Periodontal tissue responses after insertion of artificial crowns and fixed

partial dentures
Kent L. Knoernschild, DMD, MS,a and Stephen D. Campbell, DDS, MMScb
College of Dentistry, University of Illinois at Chicago, Chicago, Ill.
Purpose. The purpose of this review was, first, to critically evaluate published evidence on the effects of
artificial crowns and fixed partial dentures (FPDs) on adjacent periodontal tissue health, and second to
synthesize this evidence into meaningful summaries. Restoration qualities that contribute to inflammatory
responses were identified based on strength of evidence, and variables that should be controlled in future
investigations were outlined. Such information is necessary to accurately predict the prognosis of peri-
odontal tissues adjacent to crowns or FPDs.
Methods. Clinical trial and epidemiologic evidence published in English was collected. The effects of
crowns or FPDs on gingival inflammation, probing depths, and bone loss were evaluated based on accu-
racy of measurement, reliability of measurement, and/or appropriateness of data analysis.
Results. Crowns and FPDs increased the incidence of advanced gingival inflammation adjacent to
restorations, particularly if restorations had intracrevicular finish line placement, poor marginal adaptation,
or rough surfaces. However, because of the limitation in the accuracy and reliability of probing depth
measurements, reports of greater mean probing depths of crowned teeth, which tended to be less than
1 mm greater than control teeth, should be questioned. Finally, crowns and FPDs in general did not
accelerate the rate of adjacent bone loss.
Conclusion. Clinically deficient restorations, as well as clinically acceptable restorations, can contribute
to gingival inflammation. However, with the limitations of the applied methods of measurement, current
evidence has not shown an increased attachment loss adjacent to crowns or FPDs. Future trials should
document periodontal health before therapy and periodically after restoration insertion so that each tooth
serves as its own control. In future studies, the periodontal disease history of the patient, the influence of
the restoration on plaque formation, and the composition of the crevicular microflora must be recorded.
(J Prosthet Dent 2000;84:492-8.)

CLINICAL IMPLICATIONS
Gingivitis may develop after insertion of questionable restorations, as well as appro-
priately contoured, highly polished crowns or FPDs with well-adapted, intracrevicular
margins, but severity in response differs among patients. Specific reasons for develop-
ment of inflammation have been difficult to discern because of the diversity in
investigative design among studies. Well-controlled, clinical trials and epidemiologic
studies should be performed to further determine fundamental reasons for advanced
periodontal inflammation in some patients. Clinicians will then be able to accurately
predict the prognosis of periodontal tissues adjacent to crowns or fixed partial dentures.

T he goal of the prosthodontist is to control oral

disease while restoring esthetics and function with
durable, biocompatible restorations. Knowledge of the
responses of periodontal tissues to artificial crowns and
fixed partial dentures (FPDs) is crucial in the develop-
ment of treatment plans with predictable prognoses.
During diagnosis, treatment planning, and active ther-
apy, each patient’s needs must be considered in light of
Presented at the American Academy of Fixed Prosthodontics Annual
Meeting, February 19, 1999.
aAssociate Professor, Department of Restorative Dentistry.
bProfessor and Head, Department of Restorative Dentistry.
the available evidence, which includes published clini-
cal trials, anecdotal reports from peers, and personal
clinical experiences. Critical evaluation of evidence
should be included in the decision-making processes
for a predictable result.
Clinical research has focused on the effect of indi-
rect restorations on periodontal tissues. Studies have
reported that poor marginal adaptation,1-8 deeper
intracrevicular margin placement,9-22 rougher restoration
surfaces,23-30 and overcontoured restorations31-35 can
contribute to localized periodontal inflammation.
Inflammation commonly develops because these
restorations can provide a protected environment in

492 THE JOURNAL OF PROSTHETIC DENTISTRY VOLUME 84 NUMBER 5

KNOERNSCHILD AND CAMPBELL
Fig. 1. Gingival index score incidence in crowned and control teeth (Bader et al20).
which the indigenous microbial population matures
into a more periodontopathic flora.33 These studies
have forced clinicians and researchers to focus on the
fundamental qualities of crowns or FPDs during fabri-
cation that reduce the restoration’s contribution to
gingival inflammation.
