Studies of the association between periodontitis and certain medical conditions have reported that the surface area of periodontal pockets may be a link between periodontitis and these conditions (1±3). There are two commonly proposed biological mechanisms by which periodontal pockets may in¯uence systemic conditions. First, bacteria and their products may pass through the periodontal pockets into the bloodstream causing systemic complications. Second, cells within the connective tissues underlying periodontal pockets may secrete in¯ammatory mediators, which in turn may lead to systemic problems ranging from low birth weight to cardiovascular disease (4). Some studies reporting an association between periodontitis and systemic diseases indicate that the surface area of pockets is equivalent to that of the palm of the hand (50 cm 2 to 75 cm 2 ) or that of the ventral surface forearm (%200 cm 2 ) (1, 2, 5, 6). These estimates appear in¯ated since the root surface area of the typical den- tition (excluding 3rd molars) is approximately 75 cm 2 . Most studies reporting these large pocket surface areas have not taken into account existing work on the root surface area of the human dentition. A more accurate estimate of the surface area of periodontal pockets may be helpful in several ways. First, in non-experimental research, the assess- ment of dose-response relationships between a suspected cause and outcome may provide clues towards establishing causality (7, 8). If periodontal pockets are causally related to systemic disease, a dose-response relationship between the pocket surface area and the risk for systemic consequences may provide insight into biological mechanisms. Second, an estimate of the pocket surface area may permit a comparison with other diseases that involve ulcerated epithelium such as in¯ammatory bowel disease, and thereby allow for a re-evaluation of biological plausibility. Several studies have evaluated the relationship between linear measurements of periodontitis and lost attachment surface area (9±13). The goal of this study was to provide simple formulas to relate linear measurements of clinical periodontitis to the dentogingival epithelial surface area (DGES). These formulas were applied to a representative sample of the adult US population (1985±1986), a sample of 1021 individuals at their initial visit to The dentogingival epithelial surface area revisited Hujoel PP, White BA, GarcõÂa RI, Listgarten MA: The dentogingival epithelial surface area revisited. J Periodont Res 2001; 36: 48± 55. # Munksgaard, 2001. Recent studies implicating periodontitis as a cause of systemic diseases have reported that the surface area of periodontal pockets exposed to bacterial bio®lm ranges from 50 cm 2 to 200 cm 2 . Since the root surface area of the typical human dentition (excluding 3rd molars) is 75 cm 2 , these estimates appear too large. The goal of this study was to relate linear periodontal probing measurements to the dentogingival surface area (DGES). The DGES comprises both the sulcular and junctional epithelium, present in health, as well as any intervening pocket epithelium present in periodontitis. Formulas to estimate the DGES from clinical measures were derived from a meta-analysis of root surface areas, published values of root length, and a study that related the percent remaining root surface area to the percent remaining root length. These formulas were applied to a survey of the adult US population, the Veterans Aairs (VA) Dental Longitudinal Study, and a population of individuals visiting a periodontist. Individuals without periodontitis had a typical DGES of 5 cm 2 . Among individuals with periodontitis, the mean DGES in the three samples ranged from 8 cm 2 (ranging from 1 cm 2 to 29 cm 2 ) to 20 cm 2 (ranging from 2 cm 2 to 44 cm 2 ). It was concluded that the mean DGES among individuals with periodontitis ranges from 8 cm 2 to 20 cm 2 , considerably smaller than the range of 50 cm 2 to 200 cm 2 currently assumed. P. P. Hujoel 1,2 , B. A. White 3 , R. I. Garcõ Âa 4 , M. A. Listgarten 5 1 Department of Dental Public Health Sciences, School of Dentistry, and 2 Department of Epidemiology, University of Washington, Seattle, 3 Kaiser Permanente, Center For Health Research, Portland, Oregon, 4 VA Dental Longitudinal Study, Boston VA Outpatient Clinic, and Department of Health Policy & Health Services Research, Boston Univ. Goldman School of Dental Medicine, Boston, 5 Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, USA P. P. Hujoel, Department of Dental Public Health Sciences, School of Dentistry, Box 357475, University of Washington, Seattle, WA 98195, USA Tel: 01 206 543 2034 Fax: 01 206 685 4258 e-mail: hujoel@u.washington.edu Key words: periodontal pockets; dentogingival junction; gingival epithelium; pocket epithelium Accepted for publication May 25, 2000 J Periodont Res 2001; 36: 48± 55 Printed in UK. All rights reserved