Soft Tissue Healing Following
Subgingival curettage and root planing were per-
Curettage and Root Planing
by
S. S. S T A H L *
J. M . WEINER**
S. B E N J A M I N *
L . YAMADA*
H E A L I N G after soft tissue curettage and root planing
has been reviewed both from clinical and histologic
points of v i e w . Ratcliff noted that "studies showing
1-3 1
effectiveness of removal of crevicular epithelium by i n -
strumentation are limited" and, furthermore, that "no
horizontal study on an adequate population demon-
strated the percentage potential of curettage for ef-
fecting a longer epithelial adhesion and/or additional
connective tissue attachment." Stahl concluded that
2
"with regard to tissue responses following curettage,
reduction i n inflammation was noted universally. Differ-
ent responses, however, have been reported when total
removal of the lining epithelium following curettage was
a criterion. Epithelization of the crevice following treat-
ment has been reported within similar time limits by
various investigators; however, connective tissue repair
showed marked variations in time."
These conclusions have been supported by recent
animal and human studies. For example, Sanderson
reported that hand curettage completely removed pocket
epithelium in 5 3 % of his cases, inflammation returned
about 14 days after curettage, and no two adjacent
pockets were exactly alike with regard to inflammation.
In dogs, K o n et a l noted that pocket epithelium was
5
not completely removed in all animals by curettage and
that, at 55 days post-treatment, the degree of inflamma-
tion was similar to that seen in control specimens. E p i -
thelization of the wound was completed about seven
days after curettage.
In view of the wide usage of this therapy and re-
ported variation in results, we thought it of interest to
examine curettage healing using methods of analysis
similar to those employed i n our gingivectomy repair
studies. Comparisons of tissue responses might further
6
document similarities and variations in these therapeutic
modalities among a group of periodontal patients.
This study was supported in part by Grant No. DE-3084 from
the National Institute for Dental Research, the National Insti-
tutes of Health, Bethesda, Maryland.
*Department of Periodontics, University of Southern Califor-
nia School of Dentistry, Los Angeles, California.
** Department of Medicine and the Department of Commu-
nity Medicine and Public Health, School of Medicine, University
of Southern California, Los Angeles, California.
M A T E R I A L AND M E T H O D S
formed on 80 suprabony pockets, average pocket depth
4.6 mm ± 0.9, in 60 patients ranging in age from 18 to
71 years, mean age 43 ± 10 years. These individuals, 32
males and 28 females, 45 Caucasians, 14 Negroes, and
1 Oriental, were without any known metabolic diseases.
The periodontal condition of all patients was diagnosed
as periodontitis, and they were treated either in private
periodontal practice or at the Periodontia Clinic of the
University of Southern California School of Dentistry.
A t the time of treatment, dental and medical histories as
well as complete roentgenographic series were available.
In these individuals, adjacent facial or lingual pockets
were chosen. Every attempt was made to choose pock-
ets of similar clinical depth. The areas were anesthetized
and one of the pockets was curetted using Gracey cu-
rettes. Curettage and root planing extended to the base
of the clinical pocket. Both soft tissue curettage and
root planing were carried on until the periodontist was
satisfied that root surface smoothness and soft tissue
debridement were satisfactory.
After curettage, the adjacent nontreated gingival
pocket was excised and prepared for histologic study.
This gingiva served as the "control" specimen. The
curetted gingiva was removed at varying time intervals
over an eight-week period. Excision was performed by
straight line gingivectomy at the base of the clinical
4
pocket.
In the histologic analysis, using 80 pockets, a break-
down of the number of curettage biopsies per unit of
time indicated 14 biopsies taken immediately after cu-
rettage, 12 biopsies taken at the one-week interval, 14
biopsies at the two-week interval, 14 biopsies at the
four-week interval, 14 biopsies at the six-week interval,
and 12 biopsies at the eight-week interval. A l l patients
were instructed in home care procedures as soon as
clinically feasible.
Histologic analysis of both control and post-curettage
specimens was performed as outlined in our initial pub-
lication.
6
For the statistical analysis of post-curettage inflam-
mation fluctuation, only a control and one adjacent
pocket were used. The number of samples used were:
immediately 14, one week 8, two weeks 7, four weeks
9, six weeks 12, and eight weeks 10 samples. Statistical
analyses are based on the following models: Komol-
goroff-Smirnoff, Control Chart, and Correlated Pro-
7 8
portions. These allowed for comparison of the biopsy
9
specimen and one adjacent control specimen per pa-
tient using different assumptions in the statistical models.