The clinician must have a clear understanding of the
clinical trial or the epidemiologic study design to state
confidently that restorations can adversely affect tis-
sues. Trials have commonly started approximately 1
month after insertion of the artificial crown, and teeth
with crowns were evaluated using surrogate measures
such as probing depths, radiographically determined
alveolar bone levels, and gingival index scores. Similar
measurements were also made on each patient’s con-
tralateral tooth as the control. Means and standard
deviations of restored and control groups were usually
reported, and additional statistical analyses were per-
formed to determine differences among groups.
Epidemiologic studies reported data in a similar way,
but the dates of restoration insertion were not known.
Most studies exhibit similar basic designs, but
diversity in approach to determine the influence of
crowns or FPDs on periodontal tissue health has
made meaningful synthesis of the evidence difficult.
Investigations varied with respect to selection of
patients and types of restorations evaluated.
Moreover, 2 factors that could adversely influence the
periodontal response, the degree of marginal adapta-
tion and the intracrevicular depth of the preparation
finish line, were not reported in most studies.
Although control of important variables was not uni-
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THE JOURNAL OF PROSTHETIC DENTISTRY
form among the studies, important conclusions can
be garnered from this body of evidence that elevates
one’s awareness of how periodontal tissues respond to
fixed prosthodontic restorations.
The following sections present a critical evalua-
tion of the literature regarding the response of
periodontal tissues to artificial crowns and FPDs.
Results of clinical trials and epidemiologic studies in
humans that evaluated the degree of gingival inflam-
mation and attachment loss after crown placement
are discussed. Studies are limited to those published
in English, and the evidence is synthesized into con-
cise, comprehensive summaries based on surrogate
measure precision, surrogate measure reliability,
and/or appropriateness of data analysis. Suggestions
are also proposed that apply to the development of
future studies that address periodontal tissue
responses to restorations.
INFLAMMATION AFTER CROWN OR
FPD PLACEMENT
Most studies concluded that artificial crowns and
FPDs could contribute to periodontal inflammation.
Statistically significant differences in mean scores
between a restored tooth and contralateral control
teeth were observed in many patient populations using
the Loe and Silness36 Gingival Index (GI) scale.
Clinical trial and epidemiologic investigations consis-
tently reported mean restored tooth GI scores greater
than mean GI scores for control groups. Differences
between mean restored and control tooth groups were
as great as 0.90 units.12
493
THE JOURNAL OF PROSTHETIC DENTISTRY
Fig. 2. Gingival index score incidence in crowned and control teeth (Valderhaug et al22).
Number of teeth exhibiting index scores of “2” or “3” are presented to allow for comparisons
of incidence of more advanced gingival inflammation over 15 years.
The methods of statistical analyses in many studies
biased the interpretation of results. GI scores were
ordinal data, meaning that increasing index score cor-
related with increasing inflammation recognized by
specific criteria. However, because the data were not
continuous, a score of 2 did not indicate that the peri-
odontal tissue was twice as inflamed as tissues with a
score of 1. Therefore, reporting calculation of GI score
means and standard deviations, which is better suited for
interval or ratio scale data, was not necessarily appropri-
ate. In addition, the “statistically significant” mean
differences reported in studies that were as small as 0.2
index units cannot be recognized clinically. Finally, just
as means and mean differences between groups should
be reported with the same significance as raw data, cal-
culated differences should have been reported as
whole numbers.
Perhaps the most meaningful method to describe
associations between gingival inflammation and crown
placement was by reporting frequencies of index scores.
Valderhaug et al22 reported frequencies after a 15-year
clinical trial (Fig. 1), and one can easily appreciate that
crowned teeth more frequently exhibited GI scores of
2 and 3 compared with control teeth. A similar
approach was used in the Bader et al 20 epidemio-
logic study (Fig. 2), and trends that corroborated the
evidence of Valderhaug et al were observed. In the
Bader et al study, baseline data were not reported,
whereas in the Valderhaug et al trial, baseline data were
collected after crown insertion. No studies have recorded
each patient’s periodontal status before crown or FPD
insertion and linked the initial periodontal tissue con-
dition to the response after restoration insertion.
