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Osteocalcin (Oc) and the collagen cross-links pyridinoline (Pyr) and deoxypyridinoline (dPyr) are used as markers of bone turnover in metabolic bone diseases. The aims of this study were: 1) to establish if Oc, Pyr and dPyr can be detected in GCF and 2) using the orthodontic tooth movement model of alveolar bone resorption to evaluate GCF levels of osteocalcin and these collagen cross-links as markers of bone breakdown. Plaque, colour and bleeding indices, probing measurements and GCF samples were collected at two sites in each of 20 adolescents, during 4 stages of fixed appliance therapy: (1) prior to appliance fit, (2) post appliance fit, (3) during active retraction of the maxillary canines, (4) during retention. GCF was collected onto filter paper strips and the volume determined by weighing. An ELISA kit was used for the detection of osteocalcin, whereas Pyr and dPyr were assayed using high performance liquid chromotography (HPLC). Wilcoxon signed ranks test and Bonferroni correction revealed statistically significant increases in plaque (p= 0.012), GCF volume (p=0.024) and osteocalcin concentration (p=0.012), between stages 1 and 2. There were no statistically significant differences between the other variables at this stage or between any of the variables at stages 2 and 3, or between stages 3 and 4. All but 3 of the GCF samples yielded detectable osteocalcin, with large site and subject variation. The median values of osteocalcin and osteocalcin concentration of all the samples were 87.5 pg and 66 pg μl, with a range of 0-1,248 pg, 0-1,572 pg μl. The detection of osteocalcin in GCF during every stage, the wide variation between subjects, and the lack of a consistent pattern related to stages of orthodontic treatment, suggests that osteocalcin may merely be a constituent of GCF associated with the developing dentition, which would reduce its potential as a marker of bone turnover in this group. None of the 16 GCF samples analysed for Pyr and dPyr gave a positive result. This study confirms that fitting an orthodontic appliance results in plaque accumulation and increased gingival inflammation, and that GCF volume is the most sensitive indicator of that inflammation. Osteocalcin was detected in GCF collected from adolescents, whereas Pyr and dPyr could not be detected. Further work is required to establish whether GCF osteocalcin levels can be used as a marker of bone turnover, and whether improvements in the sensitivity of detecting Pyr & dPyr make further study of these promising bone markers worthwhile. [ABSTRACT FROM AUTHOR]

The connection between palmar plantar hyperkeratosis and severe periodontal disease was first reported in 1924 by Papillon and Lefevre. The 2 major components of this syndrome (PLS) can also occur as distinct entities. The literature describes a number of cases which do not fit the classical disease descriptions. In this paper, we report on a family with an atypical PLS. The father had marked palmar plantar hyperkeratosis but a very late onset of destructive marginal periodontitis. The son also had palmar plantar hyperkeratosis, but despite the fact that he initially harboured Actinobacillus actinomycetemcomitans, Prevotella intermedia and Porphyromonas gingivalis, he did not develop periodontal disease over a seven-year observation period when improved oral hygiene and professional tooth cleaning were instituted. [ABSTRACT FROM AUTHOR]

Gingival crevicular fluid (GCF) was collected from 16 molar and premolar sites in each of 20 chronic periodontitis patients before and after periodontal therapy using filter paper strips. These were eluted individually into buffer for determination of cathepsin B and its endogenous inhibitors. α2-macroglobulin and cystatin. Cathepsin B activity was assayed with a fluorogenic peptide substrate. α2-macroglobulin by enzyme-linked 1 mm unabsorbent assay and crystal in activity by inhibition of papain. Total amounts of enzyme and inhibitor per CCI: sample decreased after treatment and correlated positively with pocket depth and gingival bleeding and plaque indices. These comparisons were nearly always statistically significant for pooled site data and sometimes so for mean patient values. The amounts of α2-macroglobulin and cystatin were greater than those of cathepsin H and. surprisingly, enzyme and inhibitor levels correlated positively with each other. Experiments with purified reagents however, demonstrated that the cathepsin B: α2-macroglobulin complex was still active against the low molecular weight substrate and that cystatin levels in GCF are probably insufficient to inhibit the enzyme substantially. These factors may explain why GCF cathepsin H activity reflects the clinical status of periodontal lesions and has been identified in another study as a promising indicator of disease progression. [ABSTRACT FROM AUTHOR]

