Periodontal attachment loss induced by mechanical subgingival instrumentation in shallow sulci

Periodontal attachment loss induced by mechanical subgingival instrumentation in shallow sulci

Lisa A. Dufour


The fundamental periodontal conditions observed clinically are health, gingivitis, and periodontitis. In the individual dental patient, these conditions may be found separately, or in combination, and may be localized or generalized. Several clinical findings are often used as measures of periodontal health. These include shallow probing depths [less than or equal to] 3mm, with the gingival margin located at, or slightly coronal to, the cementoenamel junction (CEJ); the absence of bleeding on probing or other indications of inflammation; and the normal appearance and location of the alveolar crest as viewed radiographically. (1) The transition from a clinically healthy periodontal state to a clinically inflamed one, typically involves a change in the oral microbial burden, a change in the host response, or both. (2) When an imbalance between the oral microflora and the host’s immune response exists, inflammation of the periodontal tissues results. The imbalance may be created by a shift in either the quantity or quality of plaque or by a change in the individual’s ability to respond immunologically to the microbial plaque present. (3)

Gingivitis, inflammation of the gingiva, is often identified by clinical signs that may include redness, edema, and bleeding on probing. Gingivitis involving at least six teeth is found in nearly 50% of the United States population. (4) The evidence that there is a direct cause-and-effect relationship between the aggregation of supragingival microbial plaque and the development of gingivitis is vast and definitive. (2) Mechanical removal, and/or chemical control of supragingival dental plaque, continues to be the basic requirement for the prevention and treatment of gingivitis. (2,5) Although it is recognized that in many cases gingivitis does not proceed to periodontitis, gingivitis often does precede the destruction of the supporting tissues that occurs in periodontitis. Accordingly, the reversal of gingival inflammation has been, and continues to be, an essential objective of periodontal therapy. (4)

Watching for the signs of periodontal inflammation and measuring changes in the periodontal attachment level over time, are considered appropriate means for clinically identifying the presence, or persistence of, periodontal disease. (6,7) The attachment level refers to the point at which the fibers of the periodontal ligament are attached to the tooth root, as measured from a fixed reference point with a probe. Typically, the fixed-reference point used in a clinical setting is the cementoenamel junction (CEJ), (8) but soft acrylic onlays, stents, or margins of restorations are also used in the research setting. (6,9-12) The junctional epithelium at the base of the sulcus provides an indication of the level of the most coronally positioned connective tissue fibers of the periodontal ligament. (1) In health, the base of the sulcus is located at or near the CEJ.

Attachment loss can occur when periodontal disease progresses and destroys the fibers of the periodontal ligament, resulting in the junctional epithelium migrating apically. Measurements of probing attachment level differ from measurements of probing depth in that the reference point used in probing depth is a changeable one–the crest of the gingival margin. (8) Although traditional probing depth measurements provide the clinician with valuable information about the patient’s periodontal status or response to therapy, monitoring for attachment loss has become the gold standard for identifying progressive disease. (1,8) Measurements of attachment loss specifically monitor changes in the position of the attached periodontal tissues on the tooth root surfaces, and do not account for the inconstant positions of the gingival margins. In addition to the loss of attachment seen in disease progression, attachment loss may result from remodeling of the marginal periodontal tissues; passive eruption; and mechanical trauma from either personal oral hygiene procedures, or professional instrumentation. (6,10-11,13-17)