494
KNOERNSCHILD AND CAMPBELL
SUMMARY
Artificial crowns and FPDs increased the incidence
of advanced gingival inflammation. Moreover, studies
have shown that mean crowned tooth GI scores are
consistently greater than mean control tooth scores,
which further supported that trend. Restoration fac-
tors such as intracrevicular margin placement, poor
margin adaptation, poor restoration contours, and
restoration surface roughness were frequently associated
with inflammation.
ATTACHMENT LOSS AFTER CROWN
PLACEMENT
Accelerated loss of alveolar bone height or an
increase in probing depths compared with other teeth
in a dentition could indicate that restoration fabrica-
tion procedures or the restoration itself contributed to
injury of periodontal architecture. Pihlstrom37 stated
that in long-term clinical trials of periodontal health,
the radiographically determined attachment level
should be the primary focus, but probing depths
should be recorded. The following sections present
studies that address how crowns affected probing
depths and alveolar bone loss.
PROBING DEPTHS
Trials9,10,13-17,19,20,22 in which patients were fol-
lowed up for as long as 15 years after the insertion of
crowns or FPDs reported mean crowned tooth prob-
ing depths 0.05 to 0.5 mm greater than mean control
depths. Mean probing depth increases could be com-
pared over time because these studies tracked probing
depth changes from known dates of insertion. In general,
VOLUME 84 NUMBER 5
KNOERNSCHILD AND CAMPBELL
mean crowned tooth probing depths of 0.1 to 0.2 mm
greater than mean control depths were frequently
reported. No studies reported mean crowned tooth
probing depths significantly less than those of teeth
not restored.
Although these studies reported similar results, they
had different research designs. Careful control of
numerous variables such as initial health of the peri-
odontium, occlusogingival position of the finish line,
contour of the restoration, and adaptation of the
restoration margin are critical for accurate assessment
of probing depth outcomes. Not all studies reported
methods that controlled these and other patient selec-
tion variables. Therefore, because of the lack of
uniformity in inclusion criteria among studies, a state-
ment that crowns cause increased probing depths has
been inappropriate. Diversity in research designs dis-
guised the factor(s) that has had the most influence.
A lack of uniformity also existed in establishment of
control teeth among studies. In many studies, control
teeth were similar contralateral teeth. Sometimes the
control was previously restored with a direct restora-
tion. In other studies, caries developed in the control,
which was restored during the trial but remained in
the control group. The influence of the control groups
on observed differences in probing depths is uncertain
because directly restored teeth in some studies served
as controls. Previously reported minute differences in
probing depth changes after crown insertion could
have been greater if controls remained unrestored.
Conversely, with carefully selected controls and con-
trolled experimental variables, minimal differences
between crowned and control tooth groups may have
been observed.
A third consideration relates to accuracy of probing
depth measurement techniques. A mean increase in
probing depths after artificial crown insertion of 0.1 to
0.2 mm was often reported and could be meaningful.
However, this should be interpreted in light of mea-
surement accuracy. Variations in probing force, size
and shape of tip, location of tip placement, detection
of reference landmarks for attachment level probing,
and degree of gingival inflammation could adversely
influence accuracy.38 Moreover, error in conventional
probing measurements can be 0.5 mm or greater39
with errors depending on pocket depth, tooth, site
location, and patient.40 Finally, probes of the same
design and batch from the manufacturer have varied in
marking placement by as much as 0.5 mm.41
Therefore, only probing depths that have increased
more than 1 mm should serve as a diagnostic test with
high sensitivity and specificity.42
SUMMARY
Although mean probing depth increases after artifi-
cial crown or FPD placement were often reported,
NOVEMBER 2000
THE JOURNAL OF PROSTHETIC DENTISTRY
these reports must be evaluated individually on the
basis of each study’s research design. The lack of con-
trol of experimental variables and the use of
questionable controls in some studies diminished the
credence of their conclusions. Moreover, because an
examiner’s accuracy in evaluating probing depths is
±1 mm, commonly reported mean changes in prob-
ing depth of 0.2 mm have limited clinical meaning, as
the changes were within the error of probing depth
measurements.
