The dentogingival junction to the
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1 Volume 79 Number 10 RedefiningtheBiologicWidthinSevere, Generalized, Chronic Periodontitis: Implications for Therapy M. John Novak,* Huda M. Albather, and John M. Close Background: Previous studies demonstrated significant variability in the histologic biologic width in periodontal health and mild periodontitis. The purpose of this study was to determine whether the previously established dimensions of the biologic width applied to subjects with severe, generalized, chronic periodontitis. Methods: Twenty-eight subjects, aged 29 to 45 years, with severe, generalized, chronic periodontitis were included in the study. There were 18 males and 10 females, and 19 (68%) of the patients were smokers. Clinical and radiographic measures were taken by calibrated examiners. The clinical biologic width was determined from the most coronal level of clinical attachment to the crest of the alveolar bone for proximal surfaces only and compared to the histologic biologic width previously reported. Results: The clinical biologic width in subjects with severe, generalized periodontitis was significantly greater than previously reported (). For all evaluable proximal sites, the mean clinical biologic width was 3.95 mm versus the mean histologic biologic width of 2.04 mm. The greatest clinical biologic widths were seen with pockets <2 mm ( mm; range: 1.60 to 9.00 mm) and 2 to 4 mm ( mm; range: 0.20 to 6.40 mm). Conclusions: The mean clinical biologic width in subjects with severe, generalized, chronic periodontitis seemed to be significantly greater than the histologic biologic width previously reported for subjects not demonstrating significant periodontal pathology. In addition, sites with shallow probing depths demonstrated the greatest biologic width, suggesting that these sites may be at increased risk for losing clinically significant attachment during surgical procedures. J Periodontol 2008;79: KEY WORDS Periodontitis; surgery. * Center for Oral Health Research, University of Kentucky, Lexington, KY. Private practice, Bellevue, WA. Department of Dental Public Health, University of Pittsburgh, Pittsburgh, PA. The dentogingival junction to the tooth surface is composed of a fibrous, supracrestal connective tissue attachment and an epithelial attachment (junctional epithelium), and its dimensions have been delineated from autopsy jaw specimens (Fig. 1). 1,2 The supracrestal soft tissue attachment of the periodontal tissues to the tooth/root surface has been termed the biologic width (BW) and was introduced as an important concept in periodontics and restorative dentistry. 3 The histologic dimensions of the BW were comprehensively evaluated on teeth from autopsy specimens of subjects 19 to 50 years of age; these dimensions varied considerably with age and level of apical migration of the epithelial attachment. 2 Concern has been expressed that the mean values obtained from these studies do not truly reflect the variability that exists in the dimensions of the dentogingival junction. 4 In addition, it was suggested that BW measurements taken from the tissues of a healthy periodontium should not be extrapolated for use in pathologic situations. 4 However, to the best of our knowledge, no studies have been done on BW measurements in animals or humans with clinically diagnosed periodontitis or in subjects with the more aggressive forms of disease. The progression of periodontal destruction is generally considered to be chronic in nature and slowly progressing. However, under certain circumstances, doi: /jop
2 J Periodontol October 2008 Novak, Albather, Close Figure 1. A bucco-lingual histologic specimen of a healthy periodontium showing the components of the dentogingival junction or BW. BW is composed of the junctional epithelium (epithelial attachment) and the supracrestal connective tissue attachment. E = enamel; D = dentin; AC = alveolar crest. disease progression may be more aggressive, resulting in severe bone and attachment loss at an early age. More severe disease has been observed when the host bacterial interaction and subsequent pathologic changes in the periodontal tissues have been impacted by environmental and/or acquired risk factors, such as in smokers and patients with systemic conditions and in certain individuals who express an altered inflammatory genotype. 5 It has been believed for many years that the distance from the most apical extent of subgingival calculus or plaque to the crest of the alveolar bone remains generally constant, with mean values of 1.94 to 1.97 mm. 1,6 An average value of 2.04 mm for the BW, the distance from the most coronal extent of the epithelial attachment to the crest of the alveolar bone, is considered to be the norm for most patients and most teeth, although significant variations can occur, especially in the length of the epithelial attachment. 