Professional dental hygiene therapy has traditionally targeted the prevention, arrest, control, or elimination of infection in the gingival tissues (gingivitis) and the underlying periodontal structures (periodontitis). This endeavor has been accomplished successfully through the careful general and periodontal assessment of the patient, the planning of treatment that is specific and individualized, the implementation of appropriate therapy, the evaluation of the response to therapy, and re-treatment when indicated. (8) When supra- and subgingival instrumentation are included as part of the dental hygiene therapy, the goal is to create an environment that is conducive to periodontal health, by producing crown and root surfaces that are biologically acceptable to the periodontal tissues. (3,18) It is quite clear that mechanical instrumentation of the root surfaces is an effective therapy for a majority of patients with mild to moderate periodontitis. (4,9-10,19-20) However, as discussed by Sheiham (in Genco et al.), (21) efforts to improve periodontal health through instrumentation, can sometimes inadvertently cause harm–damage that is generally referred to as clinical iatrogenesis. Sheiham states that operative procedures or dental materials are the more widely recognized causes of clinical iatrogenesis in dentistry. To illustrate, he uses the example that an undesirable physical relationship between a dental restoration and the tissues of the periodontium, can adversely affect periodontal health. Sheiham asserts that a lesser-acknowledged form of dental clinical iatrogenesis is the damage that is caused by subgingival scaling and root planing in sulci measuring [less than or equal to] 3.0mm in depth.

In February of 1985, a three-day state-of-the-science workshop sponsored by the National Institute of Dental Research (NIDR) was held in Bethesda, Maryland. (18) Dental practitioners, researchers, and academicians from all over the world participated. Literature related to the current status of dental plaque control measures and oral hygiene procedures was reviewed extensively by the NIDR workshop working groups. Following the comprehensive review of “professionally administered oral hygiene procedures,” one workshop group concluded that scaling and root planing of shallow crevices (<3.0mm) resulted in permanent loss of periodontal attachment. They further concluded that professional care should be directed only at areas exhibiting clinical signs of disease and that regular instrumentation should not be performed on periodontal disease-free areas. They added that it would be "ironical and regrettable if a substantial part of the `prophylaxes' carded out were deleterious to dental health."

In light of these NIDR workshop conclusions, the purpose of this paper is to examine more recent studies related to the periodontal outcome of mechanical subgingival instrumentation in shallow sulci.

Review of the Literature

Thirteen clinical studies–1 animal and 12 human–were reviewed for the effects of subgingival instrumentation on the level of probing attachment in shallow sulci. The studies, in subjects with varying degrees of periodontitis, ranged in length from six months to five years, and in part assessed periodontal attachment loss in sites <4.0 mm, that resulted from various treatments. Included among the procedures received by the subjects in these studies were manual and/or ultrasonic supra-and subgingival instrumentation, performed at various intervals, with or without the use of local anesthesia (Table I).

In six-month human trials conducted by Westfelt et al. (9) and Hammerle et al., (19) hand scaling and root planing were performed during initial (active) therapy; the use of local anesthesia was not specified. Subjects in both trials received “professional tooth cleanings” (as described by Axelsson and Lindhe) (22) throughout the duration of the study, but received no further subgingival instrumentation. The results of these singular episodes of mechanical sub gingival instrumentation ranged from “minor apical shift” of the probing attachment level in sulci measuring 2.0 mm loss in 20% of sulci initially categorized as shallow ([less than or equal to] 3.0 mm). (19) In both studies, multiple measurements of attachment loss were made by the same examiner. Student t-tests (19) and regression (9) were used for statistical analysis. Lindhe et al. (23) also tested the results of subgingival instrumentation on attachment levels. Scaling and root planing was executed in “normal” sulci of two young adult monkeys, once every two weeks, for six months. Instrumentation was carried out “`to the bottom’ of the clinical pocket and resulted in some bleeding from the adjacent soft tissue.” This repeated instrumentation, beyond the CEJ, yielded a mean loss of attachment approaching 0.4 mm (P<0.001). Results were obtained through the histometric assessment of biopsy material recovered from the animals.