BONE LOSS
Change in periodontal probing depths or in radio-
graphic bone height should be used separately and in
combination43 for the determination of attachment
loss. Visual interpretation, direct measurement, or dig-
ital image analysis can identify radiographically
determined alveolar bone loss. The most precise mea-
surement of bone loss has been determined through
standardized radiographs, which permit measurement
of changes as small as 0.2 mm when computerized
methods are used.44
Attachment loss after crown placement has been
reported in longitudinal studies13,16,17,19,22 with clini-
cal data that extended from 1 to 15 years. Attachment
loss was reported using probing depth measure-
ments or radiographic examinations, but these
studies did not use the precise computerized method.
Investigators who used probing depths reported
means and standard deviations by making measure-
ments from the crown margins to the depth of the
sulcus. Studies that used radiograph measurements did
not report data in such detail, but they presumably
measured interproximally from radiographic crown
margin to alveolar crest. These studies reported mean
attachment losses ranging from 0.15 to 1.3 mm dur-
ing trial periods, which can be calculated to a reported
loss of 0.04 and 0.24 mm per year.
One longitudinal report22 recorded no difference in
incidence of crowned or control teeth that developed 0 to
1 mm horizontal bone loss or 1 to 2 mm horizontal
bone loss. The lack of increase in bone loss after crown
insertion is also corroborated by the comparison of
studies that evaluated crowned teeth to other studies in
which crowned teeth were not the investigative focus.
Several studies45-48 reported alveolar bone resorption
in controlled periodontal patients of 0.03 to 0.07 per
year. These reports did not assess differences in
crowned versus unrestored teeth, and one could
assume that both types were present in the patient pop-
ulations. Evidence also suggested that crowns did not
increase the rate of bone loss because attachment loss
between these 2 groups of studies was similar.
Other factors could influence attachment loss after
insertion of crowns or FPDs. Valderhaug and
Birkeland13 reported an accelerated rate of attachment
495
THE JOURNAL OF PROSTHETIC DENTISTRY
loss during the first 2 years after crown insertion.
These results suggested that factors related to crown
fabrication could contribute to increased attachment
loss. Albandar et al49 have reported that, in descend-
ing order of importance, that tooth type, initial bone
level, age, sex, calculus, restoration margins, and prox-
imal surface are responsible for only 20% of the
variance leading to alveolar bone loss. Thus, many fac-
tors could be influential, and future, well-controlled
studies should address these issues in detail.
SUMMARY
Evidence has not shown that artificial crown or
FPD insertion results in accelerated bone loss.
Investigators have reported that the distance from the
crown margin to the probed depth of the sulcus or the
distance from the crown margin to the radiographic
alveolar bone level increased over time. However,
mean attachment loss in crowned teeth was similar to
loss observed with control teeth.
FUTURE RESEARCH
Although investigators have focused mainly on
restoration qualities and biomaterial properties to
improve tissue responses adjacent to restored teeth,
other factors not related to the restoration could be
more critical. For example, the history of the patient’s
periodontal disease before therapy could be a contrib-
utor to periodontal inflammation that develops after
crown or FPD insertion. Previous trials and epidemio-
logic studies have not reported the patient’s
periodontal disease background, which could influ-
ence observed gingival inflammation, probing depths,
or attachment loss throughout a study. Future clinical
trials should include this history as a contributing vari-
able. If greater inflammation and/or recession were
expected because of the patient’s history, the clinician
could better predict final tissue responses before the
initiation of therapy.
The indigenous microbial flora composition and the
patient’s response to toxins produced by that flora are
probably important contributors to periodontal health
during and after therapy. If a cast restoration has pro-
vided a protected environment in which a pathogenic
flora can develop, patients with a more aggressive
indigenous flora could have greater inflammation devel-
op. However, inflammation could occur only if a patient
were not resistant to the pathogenic flora’s metabolic
products. Considerable research has been conducted
regarding immunologic responses to periodontal
pathogens, and further research is needed relating to the
pathogenesis of periodontal inflammation.