This paper describes the prevalence and severity of gingival recession in Tanzanian adults covering the age range from 20 to 64 years. In addition, it attempts to assess the relationship between the degree of gingival recession and the presence and amount of calculus. In the 20-34 years age group recession occurred in ⩾ = 32% of the buccal, ⩾ = 25% of the lingual, and ⩾ = 13% of the approximal surfaces. These %s increased to ⩾ = 64%, ⩾ = 52%, and ⩾ = 48%, respectively, in the 45-64 years age group. In the 20-34 years age group, lingual surfaces of mandibular incisors and canines followed by buccal surfaces of these teeth were the sites most severely affected with gingival recession. With increasing age, all sites became gradually more severely affected, particularly the buccal and lingual surfaces of the maxillary first molar. The lingual surfaces of mandibular incisors exhibited on an average 1.3 mm, 2.4 mm and 3.2 mm recession in the 20-34 years, 35-44 years and 45-64 years age group, respectively. Most of the correlation coefficients between gingival recession and calculus at the individual tooth surface in three age groups were statistically significant. The highest correlation coefficients (0.50-0.67) were found in the youngest (20-34 years) age group at the lingual surfaces of the mandibular incisors, canine and first premolar and at the buccal surfaces of the mandibular incisors. Based on these findings, the working hypothesis is advanced that longstanding calculus is an important determinant in the onset of gingival recession at sites exhibiting pronounced recession at a young age in populations deprived of prophylactic dental care. [ABSTRACT FROM AUTHOR]

Gingival crevicular fluid (GCF) was collected from chronic periodontitis patients using plastic micropipettes and coverslip smears stained with antibodies for leukocyte markers and Toluidine Blue for mast cells. The smears consisted of 70-80% granulocytes, 10-20% monocytes/macrophages, 5% mast cells and 5% T lymphocytes; no B lymphocytes were found. Proteases and inhibitors in GCF cells were investigated by enzyme cytochemistry using 2-methoxy-4-naphthylamine-linked peptide substrates and simultaneous coupling to Fast Blue B and immunocytochemistry using biotinylated secondary antibodies and an alkaline phosphatase/new fuchsin detecting system. Elastase was detected in granulocytes, cathepsin B in macrophages, dipeptidyl peptidases II and IV in a small proportion of macrophages, dipeptidyl peptidase IV in a few T lymphocytes, tryptase in mast cells and α-1-proteinase inhibitor and α-2-macroglobulin in some macrophages. GCF was also collected on filter paper strips and eluted into buffer for biochemical enzyme assays. Lysis of cells by addition of detergent to the elution buffer increased activities to 140-240% of control values. Removal of cells by centrifugation reduced measured activities to 1-30% of original figures; this effect was less if samples were pre-treated with detergent. Proteases from inflammatory cells therefore appear to make up most of the measured enzyme activity in GCF, and this association may explain recent correlations with periodontal disease progression. [ABSTRACT FROM AUTHOR]

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Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The Papillon-Lefevre syndrome (PLS) is a rare, autosomal recessive trait that is characterized by palmar plantar keratosis (PPK) and severe, early onset periodontitis, affecting both deciduous and permanent dentitions. The clinical presentation of PLS is variable; the disease occurs so infrequently as to limit clinical cases for study. The exception is a few families with extensive consanguinity in which numerous cases occur. Of particular interest to mapping the genetic origin of the syndrome is the co-expression of the major traits of hyperkeratosis and periodontitis, and their severity. In this paper, we report 2 families with multiple affected individuals from geographically remote areas. A large extended family, from the Cochin region of India, currently residing in Israel, in which there is documented consanguinity and a family from the southwest region of Germany. In each family, 1 individual presents with hyperkeratotic lesions with the complete absence of periodontal lesions. Further, the difference in severity of the hyperkeratotic lesions between families is marked, and one sibling in the German family expressed rapid, early onset periodontitis in the absence of PPK. The genetic nature and penetrance of the genetic defect are discussed. [ABSTRACT FROM AUTHOR]