The effects of mechanical instrumentation in shallow sulci have also been examined in several one-year experiments. A singular episode of ultrasonic scaling and root planing was completed by Claffey et al. on nine subjects with severe periodontitis, with the use of local anesthesia. (10) The ultrasonic instrument was set at maximum power, and instrumentation continued until the operator was confident that the root surfaces were debrided adequately. During the 12-month observation period, probing depths did not change in sites initially measured at [less than or equal to] 3.5 mm, but a mean probing attachment loss was recorded at 0.6 mm in these same shallow sites. Longitudinal measurements were obtained with an electronic, pressure-sensitive probe, by the same examiner and confirmed by three independent examiners. Changes in attachment loss were evaluated using the Student paired t-test. A lesser mean attachment loss–0.2mm–was seen by Christie et al. (24) When 10 subjects with advanced periodontitis received a one-time combination of hand and ultrasonic instrumentation under local anesthesia. The power setting for the ultrasonic instrument was not provided. One examiner obtained longitudinal measurements using an electronic, pressure sensitive probe. Analysis of linear regression was used to detect attachment level changes. Vouros et al. also provided initial hand scaling and root planing to 17 subjects with advanced periodontitis. (20) However, instrumentation was repeated every one to two weeks for the first three months of the study and was carried out until the root surfaces were clinically hard, smooth, and adequately cleaned, as judged by the supervising periodontist. The use of local anesthesia was not specified. Repeated instrumentation in this experiment resulted in a mean attachment loss of 0.28 mm in sulci initially measuring [less than or equal to] 3.0 mm. Longitudinal measurements were obtained by the same examiner and the intra-examiner variability test was used to ensure the objectivity of attachment level measurements. Changes were statistically analyzed using the two-way analysis of variance (ANOVA).

Longer-term studies, ranging in length from 24 to 60 months, also have demonstrated attachment loss in shallow sulci following singular or multiple episodes of scaling and root planing, completed by hand, ultrasonic, and a combination of these. Claffey relates his observations from two of his previous studies. (6) In the first study, seven subjects with generalized periodontitis received a singular treatment of ultrasonic scaling and root planing at maximum power setting, with local anesthesia. The instrumentation continued until the operator was confident of adequacy. The subjects were observed for two years, during which time no further instrumentation was provided. Fifty-three percent of the sites initially measured as [less than or equal to] 3.5 mm showed a probing attachment loss of [greater than or equal to] 1.0 mm. In Claffey’s second study lasting 42 months, 17 subjects with generalized periodontitis underwent therapy similar to that described in his first study, except that deep and/or bleeding sites received isolated root debridement between the 12 to 24 month period. (6) A gradual mean attachment loss of approximately 1.0 mm was observed in sites initially recorded at [less than or equal to] 3.5 mm. Longitudinal measurements were obtained with an electronic, pressure-sensitive probe by one examiner and confirmed by independent examiners. In these studies, changes in probing attachment were analyzed by two-way ANOVA and linear regression, respectively. In their two year study, Badersten et al. documented probing attachment loss of >1.0 mm in 23% of shallow sulci in 49 subjects with adult periodontitis, and a >1.5 mm loss in 10% of these same sites. (25) Subjects underwent either one or three scaling and root planing sessions, either by hand or ultrasonic instrumentation, during the first nine months of the study. The use of local anesthesia was not specified. One examiner obtained longitudinal measurements with an electronic, pressure-sensitive probe. Measurements identifying attachment loss were subjected to linear analysis of regression. After five years of observation, Badersten et al. reported a loss of [greater than or equal to] than or equal to] 1.5 mm in 36% of sites initially categorized as shallow. (16) These findings were seen in 39 subjects with adult periodontitis, who received similar therapy to that described above, (25) with the exception that professional dental cleanings (including subgingival scaling of deep and/or bleeding sites) were provided every 6 months beginning at 24 months. These results also were subjected to linear analysis of regression. In experiments by Lindhe et al. (26) and Vanooteghem et al., (11) comparable results of mean attachment loss were obtained–0.6mm and 0.8mm, respectively–when shallow sulci of subjects with moderate to advanced periodontitis received repeated hand or ultrasonic instrumentation. Results were statistically analyzed with Student t-tests (26) and analysis of regression. (11)