The restoration history of a specific tooth before
fixed prosthodontic therapy is likely to be a third vari-
able that contributes to alveolar bone resorption.49
Trial and epidemiologic evidence have suggested that
496
KNOERNSCHILD AND CAMPBELL
crowned teeth may have a greater incidence of
advanced gingival inflammation. However, studies
have not confirmed that gingival tissues consistently
developed an increase in inflammation after crown
insertion. Teeth generally have received extensive
direct restorative therapy that included intracrevicular
restorations before crown therapy. Amalgam or com-
posite restorations could contribute to gingival
inflammation before fixed prosthodontic therapy that
would not resolve after crown or FPD insertion. In
fact, removal of caries and the replacement of poorly
contoured or poorly adapted direct restorations with
well-fabricated crowns or FPDs could improve peri-
odontal tissue health. Therefore, before fixed
prosthodontic therapy, future clinical investigations
should document the tooth’s restorative history and
initial periodontal status as contributing variables so
that each crowned tooth serves as its own control.
A fourth consideration relates to the limited infor-
mation available regarding the effects that preparation,
tissue retraction, impression, provisionalization, and
luting procedures have on periodontal health. This
broad-based consideration is complicated and difficult
to control because one procedure must be completed
immediately after the last. If a tooth is prepared for a
crown, impressed, and provisionally restored, one can-
not determine which of the previous procedures
contributed to the inflammation that might develop.
Moreover, with clinical trials, baseline gingival index
scores collected after crown insertion could represent
only partial resolution of inflammation that developed
from previous procedures. This further underscores
the importance of tracking the periodontal health of
individual teeth before the initiation of therapy.
Finally, the influence of restorative materials on peri-
odontal health must be considered. Biomaterials must
be developed with low surface-free energies, as higher
surface energy materials such as casting alloys and
ceramics may lead to greater plaque adherence and mat-
uration.28,50-52 The degree of in vivo plaque formation
differs among materials.53-55 Therefore, a fundamental
understanding of initial pellicle biofilm formation,
which influences initial bacterial adhesion through spe-
cific and nonspecific mechanisms,56-61 is necessary. In
addition, bacterial toxins adhere to a variety of restora-
tive materials,62-65 and a greater understanding must be
developed regarding bacterial toxin contribution to
biofilm formation and bacterial adhesion.
The influences of restorative materials on the
mature crevicular microflora composition could be
critical because microflora composition beneath porce-
lain pontics adjacent to inflamed tissues differed from
microflora beneath alloy pontics adjacent to inflamed
tissues.66 Clinicians and researchers are expected to
develop a more fundamental understanding of how
restorative materials influence the crevicular environ-
VOLUME 84 NUMBER 5
KNOERNSCHILD AND CAMPBELL
ment. New biocompatible materials can then be devel-
oped that favorably influence the microflora
composition for periodontal health.
CONCLUSIONS
Evidence suggests that restoration factors such as
poor margin adaptation, intracrevicular margin place-
ment, rough surfaces, and overcontouring could
contribute to localized gingival inflammation,
increased probing depths, and bone resorption.
Crown insertion increased the incidence of advanced
gingival inflammation adjacent to restorations.
However, because of the limitation in accuracy of
probing depth measurements, commonly reported
greater mean probing depths of crowned teeth com-
pared with control teeth should be questioned.
Horizontal bone loss was not accelerated after crown
placement.
Although studies have reported a greater incidence
of gingival inflammation adjacent to crowns, studies
have not documented an increase in inflammation
compared with periodontal status before the insertion
of crowns or FPDs. Every tooth accumulates a unique
restorative history, so future trials should document
periodontal health before crown therapy and periodi-
cally after crown insertion. Each tooth would then
serve as its own control. Future studies should also
document the periodontal disease history of the
patient as well as the influence of the restoration on
pellicle formation, plaque formation, and microflora
composition. These considerations will improve the
understanding of the influences of crowns and FPDs
on periodontal health such that the clinician can
obtain the most predictable periodontal tissue
response after restoration insertion.
REFERENCES
1. Bjorn AL, Bjorn H, Grkovic B. Marginal fit of restorations and its relation
to periodontal bone level. II. Crowns. Odontol Revy 1970;21:337-46.
2. Gilmore N, Sheiham A. Overhanging dental restorations and periodon-
tal disease. J Periodontol 1971;42:8-12.
