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The Impact of the Stone Age Diet on Gingival Conditions in the Absence of Oral Hygiene


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The objective of this study was to assess the oral microbiota and clinical data in subjects without access to traditional oral hygiene methods and who ate a diet available in the Stone Age. Ten subjects living in an environment replicating the Stone Age for 4 weeks were enrolled in this study. Bleeding on probing (BOP), gingival and plaque indices, and probing depth (PD) were assessed at baseline and at 4 weeks. Microbiologic samples were collected at the mesio-buccal subgingival aspects of all teeth and from the dorsum of the tongue and were processed by checkerboard DNA-DNA hybridization methods. No subject had periodontitis. Mean BOP decreased from 34.8% to 12.6% (P <0.001). Mean gingival index scores changed from 0.38 to 0.43 (not statistically significant) and mean plaque scores increased from 0.68 to 1.47 (P <0.001). PD at sites of subgingival sampling decreased (mean difference: 0.2 mm; P <0.001). At week 4, the total bacterial count was higher (P <0.001) for 24 of 74 species, including Bacteroides ureolyticus, Eikenella corrodens, Lactobacillus acidophilus, Capnocytophaga ochracea, Escherichia coli, Fusobacterium nucleatum naviforme, Haemophilus influenzae, Helicobacter pylori, Porphyromonas endodontalis, Staphylococcus aureus (two strains), Streptococcus agalactiae, Streptococcus anginosis, and Streptococcus mitis. Bacterial counts from tongue samples were higher at baseline (P <0.001) for 20 species, including Tannerella forsythia (previously T. forsythensis), Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans; serotype a), and Streptococcus spp. The experimental gingivitis protocol is not applicable if the diet (e.g., Stone Age) does not include refined sugars. Although plaque levels increased, BOP and PD decreased. Subgingival bacterial counts increased for several species not linked to periodontitis, whereas tongue bacterial samples decreased during the study period.
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on Gingival Conditions in the Absence
of Oral Hygiene
Stefan Baumgartner,* Thomas Imfeld,
Olivier Schicht,
Christian Rath,
Rigmor E. Persson,*
and G. Rutger Persson*
Background: The objective of this study was to assess the oral
microbiota and clinical data in subjects without access to traditional
oral hygiene methods and who ate a diet available in the Stone Age.
Methods: Ten subjects living in an environment replicating the
Stone Age for 4 weeks were enrolled in this study. Bleeding on probing
(BOP), gingival and plaque indices, and probing depth (PD) were
assessed at baseline and at 4 weeks. Microbiologic samples were col-
lected at the mesio-buccal subgingival aspects of all teeth and from
the dorsum of the tongue and were processed by checkerboard
DNA-DNA hybridization methods.
Results: No subject had periodontitis. Mean BOP decreased from
34.8% to 12.6% (P<0.001). Mean gingival index scores changed
from 0.38 to 0.43 (not statistically significant) and mean plaque
scores increased from 0.68 to 1.47 (P<0.001). PD at sites of subgin-
gival sampling decreased (mean difference: 0.2 mm; P<0.001). At
week 4, the total bacterial count was higher (P<0.001) for 24 of 74
species, including Bacteroides ureolyticus,Eikenella corrodens,Lac-
tobacillus acidophilus,Capnocytophaga ochracea,Escherichia coli,
Fusobacterium nucleatum naviforme,Haemophilus influenzae,Helico-
bacter pylori,Porphyromonas endodontalis,Staphylococcus aureus
(two strains), Streptococcus agalactiae,Streptococcus anginosis,and
Streptococcus mitis. Bacterial counts from tongue samples were higher
at baseline (P<0.001) for 20 species, including Tannerella forsythia
(previously T. forsythensis), Aggregatibacter actinomycetemcomitans
(previously Actinobacillus actinomycetemcomitans; serotype a), and
Streptococcus spp.
Conclusions: The experimental gingivitis protocol is not applicable if
the diet (e.g., Stone Age) does not include refined sugars. Although pla-
que levels increased, BOP and PD decreased. Subgingival bacterial
counts increased for several species not linked to periodontitis, whereas
tongue bacterial samples decreased during the study period. JPeri-
odontol 2009;80:759-768.