Lindhe et al. observed 15 subjects with advanced periodontitis for changes in attachment level following scaling and root planing alone (RPL group), or when performed in conjunction with a modified Widman flap (MWF group). (27) The investigators established that an initial probing depth existed that was a critical determinant of attachment gain or loss (critical probing depth [CPD]), and that the CPD varied for different surgical and nonsurgical procedures. In the RPL group, the initial probing depth considered critical in determining whether attachment loss occurred as a consequence of root instrumentation was 2.9 mm, receiving the same treatment, were likely to show clinical attachment gain. For comparison, the CPD for the MWF group was 4.2 mm. Westfelt et al. calculated slightly shallower CPD of 2.33 to 2.39 mm in subjects with moderately advanced periodontitis, undergoing scaling and root planing as the sole experimental therapy. (9)

To evaluate the effects of nonsurgical maintenance therapy provided at varying recall intervals of 3, 6, 12, and 18 months, Rosen et al. observed several parameters of periodontal health, including changes in probing attachment levels. (13) The 153 study participants were recruited from a public general dentistry clinic. The subjects were divided into four experimental recall groups, but the periodontal status of the subjects was not described. Maintenance appointments provided at the various intervals usually lasted 30 to 60 minutes, and included supra- and subgingival scaling completed by hand; the use of local anesthesia was not specified. Longitudinal measurements were obtained by two independent examiners and were subjected to analysis of regression. Five years after baseline measurements were taken, there was a gradual mean loss of attachment approaching 0.4 mm in sites initially measured at 1 to 3 mm, for all four groups.


There is no question that loss of attachment occurs as a result of periodontal disease progression, but it can also result from other causes. (11) Research has shown that mechanical instrumentation in shallow sulci ( 2.0 mm. (6,10,13,24) On the contrary, following an initial loss of attachment, scaling and root planing in deeper pockets has led to attachment gain. (9-11,13,19-20,27)

Repeated instrumentation in shallow, healthy sites, particularly when no calculus is present, can result in detachment of the periodontal ligament fibers that do not reattach upon healing. Lindhe et al. postulate that repeated instrumentation in shallow sulci, beyond the cementoenamel junction, mechanically wounds the principal fibers of the periodontal ligament and leads to their detachment from the root surface. (23) This theory is one that is broadly accepted in the literature. The investigators speculate that during the healing phase, connective tissue reattachment is prevented because junctional epithelial cells repopulate the debrided root surfaces. The result is an apical displacement of the epithelial attachment.

Various other reasons for attachment loss in shallow sulci have been proposed. Badersten et al. offered “vigorous tooth cleaning procedures” as the most plausible explanation for the slight, but gradual attachment loss that continued in some shallow sites throughout their 24-month study. (25) Smith contends that trauma from mechanical tooth-brushing evokes a chronic inflammatory host response that may lead to the destruction of periodontal connective tissues. (15) Claffey et al. have suggested that attachment loss from instrumentation in shallow sites, may be due to a “remodeling phenomenon” generated by the significant connective tissue changes that result from instrumentation of adjacent deep sites. (10) In a separate study, Claffey et al. concluded that the buccolingual thickness of the gingiva–or lack thereof–may be related to the probing attachment loss seen in shallow sulci, following nonsurgical periodontal therapy, including scaling and root planing. (12) Lastly, Vanooteghem et al. implicate age-related remodeling (or passive eruption) as a possible cause of probing attachment loss in sites lacking clinical signs of disease. (11) It is conceivable that as the tooth continues to erupt, the distance between the CEJ and the junctional epithelium (JE) would increase, without implying that the JE has migrated apically.