678
Volume 42
Number 11
HISTOLOGIC OBSERVATIONS
C o n t r o l Specimens (60 Specimens)
Sixty gingival marginal samples were analyzed. These
specimens showed varying degrees of inflammation.
Twenty-three were classified as mild, 28 as moderate,
and 9 as severely inflamed. Increased vascularity and
degenerative changes in the connective tissue correlated
well with increase in inflammation. Nine specimens
showed facial or lingual keratinization. The remaining
specimens demonstrated a parakeratinized surface.
I M M E D I A T E L Y P O S T - C U R E T T A G E ( 1 4 SPECIMENS)
Crevicular epithelial lining was either disrupted or
absent in all biopsy specimens. Disruption was present
in 7 of 14 biopsies, with epithelium being frequently
present at the gingival margin area. In seven specimens,
step serial sectioning revealed no evidence of epithe-
lium. Inflammation was present adjacent to the crevicu-
lar epithelium area in all biopsy specimens. It varied in
intensity from mild to severe. Clinical pocket depth
did not correlate with degree of inflammation. Further-
more, histologic evaluation of the curetted and adja-
cent non-curetted pocket wall showed variation in de-
gree of inflammation, even though pocket depth was
identical. These findings strongly question the use of an
adjacent papilla or margin as a control site if inflam-
matory responses to therapeutic modalities are to be
evaluated. Yet, in a study of curettage effects, one ob-
viously cannot use the identical site for both pre- and
post-therapy histologic diagnosis. Thus, there are severe
limitations in properly controlling a histologic evalua-
tion of the effects of soft tissue curettage.
Degree of vascularity correlated significantly with de-
gree of inflammation within each specimen, as did de-
gree of collagen disorganization.
The surface (facial or lingual) epithelium showed
parakeratinization in 12 of 14 specimens and P A S posi-
tive, diastase labile material was present in crevicular
and marginal epithelium in 6 of 14 specimens.
O n e Week Post-Curettage (12 specimens)
A l l curetted specimens showed an intact crevicular
epithelial lining. Inflammation varied in intensity, with
six specimens showing mild inflammation and three
showing severe inflammation. Since degrees of vascu-
larity and collagen appearance correlated well with de-
gree of inflammation, they will not be described as sep-
arate entities. Parakeratinization was predominant at
lingual or facial epithelial surfaces. P A S positive d i -
astase labile material was present in all crevicular epi-
thelia and continued to be present in the great majority
of specimens taken at later time intervals.
Soft Tissue Healing 679
Two Weeks Post-Curettage (14 specimens)
A l l wounds had epithelialized and similar observa-
tions were made in all of the later specimens. A t this
time, mild inflammation was present in five specimens,
and severe inflammation in two specimens. Facial or
lingual surface keratinization was seen in two speci-
mens.
F o u r to E i g h t Weeks Post-Curettage
Inflammation was mild in 8 of 14 specimens taken
four weeks after curettage, and severe in one specimen.
A t six weeks after curettage, 6 of 14 specimens showed
mild inflammation, while three demonstrated a severe
infiltrate. A t eight weeks after curettage, 6 of 12 speci-
mens showed mild inflammation and three were severely
inflamed.
STATISTICAL ANALYSIS OF I N F L A M M A T I O N
As noted above, histologic analysis of curettage heal-
ing is restricted since pre- and post-treatment speci-
mens cannot be obtained from the same tooth. Accord-
ingly, adjacent teeth are used as possible controls. Since
the adjacent gingiva need not be related to the treated
site in terms of bacterial state and therefore show
10
different tissue reactions to insults, problems arise as-
11
sociated with the statistical analysis to be used.
For example, if the "control" sites are assumed to
be independent of the treated sites, then two analytic
approaches may be considered. The first of these is
the comparison of the pre-treatment distribution with
the post-treatment distribution, considering the group's
response. This analysis is shown in Figure 1. Figure 1
7
(above) shows the proportion of individuals with mild,
moderate and severe inflammation at zero time. Figure
1 (below) gives the proportion of individuals with mild,
moderate and severe inflammation at 1, 2, 4, 6 and 8
weeks after curettage. Note that this analysis uses two
results per person (pre- and post-treatment values),
but only in computing the group proportions. N o in-
formation related to the change or absence of change in
the individual is used. The small sample of individuals
per time period precludes seeing significant changes in
the pre-post distributions.