3. Highfield JE, Powell RN. Effects of removal of posterior overhanging
metallic margins of restorations upon the periodontal tissues. J Clin
Periodontol 1978;5:169-81.
4. Jeffcoat MK, Howell TH. Alveolar bone destruction due to overhanging
amalgam in periodontal disease. J Periodontol 1980;51:599-602.
5. Turner CH. A retrospective study of the fit of jacket crowns placed
around gold posts and cores, and the associated gingival health. J Oral
Rehabil 1982;9:427-34.
6. Lang NP, Kiel RA, Anderhalden K. Clinical and microbiological effects of
subgingival restorations with overhanging or clinically perfect margins. J
Clin Periodontol 1983;10:563-78.
7. Sorensen SE, Larsen IB, Jorgensen KD. Gingival and alveolar bone reac-
tion to marginal fit of subgingival crown margins. Scand J Dent Res
1986;94:109-14.
8. Felton DA, Kanoy BE, Bayne SC, et al. Effect of in vivo crown margin dis-
crepancies on periodontal health. J Prosthet Dent 1991;65:357-64.
9. Silness J. Periodontal conditions in patients treated with dental bridges.
3. The relationship between the location of the crown margin and the
periodontal condition. J Periodontal Res 1970;5:225-9.
10. Bergman B, Hugoson A, Olsson CO. Periodontal and prosthetic condi-
NOVEMBER 2000
THE JOURNAL OF PROSTHETIC DENTISTRY
tions in patients treated with removable partial dentures and artificial
crowns. A longitudinal two-year study. Acta Odontol Scand 1971;29:621-
38.
11. Larato DC. Effects of artificial crown margin extension and tooth brush-
ing frequency on gingival pocket depth. J Prosthet Dent 1975;34:640-3.
12. Newcomb GM. The relationship between the location of subgingival
crown margins and gingival inflammation. J Periodontol 1974;45:151-4.
13. Valderhaug J, Birkeland JM. Periodontal conditions in patients 5 years
following insertion of fixed prostheses. Pocket depth and loss of attach-
ment. J Oral Rehabil 1976;3:237-43.
14. Valderhaug J, Heloe LA. Oral hygiene in a group of supervised patients
with fixed prostheses. J Periodontol 1977;48:221-4.
15. Jameson LM. Comparison of the volume of crevicular fluid from restored
and non-restored teeth. J Prosthet Dent 1979;41:209-14.
16. Valderhaug J. Periodontal conditions and carious lesions following the
insertion of fixed prostheses: a 10-year follow-up study. Int Dent J
1980;30:296-304.
17. Muller HP. The effect of artificial crown margins at the gingival margin
on the periodontal conditions in a group of periodontally supervised
patients treated with fixed bridges. J Clin Periodontol 1986;13:97-102.
18. Orkin DA, Reddy J, Bradshaw D. The relationship of the position of
crown margins to gingival health. J Prosthet Dent 1987;57:421-4.
19. Reichen-Graden S, Lang NP. Periodontal and pulpal conditions of abut-
ment teeth. Status after four to eight years following the incorporation of
fixed reconstructions. Schweiz Monatsschr Zahnmed 1989;99:1381-5.
20. Bader JD, Rozier RG, McFall WT Jr, Ramsey DL. Effect of crown margins
on periodontal conditions in regularly attending patients. J Prosthet Dent
1991;65:75-9.
21. Freilich MA, Niekrash CE, Katz RV, Simonsen RJ. Periodontal effects of
fixed partial denture retainer margins: configuration and location. J
Prosthet Dent 1992;67:184-90.
22. Valderhaug J, Ellingsen JE, Jokstad A. Oral hygiene, periodontal condi-
tions and carious lesions in patients treated with dental bridges. A
15-year clinical and radiographic follow-up study. J Clin Periodontol
1993;20:482-9.
23. Waerhaug J. Effect of rough surfaces upon gingival tissue. J Dent Res
1956;35:323.
24. Schwarz ML, Phillips RW. Comparison of bacterial accumulations on
rough and smooth enamel surfaces. J Periodontol 1957;28:304-7.
25. Mormann W, Regolati B, Renggli HH. Gingival reaction to well-fitted
subgingival proximal gold inlays. J Clin Periodontol 1974;1:120-5.