As alluded to earlier in this paper, the goal of mechanical instrumentation is to produce a biologically compatible relationship between the root surfaces and the remaining tissues of the periodontium. When accomplished successfully, the therapy should arrest inflammation, promote healing and repair, or prevent disease recurrence. (3,18) However, if after thorough assessment the patient is deemed periodontally healthy, with no evidence of periodontal infection to arrest, control, or eliminate, how should the clinician proceed with the preventive appointment? Needless to say, as many patients as possible with periodontal disease (gingivitis and periodontitis) should be treated, but for those without disease, mechanical instrumentation can have some undesirable effects. (28) Slots recommends that when dental professionals consider preventive therapies, they should weigh the risk of patients’ acquiring destructive periodontal disease against the potentially adverse effects. (5) He adds that inappropriate treatment can result in several detrimental outcomes. For example, overly aggressive scaling and root planing can lead to an hourglass shape of the root where it meets the crown; and subgingival scaling in shallow sulci can lead to attachment loss, recession, tooth sensitivity, and root caries. Since it is not uncommon to find healthy sulci ranging from 1 to 3 mm in depth in patients being examined periodontally, clinicians should consider measures to ensure that shallow sulci are not deepened iatrogenically through unnecessary mechanical instrumentation. (21) Shallow sulci that do not bleed upon probing are highly predictable of periodontal health, (14,29,39-23) and may not require subgingival instrumentation, (30-31) particularly if no calculus is present. (5)

Inasmuch as the studies selected for review suggest important implications for dental hygiene clinical practice, the limitations must be noted. Of the 13 studies reviewed, only the animal study by Lindhe et al. (23) and the study by Rosen et al. (13) included periodontally healthy subjects. All other study subjects had moderately to severely advanced periodontitis with some shallow sulci. (6,9-11,16,19,20,24-27) Whether attachment loss would occur following mechanical instrumentation in shallow sulci of the periodontally healthy individual is not clear. Furthermore, if it did occur, whether the damage would continue to accumulate over time is unknown. These questions would need to be investigated. Also unclear is the degree of aggressiveness–or lack thereof–used during instrumentation procedures described in the studies. The specified use of local anesthesia in some of the studies, (6,9-11,24) and the use of the ultrasonic scaling unit at maximum power, (6,10) may imply a more aggressive approach to instrumentation, but that is left to interpretation. Instrumentation in most of the studies was continued until the operator felt confident that the root surfaces were adequately debrided–a subjective evaluation, but an alternative evaluation does not currently exist. Whether the varying levels of subgingival instrumentation procedures, including gentle debridement, would lead to attachment loss is also not known, and should be furthered studied.


The evidence from scientific research–that subgingival instrumentation in shallow sulci (<4.0 mm) of periodontally involved individuals induces attachment loss–is compelling. Such findings may have important implications for the clinical management and maintenance of periodontally healthy patients with shallow sulci and warrant further study.

Table I. Effect of subgingival instrumentation on level of

probing attachment in shallow sulci


Author/Date Study # Subjects/Sites Scaling

Duration Human/Animal and Root

Perio Status Planing

Lindhe et 30 months 15 Humans Hand

al. 1982a. Adv. Perio

Lindhe et 30 months 15 Humans Hand

al. 1982b. Adv. Perio

Lindhe et 6 months 2 Animals Hand

al. 1982c. “normal” sulci

Westfelt et 6 months 16 Humans Hand

al. 1985 Mod.-Adv. Perio

Badersten 24 months 49/2532 Humans 1 or 3

et al. 1985 Adult Perio Hand or


Claffey et 12 months 9/1248 Humans Ultrasonic

al. 1988 Severe Perio

Badersten 60 months 39/1956 Humans 1 or 3 Hand

et al. 1990 Adult Perio or


Vanooteghem 24 months 11 Humans Hand and

et al. 1990 Mod.-Adv. Perio Ultrasonic

Hammerle 68/4764 Humans Hand

et al. 1991 6 months Mod.-Adv. Perio



Study #1 24 months 7/938 Humans Ultrasonic

Generalized Perio

Study # 2 42 months 17 Humans Ultrasonic

Generalized Perio

Vouros et 12 months 17/1899 Humans Hand

al. 1992 Adv. Perio

Christie et 12 months 10 Humans Hand and

al. 1998 Adv. Perio Ultrasonic

Rosen et 60 months 153 Humans Hand

al. 1999 Varying Perio


Attachment Loss in

Author/Date Subsequent Use of Local Sulci [less than or

Subgingival Anesthesia equal to] 3-4 mm


Lindhe et After 6 months Not specified Mean loss 0.6mm

al. 1982a.