Diet; gingivitis; microbiology; periodontitis.
Dental plaque is a com-
plex biofilm accumulat-
ing on teeth and oral
tissues. Environmental and ge-
netic factors are influential in the
development of dental plaque bio-
Although dental plaque
is made up of a large variety of
bacterial species, the coloniza-
tion follows a regimented pat-
tern: adhesion of initial colonizers
to the acquired pellicle, followed
by secondary colonization through
interbacterial adhesion.
It is
well established that many of
the early colonizing bacteria
in the development of dental
biofilms include Actinomyces,
However, microbial
communities in the oral cavity
are polymicrobial.
Many of
the individual microorganisms
in such communities cannot sur-
vive outside that community.
The role of dental plaque in
gingivitis is well established.
Thus, within 8 days of the begin-
ning of plaque accumulation, an
early lesion exhibiting many fea-
tures characteristic of delayed
hypersensitivity develops.
creased gingival crevicular fluid
during gingivitis affects pellicle
formation, and increased plasma
proteins in the pellicle may modify
* Laboratory of Oral Microbiology, Department of Clinical Research, School of Dental Medicine,
University of Bern, Bern, Switzerland.
† Department of Preventive Dentistry, Periodontology, and Cariology, Center for Dental Medicine,
University of Zu
¨rich, Zu
¨rich, Switzerland.
Regional Clinical Dental Research Center, University of Washington, Seattle, WA.
§ Department of Oral Medicine, University of Washington.
iDepartment of Periodontics, University of Washington.
doi: 10.1902/jop.2009.080376
J Periodontol • May 2009
bacterial attachment and early dental plaque com-
The complement system may also be ac-
tivated in gingival crevice material from inflamed
Animal studies
showed that diet may play an
important role in the development of gingivitis. Stud-
in humans demonstrated that subjects on a
high-carbohydrate diet developed gingivitis com-
pared to subjects on a low-carbohydrate diet. An in-
crease in dietary sucrose has been associated with
more accumulation of plaque and evidence of gingi-
vitis in humans.
Thus, an assessment of sucrose in-
take followed by appropriate changes in diet seems
appropriate in clinical efforts to reduce the extent of
gingivitis. Studies
also demonstrated that exper-
imental gingivitis and chronic gingivitis may not be
comparable. After 4 weeks of experimental gingivitis,
more plaque accumulation and higher interleukin
(IL)-1blevels, but lower IL-8 levels, were demon-
strated in the gingival crevicular fluid.
Data also
demonstrated that levels of aspartate aminotrans-
ferase in gingival crevicular fluid were much higher
in experimental gingivitis than in chronic gingivitis.
A decrease in the prevalence of gingivitis has been
recognized through the analysis of trends over 30
Nevertheless, high prevalence scores for
supragingival plaque and gingivitis have been re-
ported in adolescent subjects.
The prevalence
of periodontitis seems to have remained virtually
constant during the past 3,000 years in Great Britain,
despite considerable changes in the oral environ-
In an isolated community (Isla Grande, Co-
lombia) with no dental services and a low educational
level, a Community Periodontal Index of Treatment
Needs (CPITN) score of 1 (presence of bleeding on
probing [BOP]) was found in only 18% of subjects,
and 11% presented with probing depths (PDs) 5mm
(CPITN =4).
To the best of our knowledge, there
are no studies on the periodontal and oral microbio-
logic conditions in subjects without access to oral hy-
giene measures or a modern diet.
The purpose of the present longitudinal case series
was to assess the oral microbiota and clinical data in a
cohort of 10 subjects with no access to traditional oral
hygiene methods and who ate a diet available to Stone
Age humans over a 4-week period.
In 2007, Swiss National Television approached fac-
ulty members at the University of Bern and at the Uni-
versity of Zu
¨rich to monitor a group of subjects who
had committed themselves to living in a confirmed en-
vironment replicating that of the Stone Age. Archeo-
logic experts were consulted about the environment,
which included replication of housing, clothing, uten-
sils, and food (fishing and hunting) known from ar-
cheologic sites in Switzerland. The project received
ethics approval (University of Zu
¨rich), and all subjects
signed approved informed consent/assent forms.