26. Keenan MP, Shillingburg HT Jr, Duncanson MG Jr, Wade CK. Effects of
cast gold surface finishing on plaque retention. J Prosthet Dent
1980;43:168-73.
27. Shafagh I. Plaque accumulation on cast gold complete crowns polished
by a conventional and an experimental method. J Prosthet Dent
1986;55:339-42.
28. Quirynen M, Marechal M, Busscher HJ, Weerkamp AH, Darius PL, van
Steenberghe D. The influence of surface free energy and surface rough-
ness on early plaque formation. An in vivo study in man. J Clin
Periodontol 1990;17:138-44.
29. Quirynen M, van der Mei HC, Bollen CM, Schotte A, Marechal M,
Doombusch GI, et al. An in vivo study of the influence of the surface
roughness of implants on the microbiology of supra- and subgingival
plaque. J Dent Res 1993;72:1304-9.
30. Bollen CM, Papaioanno W, Van Eldere J, Schepers E, Quirynen M, van
Steenberghe D. The influence of abutment surface roughness on plaque
accumulation and peri-implant mucositis. Clin Oral Implants Res
1996;7:201-11.
31. Perel ML. Periodontal considerations of crown contours. J Prosthet Dent
1971;26:627-30.
32. Silness J, Ohm E. Periodontal conditions in patients treated with dental
bridges. V. Effects of splinting adjacent abutment teeth. J Periodontal Res
1974;9:121-6.
33. Parkinson CF. Excessive crown contours facilitate endemic plaque nich-
es. J Prosthet Dent 1976;35:424-9.
34. Sackett BP, Gildenhuys RR. The effect of axial crown overcontour on
adolescents. J Periodontol 1976;47:320-3.
35. Ehrlich J, Hochman N. Alterations on crown contour—effect on gingival
health in man. J Prosthet Dent 1980;44:523-5.
36. Loe H, Silness J. Periodontal disease in pregnancy. I. Prevalence and
severity. Acta Odont Scand 1963;21:533-51.
37. Pihlstrom B. Issues in the evaluation of clinical trials of periodontitis: a
clinical perspective. J Periodontal Res 1992;27:433-41.
497
THE JOURNAL OF PROSTHETIC DENTISTRY KNOERNSCHILD AND CAMPBELL

38. Reddy MS, Palcanis KG, Geurs NC. A comparison of manual and con-
trolled-force attachment-level measurements. J Clin Periodontol
1997;24:920-6.
39. Grossi SG, Dunford RG, Ho A, Koch G, Machter EE, Genco RJ. Sources
of error for periodontal probing measurements. J Periodontal Res
1996;31:330-6.
40. Gunsolley JC, Williams DA, Schenkein HA. Variance component model-
ing of attachment level measurements. J Clin Periodontol 1994;21:289-95.
41. Van der Zee E, Davies EH, Newman HN. Marking width, calibration
from tip and tine diameter of periodontal probes. J Clin Periodontol
1991;18:516-20.
42. Aeppli DM, Boen JR, Bandt CL. Measuring and interpreting increases in
probing depth and attachment loss. J Periodontol 1985;56:262-4.
43. Hausmann E, Allen K, Norderyd J, Ren W, Shibly O, Machtei E. Studies
on the relationship between changes in radiographic bone height and
probing attachment. J Clin Periodontol 1994;21:128-32.
44. Benn DK. Limitations of the digital image subtraction technique in
assessing alveolar bone crest changes due to misalignment errors during
image capture. Dentomaxillofac Radiol 1990;19:97-104.
45. Selikowitz HS, Sheiham A, Albert D, Williams GM. Retrospective longi-
tudinal study of the rate of alveolar bone loss in humans using bite-wing
radiographs. J Clin Periodontol 1981;8:431-8.
46. Rohner F, Cimasoni G, Vuagnat P. Longitudinal radiographical study on
the rate of alveolar bone loss in patients of a dental school. J Clin
Periodontol 1983;10:643-51.
47. Papapanou PN, Wennstrom JL, Grondahl K. A 10-year retrospective study
of periodontal disease progression. J Clin Periodontol 1989;16:403-11.