Lindhe et After 6 months Not specified Critical Probing Depth

al. 1982b. <2.9mm established

Lindhe et Every 2 weeks Not specified Mean loss 0.39mm

al. 1982c.

Westfelt et None Yes “minor apical shift”

al. 1985

Badersten None Not specified 10% lost >1.5mm

et al. 1985 23% lost >1.0mm

Claffey et None Yes Mean loss 0.6mm

al. 1988

Badersten After 24 months Not specified 36% lost [greater than

et al. 1990 or equal to] 1.5mm

Vanooteghem After 12 months Yes Mean loss 0.5mm

et al. 1990

Hammerle None Not specified 20% lost >2.0mm

et al. 1991



Study #1 None Yes 53% lost [greater than

or equal to] 1.0mm

Study # 2 None in Yes Mean loss <1.0 mm




Vouros et Every 1-2 wks. Not specified Mean Loss 0.28mm

al. 1992 for 3 months

Christie et None Yes Mean loss 0.2mm

al. 1998

Rosen et Every 3-18 Not specified Mean loss 0.4mm

al. 1999 months


(1.) Wilson TG Jr., Kornman KS (eds): Fundamentals of Periodontics, Chicago, Quintessence Publishing Co, Inc., 1996, p.30, 198.

(2.) Lang NP, Attstrom R, Loe H (eds): Proceedings of the European Workshop on Mechanical Plaque Control, Chicago, Quintessence Publishing Co, Inc., 1998, p.99, 108.

(3.) Young NA: Periodontal debridement: Re-examining nonsurgical instrumentation. Seminars in Dental Hygiene 1994;4:1-7.

(4.) Greenstein G: Nonsurgical periodontal therapy in 2000: A literature review. J Am Dent Assoc 2000; 131:1580-92.

(5.) Slots J, Jorgensen MG: Efficient antimicrobial treatment in periodontal maintenance care. J Am Dent Accoc 2000;131:1293-1304.

(6.) Claffey N: Decision making in periodontal therapy. J Clin Perio 1991;18:384-89.

(7.) Grbic JT, Lamster IB: Risk indicators for future clinical attachment loss in adult periodontitis. Tooth and site variables. J Perio 1992;63:262-69.

(8.) Wilkins EM: Clinical Practice of the Dental Hygienist, 8th ed. Philadelphia, Lippincott Williams & Wilkins, 1999, p.191, 209-210, 325, 561.

(9.) Westfelt E, Bragd L, Socransky S. et al.: Improved periodontal conditions following therapy. J Clin Perio 1985;12:283-93.

(10.) Claffey N, Loos B, Gantes B, et al.: The relative effects of therapy and periodontal disease on loss of probing attachment after root debridement. J Clin Perio 1988;15:163-69.

(11.) Vanooteghem R, Hutchens L, Bowers G, et al.: Subjective criteria and probing attachment loss to evaluate the effects of plaque control and root debridement. J Clin Perio 1990;17:580-87.

(12.) Claffey N, Shanley D: Relationship of gingival thickness and bleeding to loss of probing attachment in shallow sites following nonsurgical therapy. J Clin Perio 1986;13:654-657.

(13.) Rosen B, Olavi G, Badersten A, et al.: Effect of different frequencies of preventive maintenance treatment on periodontal conditions. 5-year observations in general dentistry patients. J Clin Perio 1999;26:225-33.

