in serum, saliva and gingival crevicular fluid; (3) the finding that localized juvenile periodontitis can be successfully treated by eliminating A. actinomycetemcomitans from periodontal pockets; (4) histopathologic investigations showing that A. actinomycetemcomitans invades the gingival connective tissue in localized juvenile periodontitis lesions; (5) the demonstration of several pathogenic products from A. actinomycetemcomitans including factors which may: (a) facilitate its adherence to mucosal surfaces such as capsular polysaccharides; (b) inhibit host defense mechanisms including leukotoxin, a polymorphonuclear leukocyte chemotaxis inhibiting factor, and a lymphocyte suppressing factor (c) cause tissue destruction such as lipopolysaccharide endotoxin, a bone resorption-inducing toxin, acid and alkaline phosphatases, collagenase, a fibroblast inhibiting factor and an epitheliotoxin.(ABSTRACT TRUNCATED AT 400 WORDS)

Actinobacillus actinomycetemcomitans in human periodontal disease

There have been many advances in the past decade in our knowledge of the microflora associated with periodontal diseases, the potential of specific periodontal bacterial species to destroy periodontal tissues, and the host responses to bacterial infections of the periodontium. It is the purpose of this and an accompanying paper, to present important features of the host-parasite interaction in human periodontal disease. The present communication emphasizes characteristics of periodontopathic bacteria which may enable them initially to colonize the host, to survive in the periodontal pocket, and possibly to invade the gingival tissue despite potentially effective host defense systems, and to destroy the collagenous periodontal ligament, the alveolar bone, and other tissue components surrounding the tooth. It seems reasonable to assume that a bacterial species must possess factors applicable to most if not all of the above aspects of the infectious process of periodontal disease in order to produce periodontitis.

Black-pigmented Bacteroides species, Capnocytophaga species, and Actinobacillus actinomycetemcomitans in human periodontal disease: virulence factors in colonization, survival, and tissue destruction.

This article describes the subgingival microflora of the healthy periodontium, gingivitis, advanced adult periodontitis, and juvenile periodontitis. A total of seven to nine subjects were examined in each of the four periodontal clinical entities listed. The individual bacteriological samples included material from the base of a single periodontal pocket. The sampling, the treatment of the samples, and the bacteriological cultivations were carried out using continuous anaerobic techniques.

Briefly, the healthy gingival sulcus harbored a scant microflora dominated by Gram-positive organisms (85%), usually Streptococcus and facultative Actinomyces species. The development of gingivitis was accompanied by a marked increase in the total number of Gram-negative organisms. Fusobacterium nucleatum, Bacteroides melaninogenicus ss. intermedius, Haemophilus species, and other Gram-negative organisms comprised about 45% of the total gingivitis isolates. Streptococcus and facultative and anaerobic Actinomyces species constituted the majority of the Gram-positive gingivitis isolates. The micro-flora of advanced adult periodontitis was comprised mainly of Gram-negative anaerobic rods (about 75%), B. melaninogenicus ss. asaccharolyticus and F. nucleatum being the most predominant isolates. The deep pocket microflora in juvenile periodontitis was also made up mainly of Gram-negative organisms (about 65%), but was of a nature different from that of adult periodontitis, being predominated by isolates of Bacteroides species and other organisms of unknown species.

The present article also concerns factors of importance for the colonization of Gram-negative anaerobic rods in the oral cavity and periodontal pockets. In vitro experiments showed that cells of B. melaninogenicus ss. asaccharolyticus and other Gram-negative organisms attached in high numbers to epithelial cells, hydrosyapatite (HA) surface, and Gram-positive bacteria when suspended in phosphate-buffered saline; however, the bacterial attachment to epithelial cells and HA was strongly inhibited in the presence of human saliva and serum. In contrast, saliva and serum had little effect upon the attachment of Gram-negative bacteria to Gram-positive bacterial cells. These findings agreed well with data from an in vivo study, in which streptomycin-labeled cells of B. melaninogenicus ss. asaccharolyticus were introduced into the mouth of two volunteers. A significantly higher number of B. melaninogenicus cells was recovered from dental plaque than from the other oral surfaces studied.

The present series of studies has pointed to certain Gram-negative organisms as potential pathogens in rapidly progressing periodontal lesions. The available data on oral microbial ecology suggest that the presence of dental plaque containing Gram-positive organisms may be essential for the attachment and colonization of several Gram-negative species after their initial introduction into the mouth and the periodontal pocket area. The clinical relevance of these findings is discussed.

Subgingival microflora and periodontal disease

A clinical trial was undertaken to test the hypothesis that periodontitis can be cured and that bone regeneration occurs in infrabony pockets in patients maintained on an optimal standard of oral hygiene. The material comprised 24 patients with advanced periodontal disease. After an initial examination, the patients were randomly distributed into one test group and one control group. All the patients were given instruction and practice in a proper oral hygiene technique, and then subjected to periodontal surgery using the modified Widman flap procedure. Following treatment, during a 2-year period the patients of the test group were recalled once every second week for professional tooth cleaning. The control patients were recalled once every 12 months for prophylaxis. The results showed that all osseous defects of the patients of the test group were refilled with bone. The control patients, on the other hand, could not maintain a high standard of oral hygiene, and exhibited a progressive deterioration of the periodontal tissues during the postsurgical observation time.

The effect of systematic plaque control on bone regeneration in infrabony pockets.