These subjects were confined to living conditions that
archeologic experts had identified as typical for Stone
Age humans along the Rhine River. Nutrition and
health experts monitored the daily activities and eat-
ing habits of the participants.
Ten subjects were enrolled, including two families
(husband, wife, and two children each) and two single
young adult males. These volunteers lived under
Stone Age conditions for 4 weeks. Daily television
reports were broadcast about their experiences. A
thorough medical (data not shown) and dental exam-
ination was performed before the study and 4 weeks
All subjects were examined before and after the
4-week study at the University of Zu
¨rich, School of
Dentistry; assessments included extra- and intraoral
examinations, periodontal screening index, and
partial-mouth recording of plaque index (PI)
gingival index (GI).
Thus, PI was recorded in the
first (upper right) and third quadrants, whereas GI
was recorded in the second and fourth quadrants
(lower left) at the University of Zu
¨rich (by OS and
CR). Bitewing radiographs were taken (only at base-
line) of areas for which no recent radiographic docu-
mentation was available, and dental photographs
were taken. At baseline and at week 4, faculty mem-
bers at the University of Bern (GRP and REP) collected
subgingival microbiologic samples at the mesio-
buccal aspects of all teeth present in each subject.
The same examiner took the bacterial samples and
recorded the measurements of the subject at both
visits. The examiners had no access to baseline data
or the results from the other center. It was not possible
to mask them in terms of the order of examination.
None of the subjects had access to toothbrushes,
toothpaste, dental floss, toothpicks, or other oral hy-
giene products during the study period. No advice was
given about how to clean teeth without access to such
oral hygiene aids; the use of twigs and any other nat-
ural material was allowed. Swiss television crews and
security guards ensured that all subjects maintained
the appropriate lifestyle for Stone Age humans.
Stone Age Diet and Living Conditions
The study subjects signed a contract with the Swiss
television system. The environment was developed
by anthropologists to be as similar as possible to what
had been identified in archeologic findings from an
area close to the Rhine River in Switzerland and dated
early Stone Age or between ;4000 and 3500 BC. Liv-
ing quarters, clothing, tools, and types of food stock
were provided as known from archeologic findings
in the region. Therefore, the diet was restricted to
Natural Experimental Gingivitis Volume 80 • Number 5
include a basic supply of whole grains of barley,
wheat, spelt (‘‘einkorn,’’ ‘‘emmer’’ =local ancient ag-
ricultural wheat), some salt, herbs, honey, milk, and
meat from domestic animals (goats and hens). A
hunter would shoot one of the goats at the partici-
pants’ request. This food supply would not provide
the participants with a full diet over 4 weeks. Hence,
they were forced to seek supplemental food from na-
ture, including berries, edible plants, and fish without
nets. A sports medicine physician monitored the sub-
jects. The location was within a nature reservation,
and subjects were restricted in how they could move
and use natural resources. The subjects had to make
fire by themselves. They had no access to refined sug-
ars or modern kitchen utensils. Huts were available for
them as living quarters.
Microbiologic Sampling
All sampled areas were isolated from saliva contam-
ination. Supragingival plaque was gently removed
with a curet.
Subgingival plaque samples were col-
lected with sterile endodontic paper points (size 55)
inserted into the pocket for 20 seconds. Samples were
placed individually in 1.5-ml natural flat-cap micro-
centrifuge tubes free of DNase and DNA and sterile.
Bacterial samples were also collected from the back
of the tongue using sterile swabs,** which were
placed in labeled sterile containers. All samples were
placed in boxes at 4C, transported within 4 hours to
the laboratory, and immediately frozen at -20C.
Following bacterial sampling, clinical PD measure-
ments were made, using Michigan periodontal probes,
at the mesio-buccal aspect of all teeth that had
been sampled. In addition, the extent of bleeding on
probing (BOP) was assessed 10 seconds after prob-
ing. All clinical examinations were performed with
no access to previous data and with no information
about the results of the examinations at the University
of Zu
Microbiologic Processing
We analyzed the samples with the checkerboard
DNA-DNA hybridization technique. Seventy-four
bacterial species were included in the checkerboard
panel (Table 1). The checkerboard DNA-DNA hy-
bridization method was performed as described by
Socransky et al.