A number of gingival indices have been described which include visual and invasive components, either separately or in combination. In selecting indices for use in gingivitis therapeutic trials, some investigators maintain that only invasive indices should be used, since indices that include a bleeding-on-provocation component are deemed to be the most objective. Other investigators, however, maintain that non-invasive indices are the more appropriate insofar as invasive procedures will not only disrupt the plaque at the gingival margin, but could also mildly traumatize the tissue and present an impediment to assessing examiner standardization and reproducibility. This paper discusses these aspects of gingivitis evaluation. The data indicate that all validated indices, whether invasive or non-invasive, have some degree of both objectivity and subjectivity. Therefore, the selection of an appropriate index will depend upon the ability of a given index to achieve the objectives of the clinical trial in which it is to be utilized. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This paper reviews the development of various rapid microbial identification techniques and their potential role in the diagnosis of active periodontal tissue destruction. It also explores the concerns expressed by some, that although these techniques offer enormous promise as research tools, validation and translation of test results to clinical diagnosis, prognosis and treatment planning are still problematic. It may be premature to recommend these tests to clinicians in practice. Further longitudinal studies are required to establish the best use of these techniques in a clinical setting. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Gingival hyperplasia caused by the use of nifedipine has been extensively reported. In this paper, the gingiva of 18 patients suffering from cardiopathy and treated with nifedipine were compared with those of 10 patients with cardiac disorders who had not been treated with calcium antagonists and with a no-treatment group of 12 patients. Nifedipine produced gingival hyperplasia, although patients who had not been treated with calcium antagonists also had mild hyperplasia. Hyperplasia first appeared in the interproximal areas, an observation which may be important for early detection. There was a direct correlation between the degree of hyperplasia and the bacterial plaque score. When we studied the influence of administration time and dose of nifedipine with the degree of hyperplasia, no statistically significant differences were found. [ABSTRACT FROM AUTHOR]

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Hypophosphatasia is rare enzymopathy that normally presents within the first few years of life and often has profound effects upon the periodontium. It is a heritable disorder characterised by defective mineralisation of the skeletal and dental structures of the body and a deficiency in the liver/bone/kidney (L/B/K) isoenzyme of alkaline phosphatase (ALP). There has been a tremendous advance in our knowledge of this condition over the last decade due to the advent of highly specific DNA probes and novel microanalytical techniques. This paper aims to review current literature about hypophosphatasia with special reference to the dental aspects of the condition and to shed light upon the controversial area of its mode of genetic inheritance. It is concluded that hypophosphatasia may result from the existence of 2 defective alleles, which alone or in combination may cause the condition. One allele is expressed in an autosomal dominant mariner producing milder phenotypic characteristics, whilst the other is expressed in an autosomal recessive manner producing the more severe clinical form that often results in neonatal death. The milder phenotypes may go undiagnosed and the consequence of this in genetic counselling terms is extremely important. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This paper reports the treatment of prepubertal periodontitis in a 3- year-old girl with Papillon-Lefevre Syndrome, Initially, the patient was found to have a myeloperoxidase deficiency and microbiological tests have identified Butteroides and Fusobacterium, in 60% and 25%, respectively of the total number of microbial flora cultivated. The initial treatment was extration of all the primary teeth with grade 3 mobility, scaling, root platting and daily subgingival irrigation with a 0.2% solution of chlorhexidine. Several months before the eruption of the first permanent molars, the rest of the primary teeth were extracted. The patient was treated with daily subgingival irrigation of chlorhexidine and weekly professional oral hygiene. At the age 6½ years, the permanent teeth have normal gingiva and crevice depths; microbiological investigation reveals a prevalence of the coccoid forms, and radiographs show no evidence of periodontal pathology. [ABSTRACT FROM AUTHOR]

19 patients with a total of 23 periodontal lesions were selected for the study. Following flap-elevation, an occlusive membrane (Gore Tex® adjusted to the size and shape of the lesion was applied. The membrane was removed 4- 6 weeks later by a 2nd operation. Clinical attachment levels were measured and intraoral radiographs taken prior to surgery, and 6 and 12 months postoperatively. The root length and marginal hone level were measured on paper drawings of the teeth magnified (1 5 × ) from the conventional radiographs. The radiographs were digitized for analysis of the subtraction images between the preoperative and the 6- and 12-month postoperative images. Clinical attachment gain was seen in 78% of the teeth after 6 months and 70% after 12 months. Bone gain was recorded in 56% and 22% after 6 months and in 44% and 66% after 12 months by conventional and digital subtraction radiography, respectively. The bone level measurements on conventional radiographs differed significantly (p = 0.001) between the preoperative and 6-month postoperative, but not between the 6- and 12- month, (p = 0.29) conventional radiographs. There was no significant relationship between the clinical measurements and the assessments of hone changes on conventional radiographs r - 0.28, p = 0.25), while a stronger relationship was observed between assessment of clinical attachment gain and assessment of hone changes on the subtraction images (r - 0.58, p - 0.01), [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Application of standard statistical procedures to site-specific data in periodontal research is invalid unless site-to-site dependencies are accounted for. In this paper, we present the adjustments required for valid application of matched pair procedures, including the paired t-test and McNemar's χ² test for correlated proportions. Examples are given involving data arising from: (1) the comparison of pre- and post-treatment clinical measurements; (ii) split-mouth protocols. [ABSTRACT FROM AUTHOR]