48. Lavstedt S, Bolin A, Henrikson CO. Proximal alveolar bone loss in a lon-
gitudinal radiographic investigation. II. A 10-year follow-up study of an
epidemiologic material. Acta Odontol Scand 1986;44:199-205.
49. Albandar JM, Rise J, Abbas DK. Radiographic quantification of alveolar
bone level changes. Predictors of longitudinal bone loss. Acta Odontol
Scand 1987;45:55-9.
50. Clayton JA, Green E. Roughness of pontic materials and dental plaque. J
Prosthet Dent 1970;23:407-11.
51. Quirynen M, Marechal M, Busscher HJ, Weerkamp AH, Arends J, Darius
PL, et al. The influence of surface free-energy on planimetric plaque
growth in man. J Dent Res 1989;68:796-9.
52. Tsibouklis J, Stone M, Thorpe AA, Graham P, Peters V, Heerlien R, et al.
Preventing bacterial adhesion onto surfaces: the low-surface-energy
approach. Biomaterials 1999;20:1229-35.
53. Olsson J, van der Heijde Y, Holmberg K. Plaque formation in vivo and
bacterial attachment in vitro on permanently hydrophobic and
hydrophilic surfaces. Caries Res 1992;26:428-33.
54. Savitt ED, Malament KA, Socransky SS, Melcer AJ, Backman KJ. Effects
on colonization of oral microbiota by a cast glass-ceramic restoration. Int
J Periodontics Restorative Dent 1987;7:22-35.
55. Adamczyk E, Spiechowicz E. Plaque accumulation on crowns made of
various materials. Int J Prosthodont 1990;3:285-91.
56. Busscher HJ, Cowan MM, van der Mei HC. On the relative importance
of specific and non-specific approaches to oral microbial adhesion.
FEMS Microbiol Rev 1992;8:199-209.
57. Satou J, Fukunaga A, Morikawa A, Matsumae I, Satou N, Shintani H.
Streptococcal adherence to uncoated and saliva-coated restoratives. J
Oral Rehabil 1991;18:421-9.
58. Scheie AA. Mechanisms of dental plaque formation. Adv Dent Res
1994;8:246-53.
59. Ellen RP, Lepine G, Nghiem PM. In vitro models that support adhesion
specificity in biofilms of oral bacteria. Adv Dent Res 1997;11:33-42.
60. Busscher HJ, van der Mei HC. Physico-chemical interactions in initial
microbial adhesion and relevance for biofilm formation. Adv Dent Res
1997;11:24-32.
61. Bos R, van der Mei HC, Busscher HJ. Physico-chemistry of initial micro-
bial adhesive interactions—its mechanisms and methods for study. FEMS
Microbiol Rev 1999;23:179-230.
62. Knoernschild KL, Lefebvre CA, Schuster GS, Payant LM, Gagnon FM.
Endotoxin adherence to and elution from two casting alloys. Int J
Prosthodont 1994;7:22-9.
63. Knoernschild KL, Tompkins GR, Lefebvre CA, Griffiths LL, Schuster GS.
Effect of pH on Porphyromonas gingivalis endotoxin affinity for resins. Int
J Prosthodont 1996;9:239-47.
64. Nelson SK, Knoernschild KL, Robinson FG, Schuster GS. Lipopolysaccharide
affinity for titanium implant biomaterials. J Prosthet Dent 1997;77:76-82.
65. Knoernschild KL, Tompkins GR, Schuster GS, Lefebvre CA, Russell CM.
Effect of treatment concentration on lipopolysaccharide affinity for two
alloys. Dent Mater 1997;13:111-7.
66. Wang JC, Lai CH, Listgarten MA. Porphyromonas gingivalis, Prevotella
intermedia and Bacteroides forsythus in plaque subjacent to bridge pon-
tics. J Clin Periodontol 1998;25:330-3.
Reprint requests to:
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UIC COLLEGE OF DENTISTRY (MC555)
801 S PAULINA ST
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Copyright © 2000 by The Editorial Council of The Journal of Prosthetic
Dentistry.
0022-3913/2000/$12.00 + 0. 10/1/110262
doi:10.1067/mpr.2000.110262

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