(14.) O’Reilly PG, Claffey NM: Identifying losing sites at periodontal reevaluation. Curr Opin Periodontol 1996;3:68-77.

(15.) Smith RG: Gingival recession. Reappraisal of an enigmatic condition and a new index for monitoring. J Clin Perio 1997;24:201-205.

(16.) Badersten A, Nilveus R, Egelberg J: Scores of plaque, bleeding, suppuration and probing depths to predict probing attachment loss. 5 years of observation following nonsurgical periodontal therapy. J Clin Perio 1990;17:102-107.

(17.) Claffey N, Egelberg J: Clinical characteristics of periodontal sites with probing attachment loss following initial periodontal treatment. J Clin Perio 1994;21:670-79.

(18.) Loe H, Kleinman DV (eds): Dental Plaque Control Measures and Oral Hygiene Practices, Washington DC, IRL Press LTD., 1986 p.102-103, 106, 117.

(19.) Hammerle CHF, Joss A, Lang NP: Short-term effects of initial periodontal therapy (hygienic phase). J Clin Perio 1991;18:233-39.

(20.) Vouros I, Konstantinidis A, Kirkou-Bata A: Effect of nonsurgical periodontal therapy in an undergraduate dental clinic: Results one year following treatment. J Biol Buccale 1992;20:11-17.

(21.) Genco RJ, Goldman HM, Cohen DW (eds): Contemporary Periodontics, St. Louis, The C.V. Mosby Company, 1990, p.709.

(22.) Axelsson P, Lindhe J: The effects of a preventive programme on dental plaque, gingivitis and caries in school children. J Clin Perio 1974;1:126-38.

(23.) Lindhe J, Nyman S, Karring T: Scaling and root planing in shallow pockets. J Clin Perio 1982;9:415-18.

(24.) Christie P, Claffey N, Renvert S: The use of 0.2% chlorhexidine in the absence of a structured mechanical regimen of oral hygiene following non-surgical treatment of periodontitis. J Clin Perio 1998;25:15-23.

(25.) Badersten A, Nilveus R, Egelberg J: Effect of non-surgical periodontal therapy. VI. Localization of sites with probing attachment loss. J Clin Perio 1985;12:351-59.

(26.) Lindhe J, Wetfelt E, Nyman S, al.: Healing following surgical/non-surgical treatment of periodontal disease. J Clin Perio 1982;9:115-28.

(27.) Lindhe J, Socransky S, Nyman S, et al.: “Critical probing depths” in periodontal therapy. J Clin Perio 1982;9:323-36.

(28.) Haffajee A, Socransky S, Lindhe J, et al.: Clinical risk indicators for periodontal attachment loss. J Clin Perio 1991;18:117-25.

(29.) Amato R, Caton J, Poison A, et al.: Interproximal gingival inflammation related to the conversion of a bleeding to a nonbleeding state. J Perio 1986;57:63-68.

(30.) Lang N, Joss A, Orsanic T, et al.: Bleeding on probing. A predictor for progression of periodontal disease? J Clin Perio 1986;13:590-96.

(31.) Chaves E, Caffesse R, Morrison E, et al.: Absence of bleeding on probing: An indicator of periodontal stability. J Clin Perio 1990;17:714-21.

(32.) Chaves ES et al.: Diagnostic discrimination of bleeding on probing during maintenance periodontal therapy. Am J Dent 1990;4:167-70.

(33.) Chaves E, Wood R, Jones A, et al.: Relationship of “bleeding on probing” and “gingival index bleeding” as clinical parameters of gingival inflammation. J Clin Perio 1993;20:139-43.

Lisa A. Dufour, RDH, MS, is professor of dental hygiene at the University of New England, Portland, Maine. Heather S. Bissell, RDH, BS, practices dental hygiene in periodontal and general dentistry practices in Massachusetts.

COPYRIGHT 2002 American Dental Hygienists’ Association

COPYRIGHT 2008 Gale, Cengage Learning