2,4 More than 20 years ago, we reported that the supracrestal connective tissue attachment is an important, but variable, component of the periodontal support that may provide periodontal stability to teeth that lack alveolar bone support as well as providing an unusually large BW. 7 More recently, we observed in studies of young adults with severe generalized periodontitis that the most coronal level of clinical attachment does not always relate to the crest of the alveolar bone in a manner that is consistent with previous measures of the BW (Fig. 2). Because considerable variability has been shown to exist in the dimensions of the BW in cross-sectional studies 1,2 of autopsy materials with no overt periodontal pathology, the purpose of this study was to determine whether previously observed norms in the BW apply in a previously untreated population with severe generalized periodontitis. The importance of understanding the variations in BW that may occur with periodontal pathology may impact our approach to surgical intervention if conserving the existing periodontal attachment is a clinical priority. MATERIALS AND METHODS The baseline clinical measurements and radiographs, previously gathered from 28 male and female subjects as part of a longitudinal intervention study at the University of Pittsburgh in 2000, were used for this cross-sectional study of the dimensions of the clinicalbw. 8 Allconsenting subjects were 45yearsofage (range: 29 to 45 years) and were diagnosed as having severe, generalized, chronic periodontitis using recently describedcriteria. 9 Eligible subjects had to have 20 teeth with >30% of measured sites with 5 mm clinical attachment loss, be in good health, and be willing to participate in the study. Subjects were excluded from participating in the study if they had received any non-surgical periodontal treatment or antibiotic therapy in the 3 months prior to the screening appointment or had undergone periodontal surgery in the 12 months prior to screening. Subjects were also excluded if they needed antibiotic prophylaxis for dental treatment. Smoking was not an exclusion criterion. Each subject received a clinical examination by one of two calibrated examiners consisting of full-mouth recording of probing depths (PDs) and clinical attachment levels (CALs) at six sites per tooth for all fully erupted teeth, except third molars, using a University of North Carolina 15 probe with measures rounded up to the nearest millimeter. 8 Alveolar bone levels (BLs) were measured as previously described from a fullmouth series of periapical radiographs taken for each subject using the long-cone paralleling technique. 10 All radiographs were exposed with settings at 70 kilovolt (peak) and 15 ma. Films were processed 1865
3 Biologic Width in Severe, Generalized, Chronic Periodontitis Volume 79 Number 10 Figure 2. A) The clinical and radiographic appearance of a subject with severe, generalized, chronic periodontitis. B) Clinical and radiographic appearance of a deep pocket and significant attachment and bone loss on the mesial surface of tooth #8 immediately adjacent to a shallow pocket associated with significant bone loss on the mesial surface of tooth #9 and an extended BW. Similar clinical (C) and radiographic (D) appearances of a deep pocket with significant attachment loss on the distal surface of tooth #28 adjacent to a shallow pocket with minimal clinical attachment loss on the mesial surface of tooth #29 and an extended BW. 1866
4 J Periodontol October 2008 Novak, Albather, Close under standardized conditions using an automatic processor. Radiographic analysis was performed by projecting each x-ray film onto a solid white surface at a fixed distance, providing a magnification of 3.5. All measurements were made in a darkened room with a clear plastic millimeter rule. BL was determined by measurement of the distance from the cementoenamel junction (CEJ) to the alveolar crest and was made by aligning the ruler along the outer surface of the root of the tooth and measuring the distance from the CEJ to the most coronal extent of the periodontal ligament, as previously described. 10 In situations in which the CEJ or alveolar crest could not be clearly identified, the interproximal surface was recorded as being non-measurable. Only proximal surfaces were used in the analysis, and for each evaluated radiographic surface, mean values of the buccal and lingual proximal clinical measuresforpd andcalwere usedforcomparisonwithbl at that surface. Clinical BW is defined as the distance from the most coronal level of the CAL to the BL. Because the CEJ is used to calculate CAL and BL, clinical BW was calculated as BL - CAL and was considered to consist of the supracrestal connective tissue fibers and the junctional epithelium as previously described. 