The biological principle of "guided tissue regeneration" (GTR) was developed for regenerating periodontal tissues, lost as a result of periodontal disease. This principle was based on the hypothesis that non-desirable types of tissue cells can be prevented from migrating into a wound by means of a membrane barrier and at the same time giving preference to those particular cells to repopulate the wound, which have the capacity to regenerate the desired type of tissue. This principle may have its application in many areas of surgery, aimed at regeneration of lost tissues. One such area is osseous surgery aimed at bone regeneration. In the present paper, a series of experiments in laboratory animals using the method of GTR for regeneration of various types of bone defects are presented as well as examples of application in humans for regeneration of jaw bone defects in conjunction with the placement of dental implants. [ABSTRACT FROM AUTHOR]

Psychosocial factors can influence immune functions: the brain intermediates between the outside world and the inside of the body. The functional interaction between the central nervous system and the immune system is effected by 2 different pathways: the nervous "wiring system" innervating lymphoid tissues and the "soluble connection" via the neuroendocrine system. The paper reviews data from the literature regarding changes in susceptibility to infections due to stressful conditions. Emphasis is given to information regarding infection of the oral cavity and the upper respiratory tract. [ABSTRACT FROM AUTHOR]

This paper summarizes the rationale for the application of microbiology in the management of destructive periodontal diseases. The subgingival microbiota in patients with severe periodontitis is complex and contains high numbers of obligate anaerobic bacteria as well as facultative micro-organisms. It has become clear that major differences exist in the composition of the subgingival microflora. These differences are not only quantitative but also qualitative. Difference in plaque composition is the basis for the application of clinical microbiology in the management of periodontal disease. Several bacterial species have emerged as useful indicators for progressive periodontitis. In this respect, the importance of Actinobacillus actinomycetemcomitans, Bacteroides gingivalis and Bacteroides intermedius has been shown in a number of studies. It has become clear that A. actinomycetemcomitans is not specifically associated with the local form of juvenile periodontitis, but this micro-organism is probably also of importance in severe periodontitis in adult patients. Selection of individuals with an A. actinomycetemcomitans associated periodontitis is essential since successful treatment in these patients needs an adjunctive antibiotic therapy. Microbiological testing can be useful in patients showing a poor response to periodontal treatment (refractory periodontitis). Factors which may be responsible include poor oral hygiene, poor subgingival debridement, the patient's susceptibility and a subgingival microflora resistant to therapy. In this patient category, microbiological testing is capable of diverting continuing periodontal treatment. Furthermore, microbiology can be useful in evaluating periodontal treatment. Successful elimination of specific periodontopathic microorganisms can be used to determine recall intervals. [ABSTRACT FROM AUTHOR]

In the present paper, the onset age of periodontal destruction is discussed. Results of epidemiological studies have shown that with increasing age, the prevalence of periodontitis in a population increases. Data show that after the age of 40 years, the % of the population affected by periodontitis remains rather constant. If it is supposed that the incidence of periodontitis after the age of 40 is zero (no new cases), then extractions resulting in edentulousness due to periodontitis should lead to a decrease of the prevalence of periodontitis. However, after the age of 40 years, the prevalence of periodontitis remains about the same, whereas edentulousness due to periodontitis increases. This suggests that even at a relatively old age, the onset of periodontitis may occur. On the other hand, periodontal destruction has also been found in the primary dentition. Especially on the basis of family studies and studies on localized juvenile periodontitis patients, it can be supposed that in a substantial part of the population, periodontal destruction starts early in life. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This paper describes a retrospective study in which the gingival and periodontal status was assessed at crowned and natural teeth. 510 crowned teeth and 510 natural teeth in 109 subjects were examined. The time elapsed between active therapy and the clinical examination was: (i) 1 to 3 years for 270 teeth. (ii) 3 to 5 years for 168 teeth; (iii) 6 to 9 years for 72 teeth. 90% of the patients were on a recall schedule that required prophylaxis once every 3 months; 8% returned every 6 months and 2% once a month. Plaque index and gingival index were assessed at 4 sites per tooth and pocket depth at 6 sites per tooth, the highest reading per tooth being used for the statistical analysis. The results indicated that there was no difference in plaque and gingival indices between crowned and natural teeth. In addition, the gingival status of the crowned teeth was good, irrespective of the position of the crown margin (subgingival, at the gingival margin or supragingival). [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Periodontology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)