A second method of analysis is of the "quality con-
trol chart" type commonly used in laboratory quality
8
control analyses. In this analysis, the pre-treatment
specimens, representing different individuals, yield a
pre-treatment distribution. The proportions of speci-
mens with mild, moderate and severe inflammation are
determined, together with confidence intervals for each.
The assumption to be tested is that the inflammatory
state of the gingiva after curettage is "unchanged" from
that seen at baseline time (represented by the "control"
teeth). Further, the pre-treatment description of inflam-
680 Stahl, Weiner, Benjamin, Yamada J. Periodont.
November, 1971

FIGURE 1. Analysis of inflammatory response i n gingival specimens. Statistical model used

is based on assumption of independence between tissue responses with individual. Group
responses are shown as percentage distributions. Above: Effect of immediate curettage on
inflammatory reponse—mild, moderate, severe—in specimens from untreated adjacent
teeth ( C ) and i n specimens from treated teeth ( T ) . Below: Effect of recovery time of 1 to 8
weeks on inflammatory response—mild, moderate, severe—in specimens from untreated
adjacent teeth ( C ) and i n specimens from treated teeth ( T ) .

FIGURE 2. Analysis of post-curettage inflammatory responses following 0 to 8 weeks of

recovery time. Statistical model used is based on the asumptions that specimens from adja-
cent teeth are independent with respect to inflammatory response and that the level of i n -
flammation observed i n untreated teeth describes the "expected" inflammation throughout
the recovery period. Above: Percentage of mild inflammation specimens at 0 to 8 weeks of
recovery time. Center: Percentage of moderate inflammation specimens at 0 to 8 weeks of
recovery time. Below: Percentage of severe inflammation specimens at 0 to 8 weeks of re-
covery time.
682 Stahl, Weiner, Benjamin, Yamada J. Periodont.
November, 1971

mation is appropriate to use through time. This situa- TABLE 1

Analysis of Pre-Curettage and Post-Curettage Inflammatory Re-
tion is depicted i n Figure 2. In Figure 2 (above) the
sponse in Gingival Specimens from Adjacent Teeth (Model Used
proportion of specimens with mild inflammation is is Based on Assumption of Interrelationship Between
given. Note that the groups observed at 1, 2, 4 and 6 Tissue Responses Within the Individual)
weeks post-treatment are less than at 0 week ( 5 7 % ) ,
although not significantly so, which suggests that an A. Analysis of Responses Associated with Immediate Curettage
Pre-Curettage Inflammation
increase in inflammation follows treatment. A t eight Response
weeks, the proportion with mild inflammation is now M i l d Moderate Severe Total
significantly higher than baseline ( 6 0 % ) , suggesting a Post- Mild 5 2 1 8
Curettage Moderate 2 2 1 5
decrease in inflammation of the moderate or severe Inflammation Severe 0 1 0 1
forms. In Figure 2 (center) the proportion of specimens Response Total 7 5 2 14
with moderate inflammation is seen to be somewhat B. Analysis of Responses Associated with 1-2 Weeks Recovery
lower than baseline, although not significantly so. A t from Curettage
eight weeks, moderate inflammation is significantly Pre-Curettage Inflammation
Response
less. In Figure 2 (below) the proportion of specimens M i l d Moderate Severe Total
with severe inflammation is seen to increase at one Post- Mild 6 0 0 6
week. N o significant deviations from baseline are seen. Curettage Moderate 0 5 1 6
Inflammation Severe 0 1 2 3
In the quality control chart analysis, the small samples Response Total 6 6 3 15
seen at each post-treatment period do not affect the
C. Analysis of Responses Associated with 4-8 Weeks Recovery
ability to recognize significant differences from a base- from Curettage
line state. Pre-Curettage Inflammation
Response
M i l d Moderate Severe Total
The fact that both control and treated teeth are 6 9 1 16
Post- Mild
from the same individual and hence subject to the same Curettage Moderate 4 4 1 9
metabolic, structural, and environmental influences sug- Inflammation Severe 0 4 2 6
Response Total 10 17 4 31
gests that one should rationally assume a relationship
between pre- and post-treatment responses. This as-
sumption would give rise to an analysis assessing change Keeping within this rationale, a consideration of F i g -
in the individual. Table 1 illustrates this analysis. The ure 2 illustrates two possible explanations of shifts in
first section of the table shows the effect of immediate degree of inflammatory tissue response that can be seen
treatment. The second shows the effect of 1-2 weeks of clearly even with small samples. The first, occurring at
treatment. The third shows the effect of 4 to 8 weeks. one week, was associated with an increase in the severity
Note that in each section the number of individuals is of inflammation. This may be in response to acute in-
relatively small and significant differences are not de- jury induced by curettage. Proportions of specimens
termined. This analysis is based upon correlated pro- showing severe inflammation sudsided to baseline at two
portions as is appropriate when the same individual is
9

weeks and remained within statistical variation. The

subjected to a "before and after" response. This form
of Chi-square analysis is comparable in concept to the
paired differences test using the Student "t" statistic.