2 Statistical Analyses Descriptive statistical analyses for the mean SD with 95% confidence intervals about the mean were performed. The intercorrelations among PD, CAL, BL, and BW were compared for all sites as well as for sites grouped by PD ranges of <2, 2 to 4, 5 to 7, and >7mm and CAL ranges of 0 to 2, 3 to 6, and >6 mm. A comparison was made, using a one-sample multivariate analysis of variance, of the data obtained from this study for the clinical BW in subjects with severe, generalized, chronic periodontitis and the means previously obtained for the histologic BW. 2 RESULTS The clinical analysis of this population with severe, generalized, chronic periodontitis revealed that 44% of all measured sites had PD and CAL 3 mm. These clinical observations suggested that even in the presence of a severe, generalized, horizontal pattern of alveolar bone loss, nearly half of the clinical sites in the mouth showed minimal clinical signs of disease but extensive radiographic evidence of alveolar bone loss. When we examined the relationship between PD and the calculated clinical BW (Table 1), statistically significant increases in the clinical BW were observed compared to the mean values previously reported for the histologic BW. 2 At sites with PD <2 mm, there was a mean BW of 5.02 mm across all subjects, with a median of 4.90 mm (Table 1). Consistent with previously reported histologic measures of BW, the range of measurements for all sites with PD <2 mm was considerable, ranging from 1.6 mm to as much as 9 mm. As PD increased, the associated mean BW tended to decrease. However, for all levels of PD, the clinical BW was significantly greater than that previously reported for the histologic BW. Similar findings were observed when the evaluation of BW was based on CAL at an individual site (Table 2). Sites with CAL of 0 to 2 mm had an average BW of 5.35 mm, with a median of 5.16 mm and a range of 3.00 to 9.35 mm. Consistent with the observations based on PD (Table 1), the average BW tended to decrease with increasing CAL, but it was always statistically significantly greater than previously reported for the histologic BW in subjects without significant periodontal pathology. 2 An analysis of the intercorrelation coefficients and their statistical significance was performed for PDs of 2 to 4, 5 to 7, and >7 mm and for all PDs combined (Table 3). Comparisons were made between PD and BL, PD and BW, and BL and BW for each range of PD. For all sites combined, PD was significantly correlated with BL (). However, PD was not significantly correlated with BL at the individual ranges of PD nor was it significantly correlated with BW, confirming our initial observation of a disassociation between PD and BW in subjects with severe, generalized periodontitis. BL was significantly correlated with BW for each group of PDs and for all sites combined as would be expected, because bone levels are used in the determination of the BW. Similar correlations were found when sites were examined by CAL (Table 4). Significant correlations were found between CAL and BL but only for moderate to severe attachment loss. However, no correlation was observed between CAL and BW at any range of CAL or for all sites combined. BL was significantly correlated with BW at all sites because BL is used in the calculation of BW. DISCUSSION BW is an important clinical concept in restorative dentistry and periodontics. 4,11 Although the frequently used histologic measure for BW, 2.04 mm, is the reported average from many measurements, it has not been generally understood that considerable variability exists in the dimensions of the dentogingival junction that constitute thebw. 2,4 Inthe originalstudy 2 that is frequently referenced for BW, 325 measures were taken on 287 teeth in 30 autopsy jaws. Although the investigators stated that all specimens were free of extensive pathology and fulfilled the requirements of clinically normal specimens, they had been classified by their various stages of passive eruption, a term used to characterize the exposure of the anatomic crown because of gingival recession. 12 The phases AT 2000, Air Techniques, Melville, NY. 1867
5 Biologic Width in Severe, Generalized, Chronic Periodontitis Volume 79 Number 10 Table 1. Relationship of PD to Clinical BW PD <2 mm 2to4mm 5to7mm >7 mm All Sites Clinical BW (mm; mean SD) Clinical BW (mm; median [range]) Clinical BW versus histologic BW* (1.60 to 9.00) 4.12 (0.20 to 6.40) 3.36 (0.68 to 6.33) 3.33 (1.15 to 5.41) 3.88 (1.93 to 6.41) P <0.013 * Previously reported histologic values for BW. 2 Table 2. Relationship of CAL to Clinical BW CAL 0to2mm 3to6mm >6 mm All Sites Clinical BW (mm; mean SD) Clinical BW (mm; median [range]) 5.16 (3.00 to 9.35) 3.79 (1.71 to 6.61) 3.05 (1.45 to 5.44) 3.88 (1.93 to 6.41) Clinical BW versus histologic BW* * Previously reported histologic values for BW. 2 Table 3. Intercorrelation Coefficients by PD PD versus BL r =-0.08 P = PD versus BW r =-0.42 P = BL versus BW r = 0.39 P = PD 2 to 4 mm 5 to 7 mm >7 mm All Sites r =-0.33 P = r =-0.18 P = r = 0.73 r =-0.39 P = r = 0.13 P = r = 0.47 P = r = 0.61 r = 0.02 P = r = 0.06 Table 4. Intercorrelation Coefficients by CAL CAL versus BL r =-0.12 P = CAL versus BW r =-0.36 P = BL versus BW r = 0.97 CAL 0 to 2 mm 3 to 6 mm >6 mm All Sites r = 0.60 P = r = 0.29 P = r = 0.94 r = 0.71 r = 0.09 P = r = 0.76 r = 0.76 r =-0.07 P = r = 0.06 of passive eruption are based on the location of the dentoepithelial junction (DEJ). In phase I, the DEJ is located on enamel and, therefore, is consistent with periodontal health or gingivitis, depending on the presence or absence of inflammation. In phase II, the DEJ is located on enamel and cementum and, therefore, depicts early stages of periodontitis. In phase III, the DEJ is located entirely on cementum; inphaseiv, thedej is on cementum, and the root surface is exposed. Phases III and IV would be termed periodontitis because loss of attachment had occurred. The most consistent reported component of the histologic BW was the width of the supracrestal connective tissue, which averaged 1.08 mm in phase I (range: 0.75 to 1.49 mm), 1.07 mm in phase II (range: 0.81 to 1.56 mm), 1.06 mm in phase III (range: 0.69 to 1.53 mm), and 1.06 mm in phase IV (range: 0.89 to 3.10 mm). 2,4 Greater variability was seen in the length of the junctional epithelium, averaging 1.35 mm in phase I (range: 1.14 to 1.56 mm), 1.10 mm in phase II (range: 0.80 to 1.35 mm), 0.74 mm in phase III (range: 0.44 to 0.88 mm), and 0.71 mm in phase IV (range: 0.53 to 0.88 mm). 2,4 1868