Since recent studies have implicated Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis, this investigation determined the effectiveness of subgingival debridement, topical Betadine Solution, and systemic tetracycline in suppressing subgingival A. actinomycetemcomitans and other microorganisms. A total of 20 deep periodontal pockets and 10 normal periodontal sites of 6 localized juvenile periodontitis patients was included in the study. Each patient was treated in 3 stages over a period of 22 weeks, and the result of treatment was monitored for an additional 38 weeks. The first stage of treatment included plaque control, as well as thorough scaling and root planing, composed of at least 6 h of debridement. No concomitant periodontal surgery was performed. In the second stage, Betadine saturated cotton gauze was inserted into the periodontal pockets for 10 min. Stage 3 involved systemic tetracycline therapy (1 g/day) for 14 days. The subgingival microflora was determined at frequent intervals by selective culturing of A. actinomycetemcomitans and Capnocytophaga and by direct microscopic examination. The clinical effect was assessed by measuring changes in probing periodontal attachment level, probing periodontal pocket depth, radiographic alveolar bone mass, and other relevant clinical parameters. Scaling and root planing reduced the total subgingival bacterial counts and the proportions of certain Gram-negative bacteria, but no periodontal pocket became free of A. actinomycetemcomitans. Betadine application had little or no effect on the subgingival microflora. In contrast, tetracycline administered via the systemic route suppressed A. actinomycetemcomitans, Capnocytophaga, and spirochetes to low or undetectable levels in all test periodontal pockets. A. actinomycetemcomitans reappeared in 9 of the deep periodontal pockets after the administration of tetracycline. Most of these 9 pockets became free of detectable A. actinomycetemcomitans during the second week of tetracycline administration, whereas pockets which yielded no A. actinomycetemcomitans after tetracycline therapy became free of the organisms during the first week of tetracycline treatment. This data suggests that systemic tetracycline therapy of localized juvenile periodontitis should, as a practical rule, be continued for 3 weeks. Periodontal destruction continued in 4 deep pockets which all showed high posttetracycline A. actinomycetemcomitans counts. All 6 pockets which demonstrated a marked gain in periodontal attachment yielded no cultivable A. actinomycetemcomitans. No association was found between periodontal disease status and subgingival Capnocytophaga, spirochetes or motile rods. The present study indicates that A. actinomycetemcomitans is an important etiologic agent in localized juvenile periodontitis.(ABSTRACT TRUNCATED AT 400 WORDS)

Suppression of the periodontopathic microflora in localized juvenile periodontitis by systemic tetracycline

A clinical trial was undertaken to study the healing capacity of the periodontal tissues following different modes of periodontal surgery in patients whose oral hygiene was professionally maintained at an optimal level. Fifty patients, distributed into five groups, participated in the study. Following an initial examination and presurgical treatment, the various patient groups were subjected to one of the following surgical procedures: 1) the apically repositioned flap operation including elimination of bony defects, 2) the apically repositioned flap operation including curettage of the bony defects but without removal of bone, 3) the “Widman flap” technique including elimination of bony defects, 4) the “Widman flap” technique including curettage of the bony defects but without removal of bone, 5) gingivectomy including curettage of the bony defects but without removal of bone. After surgery, all patients received oral hygiene instruction and professional cleaning of the teeth once every 2 weeks during a 2-year period.

The results showed that periodontal disease can be cured and further destruction of the periodontal tissues avoided irrespective of the surgical technique utilized for pocket elimination. Different surgical techniques, however, promoted varying degrees of regeneration of the supporting tissues. The most favourable healing was obtained when resection of bone was avoided and when complete coverage of the alveolar bone was ensured.

The healing potential of the periodontal tissues following different techniques of periodontal surgery in plaque-free dentitions. A 2-year clinical study.

A clinical trial was performed to study the result of periodontal treatment following different modes of periodontal surgery in patients not recalled for maintenance care. The material consisted of 25 patients distributed into 5 groups. Following an initial examination, all patients underwent presurgical treatment including case presentation and instruction in oral hygiene measures. This instruction was given once. The various patient groups were then subjected to one of the following surgical procedures: 1) the apically repositioned flap operation including elimination of bony defects 2) the apically repositioned flap operation including curettage of bony defects but without removal of bone 3) the "Widman flap" technique including elimination of bony defects 4) the "Widman flap" technique including curettage of bony defects but without removal of bone 5) gingivectomy including curettage of bony defects but without removal of bone. Six, 12 and 24 months after completion of the treatment, the patients were recalled for assessment of their oral hygiene standard and periodontal conditions. The results showed that case presentation and oral hygiene instruction given once, only temporarily improved the patient's oral hygiene habits. Renewed accumulation of plaque in the operated areas resulted in recurrence of periodontal disease including a significant further loss of attachment. All five different techniques for surgical pocket elimination were equally ineffective in preventing recurrence of destructive periodontitis.

Periodontal surgery in plaque‐infected dentitions

The investigation was undertaken to find out whether favourable conditions for healing after periodontal surgery would develop in patients whose oral hygiene was professionally maintained at a high standard. The study was performed on 20 patients with advanced periodontal disease. Following an initial examination, comprising plaque index and gingival index scoring, measurement of pocket depths and loss of attachment, the patients were randomly distributed between a test and a control group. The patients first received professional cleaning of the teeth once every 2 weeks. The patients of the control group were recalled for scaling of the teeth once every 6 months. All patients were reexamined after 6, 12 and 24 months. It was found that the control patients were unable to maintain a high standard of oral hygiene with the result that the treatment of the periodontal disease failed. The patients of the test group maintained a high standard of oral hygiene, and the treatment of the periodontal disease was, therefore, successful.

B. Rosling

Papers

The effect of systematic plaque control on bone regeneration in infrabony pockets.

Suppression of the periodontopathic microflora in localized juvenile periodontitis by systemic tetracycline

The healing potential of the periodontal tissues following different techniques of periodontal surgery in plaque-free dentitions. A 2-year clinical study.

Periodontal surgery in plaque‐infected dentitions

Effect of professional tooth cleaning on healing after periodontal surgery.