If the assumption of interrelationship between control
and treated teeth was appropriate, sample sizes in ex-
cess of 500 individuals would be required to detect
significant changes associated with the treatment method
being evaluated in this study.
In reviewing these analytical models, it would ap-
pear that the "control chart" approach best represents
the experimental situation since:
second shift is associated with specimens showing mod-
erate inflammation. The proportion of such specimens
fluctuated within baseline limits until the eighth week,
at which time significantly less moderate inflammation
was seen. This response, concomitant with a signifi-
cantly increased proportion of mild inflammation speci-
mens at eight weeks, suggests potential benefit, albeit
short-lived, to the patient. The proportion of severe in-
flammation in 30% of the specimens taken at eight
weeks after curettage indicates that the tissue may be
responding once more to the returning plaque.

1. Baseline observations are used to determine the DISCUSSION

proportions of subjects with inflammatory responses;
2. Within short time periods, the oral conditions
should remain relatively stable; and
3. Observations taken on the same individual in
these limited time periods should reflect the baseline
state.
Histologic responses demonstrated that, within the
limits of our experiment, degree of inflammation did
not correlate well with pocket depth, nor could the de-
gree of inflammation at one site predict the degree of
inflammation at an adjacent soft tissue site, even though
pocket depth was matched. These findings confirm
those of Zachrisson and Schultz-Haudt, who stated 11
Volume 42
Number 11
that: " A correlation between the clinical and histologi-
cal diagnoses were found in about 50% of the cases.
Hence, a diagnosis based upon clinical criteria is con-
sidered unreliable when it comes to an evaluation of
the degree of inflammation of the tissue." They further
support similar comparative findings by Sanderson and 4
Stahl and associates. 12
Removal of crevicular epithelium by soft tissue cu-
rettage was not always achieved by our approach. These
findings again support those of Sanderson and K o n4
and associates. However, epithelialization of the pocket
5
wall appeared to be complete within one week after
curettage, which seems more rapid than epithelializa-
tion after gingivectomy when analyzed by similar ap-
proaches. 6
With regard to post-curettage inflammatory fluctua-
tions, Handleman and Hess recently reported that, in
13
humans, the distribution of tooth surface flora after
prophylaxis tended to recur to pre-prophylaxis levels in
30 to 60 days. The inflammatory responses observed in
our specimens within four to eight weeks after curettage
may well reflect tissue reactions to the recurring bac-
terial plaque.
A final comment should be made relative to our use
of individual gingival sites as independent experiences.
Is such an approach valid, particularly since we must
consider the role of the host in periodontal responses to
irritation? The findings cited suggest that the local mi-
lieu is indeed different at each site. Yet we also recog-
nize that host variations exist. F o r example, of 21 i n -
dividuals i n whom oral hygiene was not practiced on
one side of their mouth for 15-17 days, 10 showed
marked inflammation, while 3 exhibited no clinical
signs of inflammation. Increase i n gingivitis has also
14
been noted during menstruation in a longitudinal study
(three months), and more severe or extensive perio-
15
dontal disease has been reported in association with
malnutrition and a g i n g . Since very severe metabolic
1618
stresses interfere significantly with repair of gingival
injury, 19,20
while less severe metabolic shifts apparently
allow for adaptation, ' we might postulate that i n
15 21
healthy patients the local tissue response is essentially
a reaction to the local milieu, while in severe metabolic
stresses the interaction of local and systemic factors be-
comes clinically evident. Thus, in clinical studies tracing
inflammatory shifts, analysis of independent sites may
be an acceptable a p p r o a c h if metabolic shifts within
22,23
the host are within normal variation.
SUMMARY AND CONCLUSION
Eighty suprabony pocket sites were curetted and
root planed in 60 adult patients suffering with perio-
dontitis. Biopsies of these sites were taken at varying
time intervals over an eight-week postoperative period.
Soft Tissue Healing 683
Adjacent pocket sites of similar clinical depth were ex-
cised and served as baseline specimens. A l l tissues were
prepared for histologic study and were graded for epi-
thelialization of the crevicular surface, degree of inflam-
mation adjacent to the crevicular epithelium, and con-
nective tissue status in this area.