6 J Periodontol October 2008 Novak, Albather, Close There are no comprehensive evaluations of BW in more advanced cases of periodontitis where significant changes in connective tissue and bone have occurred. The present study took advantage of baseline data obtained as part of an intervention study in subjects with severe, generalized, chronic periodontitis to examine the changes in BW that might occur in periodontitis. 8 The first observation was that the average clinical BW in cases of severe, generalized, chronic periodontitis was nearly twice as large as previously reported for the histologic BW in cases of health to mild periodontitis (3.95 mm versus 2.04 mm). What was even more surprising was the extreme range of values obtained for BW, based on initial PD or CAL, with values <1to >9 mm. An examination of intercorrelation coefficients confirmed our initial observation (Fig. 2) that sites with the shallowest PDs and least CAL had the greatest BW. This observation provides significant implications for the selection of surgical or non-surgical approaches in the treatment of patients with severe periodontitis. It was demonstrated that surgical intervention in sites with shallow PDs resulted in post-surgical loss of attachment at that site In cases of severe, generalized, chronic periodontitis in which the BW at shallow sites may be at least twice as much as first described, with extremes of up to 9 mm, there is considerable potential for extensive attachment loss as the result of open flap debridement with scaling and root planing or with apically positioned flaps. ACKNOWLEDGMENTS This study was supported, in part, by a grant from CollaGenex Pharmaceuticals, Newtown, Pennsylvania. The authors report no conflicts of interest related to this study. REFERENCES 1. Stanley HR Jr. The cyclic phenomenon of periodontitis. Oral Surg Oral Med Oral Pathol 1955;8: Gargiulo AW, Wentz FM, Orban B. Dimensions and relations of the dento-gingival junction in humans. J Periodontol 1961;32: Ingber JS, Rose LF, Coslet JG. The biologic width A concept in periodontics and restorative dentistry. Alpha Omegan 1977;70: Gargiulo A, Krajewski J, Gargiulo M. Defining biologic width in crown lengthening. CDS Rev 1995;88: Page RC, Kornman KS. The pathogenesis of human periodontitis: An introduction. Periodontol ; 14: Waerhaug J. The gingival pocket. Odontol Tidskr 1952; 60: Novak MJ, Polson AM, Caton J, Freeman E, Meitner S. A periodontal attachment mechanism without alveolar bone. Case report. J Periodontol 1983;54: Novak MJ, Johns LP, Miller RC, Bradshaw MH. Adjunctive benefits of subantimicrobial dose doxycycline in the management of severe, generalized, chronic periodontitis. J Periodontol 2002;73: Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4: Reed BE, Polson AM. Relationships between bitewing and periapical radiographs in assessing crestal alveolar bone levels. J Periodontol 1984;55: Hildebrand CN. Crown lengthening for optimum restorative success. Compendium 2003;24: Orban B, Kohler J. The physiologic gingival sulcus. Ztschr Stomatol 1924;22: Knowles JW, Burgett FG, Nissle RR, Shick RA, Morrison EC, Ramfjord SP. Results of periodontal treatment related to pocket depth and attachment level. Eight years. J Periodontol 1979;50: Lindhe J, Westfelt E, Nyman S, Socransky SS, Heijl L, Bratthall G. Healing following surgical/non-surgical treatment of periodontal disease. A clinical study. J Clin Periodontol 1982;9: Lindhe J, Westfelt E, Nyman S, Socransky SS, Haffajee AD. Long-term effect of surgical/non-surgical treatment of periodontal disease. J Clin Periodontol 1984;11: Pihlstrom BL, McHugh RB, Oliphant TH, Ortiz-Campos C. Comparison of surgical and nonsurgical treatment of periodontal disease. A review of current studies and additional results after 6 1/2 years. J Clin Periodontol 1983;10: Pihlstrom BL, Oliphant TH, McHugh RB. Molar and nonmolar teeth compared over 6 1/2 years following two methods of periodontal therapy. J Periodontol 1984;55: Ramfjord SP, Caffesse RG, Morrison EC, et al. 4 modalities of periodontal treatment compared over 5 years. J Clin Periodontol 1987;14: Correspondence: Dr. M. John Novak, Center for Oral Health Research, University of Kentucky, 414 Health Sciences Research Building, Lexington, KY Fax: 859/ ; mjnova2@uky.edu. Submitted January 31, 2008; accepted for publication March 21,
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