No significant correlation could be established be-
tween degrees of inflammation at adjacent pocket sites,
even though pocket depth was similar, nor was pocket
depth significantly correlated to the degree of inflam-
mation at a specific site. Immediately after soft tissue
curettage, crevicular epithelium appeared to have been
either completely removed or disrupted in all specimens.
If epithelium was only disrupted, fragments were usu-
ally seen near the gingival margin. One week after cu-
rettage, crevicular epithelial lining was present i n all
specimens examined. In the early stages after curettage,
an increase in acute inflammatory infiltrate was noted.
A t the eight-week postoperative interval, however, the
inflammatory infiltrate in our specimens appeared simi-
lar in distribution and degree to that observed in non-
treated control samples.
Postoperative inflammatory response was analyzed
using three statistical models. Each model was con-
structed using different assumptions of the host response
during healing. The first model tested shifts in "before to
after" distributions and was concerned only with group
responses. The second model tested shifts from a "base-
line inflammatory level," assuming that the groups ob-
served through varying recovery periods should not
deviate from baseline if curettage was completely inef-
fective. The third model tested for shifts within the in-
dividual, assuming that the "before and after" speci-
mens were comparable.
Tht second model yielded significant changes with
length of recovery time, even for the small samples of
specimens used. This model is consistent with the as-
sumption that individual specimens from the same host
are independent and reflect an "unchanging" inflam-
matory response, given normal metabolic variation. In-
flammatory response at each tooth then may be pri-
marily "controlled" by local factors (i.e., plaque,
trauma, etc.). This assumption, if correct, facilitates the
design and execution of clinical studies tracing inflam-
matory shifts.
REFERENCES
1. Ratcliff, P. A.: Periodontal Therapy, in World Work-
shop in Periodontics, 199, ed. S. P. Ramfjort, D . A . Kerr
and M . A . Ash, University of Michigan, Ann Arbor, pp.
291-298.
2. Stahl, S. S.: Healing of Gingival Tissues Following
Various Therapeutic Regimens—A Review of Histologic
Studies. J. Oral Ther. & Pharm., 2:145, 1965.
684 Stahl, Weiner, Benjamin, Yamada
3. Tandy, R. B.: Gingival Curettage. Periodont. Abstr.,
18:100, 1970.
4. Sanderson, A . : Gingival Curettage by Hand and U l -
trasonic Instruments: A Histologic Comparison. J. Perio-
dont, 37:279, 1966.
5. Kon, S., Novacs, A . B., Ruben, M . P. and Goldman,
H . M . : Visualization of Microvascularization of the Healing
Periodontal Wound. II. Curettage. J. Periodont., 40:96,
1969.
6. Stahl, S. S., Witkin, G . J., Heller, A . and Brown, R.:
Gingival Healing. II. Clinical and Histologic Repair Se-
quences Following Gingivectomy. J. Periodont., 39:109,
1968.
7. Dixon, W. J. and Massey, F. J.: Introduction to Statis-
tical Analysis, ed. New York, McGraw-Hill, 1969, Chapter
17, p. 291.
8. Ibid., Chapter 13, pp. 238-239.
9. Ibid., Chapter 13, pp. 233-234.
10. Egelberg, J. anl Gowley, G . : The Bacterial State of
Different Regions Within the Clinically Healthy Gingival
Crevice. Acta Odont. Scand., 21:289,1963.
11. Zachrisson, B. U . and Schultz-Haudt, S. D.: A Com-
parative Histological Study of Clinically Normal and Chron-
ically Inflamed Gingivae from the Same Individual. Odont.
T., 76-179, 1968.
12. Stahl, S. S., Witkin, G . J., DiCeasare, A . and Brown,
R.: Gingival Healing. I. Description of the Gingivectomy
Sample. J. Periodont., 39:106, 1968.
13. Handleman, S. L . and Hess, C : Effect of Dental
Prophylaxis on Tooth-Surface Flora. J. Dent. Res., 49:340,
1970.
Abstracts
INTRAORAL OCCLUSAL TELEMETRY. PART I V .
TOOTH CONTACT DURING SWALLOWING
Pameijer, J. H . N., Brion, M., Glickman, I. and Roeber, F. W.
J. Prosth. Dent. 24:396, October, 1970
Of six adult patients with intact dentitions, except for a miss-
ing lower molar, four had a discrepancy of 0.75 mm (glide)
between centric jaw relation (with the mandible in its most pos-
terior relationship to the maxillae) and centric occlusion (maxi-
mum intercuspation). The other two subjects had a discrepancy
of 1.5 mm. The missing molar was replaced with a three unit
acrylic resin fixed partial denture which contained a radio trans-
mitter embedded in the pontic with a multilayered switch which
motivated a radio transmitter when it contacted a small gold in-
lay in the opposing tooth. The signals emitted at one of several
frequencies, depending upon which part of the switch was con-
tacted, were picked up by an antenna and fed through receivers
into a six channel oscilloscope. Recordings were obtained while
each subject ate hamburger and drank coffee without instructions
or assistance. The duration of each swallow was computed on the
timer channel. The findings concerning swallowing showed that
contacts of teeth during swallowing were of longer duration than
those during chewing. Contacts of teeth occurred during swallow-
ing in 166 of 182 swallows. There were contacts of teeth in cen-
tric relation in only five of 182 swallows in the study, as com-
pared with 162 contacts in centric occlusion. The five tooth
contacts in centric relation were part of glides which started in
centric occlusion and the contact in centric occlusion was of
longer duration than the brief contact in centric relation during
J. Periodont.
November, 1971
14. Zachrisson, B. U . : A Histological Study of Experi-
mental Gingivitis in Man. J. Periodont. Res., 3:293, 1968.
15. Larato, D . C , Stahl, S. S., Brown, R. and Witkin,
G. J.: The Effect of a Prescribed Method of Toothbrushing
on the Fluctuation of Marginal Gingivitis. J. Periodont., 40:
142,1969.
16. Russel, A . L . : International Nutrition Surveys: A
Summary of Preliminary Dental Findings. J. Dent. Res., 42:
233, 1963.
17. Waerhaug, J.: Prevalence of Periodontal Disease in
Ceylon. Acta Odont. Scand., 25:205,1967.
18. Sheiham, A.: The Prevalence and Severity of Perio-
dontal Disease in Rural Nigerians. Dent. Pract., Dent. Ree.,
17:51, 1966.
19. Stahl, S. S.: The Effect of a Protein Free Diet on the
Healing of Gingival Wounds in Rats. J. Dent. Res., 7:551,
1962.
20. Malberger, E.: Acute Infectious Oral Necrosis among
Young Children in Gambia, West Africa. J. Periodont. Res.,
2:154, 1967.
21. Tiber, A . and Stahl, S. S.: Autoradiographic Evalua-
tion of Gingival Response to Injury. VI. Surgical Trauma in
Long Term, Low Protein-Fed Adult Rats, (In preparation).
22. Ramfjord, S. P., Nissle, R. R., Shick, R. A . and
Cooper, H : Subgingival Curettage Versus Surgical Elimina-
tion of Periodontal Pockets. J. Periodont., 39:167, 1968.
23. Suomi, J. O., Greene, J. C , Vermillion, J. R., Chang,
J. J. and Leatherwood, E. C : The Effect of Controlled Oral
Hygiene Procedures on the Progression of Periodontal Dis-
ease in Adults; Results after Two Years. J. Periodont., 40:
416, 1969.
swallowing. It appeared that for the subjects in this study cen-
tric occlusion rather than centric relation is the physiological
relationship of the dentition during swallowing, however, since
deflective occlusal contacts were present in all subjects it is pos-
sible that this prevented closures into centric relation. The effect
of eliminating deflective occlusal contacts upon the position of
the mandible during swallowing has been reported separately.
Department of Periodontology, Tufts University School of D e n -
t a l M e d i c i n e , Boston, Massachusetts 02111.
GLYCOGEN GRANULES IN T H E PERIODONTAL AND B O N E
C E L L S DURING PERIODONTAL DISEASE
Michel, C. and Frank, R. M .
Paradont. Acad. Rev. 24:3, March 1970 (French;
summaries in French and English)
Biopsies of marginal and deep interdental septa are made by
means of chisels or rongeurs and prepared for electron micro-
scopic examination. The presence of glycogen granules within
the cytoplasm of fibrocytes and lining osteoblasts is a constant
finding in all the cells of the periodontium. Sometimes, some
glycogen granules could be detected between the collagen fibre
bundles, while the neighboring cells showed in the break-down of
the cytoplasmic membrane. The osteocytes of the alveolar bone
presented a large accumulation of glycogen granules which is
considered as being one of the first manifestations of periodontal
disease in alveolar bone. Centre de Recherches odontologiques,
E q u i p e de Recherche associee du C N R S , Strasbourg, France.