For processing, 0.15 ml Tris
EDTA buffer (10 mM Tris-HCl, 1.0 mM EDTA, pH
7.6) was added to each vial with a subgingival bacte-
rial sample; 0.10 ml 0.5 M NaOH was added to each
Eppendorf tube with an oral bacterial sample; and 300
ml Tris EDTA buffer (10 mM Tris-HCl, 1.0 mM EDTA
and pH 7.6) was added to each Eppendorf tube with a
tongue bacterial sample. After 10 minutes, these
samples were sonicated for 10 seconds. Subse-
quently, 200 ml freshly made 0.5 M NaOH was added
to each vial, and the swab was removed.
Bacterial DNA was extracted, concentrated on ny-
lon membranes,
and fixed by cross-linking using ul-
traviolet light.
The membranes with fixed DNA were
placed in a multichannel incubation chamber.
A gel
and blot imaging system
for chemifluorescence-
based methods was used for quantification using a
setting of 200 mm and 600 V. The digitized information
was analyzed by a software program
allowing com-
parison of the density of 19 sample lanes against the
two standard lanes (10
or 10
cells). Signals were
converted to absolute counts by comparisons with
these standards.
The bacteria assayed are identified
as panel 1 and panel 2 (Table 1).
The paired ttest was used to assess changes in the
clinical indices (PD, BOP, GI, and PI) over time. Sub-
ject-based mean values were calculated for each bac-
terial species. The paired-samples ttest was used to
compare bacterial counts between baseline and
week 4. Tongue samples were analyzed with the
Wilcoxon signed-sum rank test. Significance was de-
clared at the P<0.001 level. A statistical software
package was used for the analysis.***
Subject characteristics and clinical data are presented
in Table 2. No subject presented with clinical evidence
of periodontitis. Between baseline and week 4, the
mean percentages of sites with BOP decreased from
34.8% to 12.6% (P<0.001) (Fig. 1). Decreases in
PD were also found at sites from which bacterial sam-
ples were taken (mean difference, 0.2 mm; 95% con-
fidence interval: 0.1 to 0.3 mm; P<0.001). The mean
PI at baseline and 4 weeks (partial-mouth recordings)
was 0.68 and 1.47, respectively (P<0.001). The mean
GI (partial-mouth recordings) at baseline and 4 weeks
was 0.38 and 0.43, respectively (not statistically sig-
nificant). Anterior clinical images are presented for
one of the subjects at baseline (Fig. 2) and at 4 weeks
(Fig. 3).
Tongue samples. The baseline and 4-week distri-
butions of Tannerella forsythia (previously T. forsyth-
ensis), Aggregatibacter actinomycetemcomitans (a)
(previously Actinobacillus actinomycetemcomitans),
and Streptococcus gordonii for the 10 subjects are
Gracey curet 4R/4L, Deppeler, Rolle, Switzerland.
# Starlab, Ahrensburg, Germany.
** Catch-All Sample Collection Swabs, Epicentre, Madison, WI.
†† PCP 11, Hu-Friedy, Chicago, IL.
‡‡ Roche Diagnostics, Mannheim, Germany.
§§ Stratalinker 1800, Stratagene, La Jolla, CA.
ii Miniblotter 45, Immunetics, Cambridge, MA.
¶¶ Storm 840 Fluor-Imager, Amersham Biosciences, Piscataway, NJ.
## ImageQuant, Amersham Biosciences.
*** SPSS 16.0, SPSS, Chicago, IL.
J Periodontol • May 2009 Baumgartner, Imfeld, Schicht, Rath, Persson, Persson
Table 1.
Bacterial Species and Subspecies Included in the DNA-DNA Checkerboard Kit
Species Panel 1 Collection Species Panel 2 Collection
1a. A. actinomycetemcomitans (a) ATCC 29523 1. A. neuii GUH 550898
1b. A. actinomycetemcomitans (Y4) ATCC 43718 2. Aerococcus christensenii GUH 070938
2. Actinomyces israelii ATCC 12102 3. A. vaginalis GUH 290486
3. A. naeslundii (type I +II) ATCC 43146 4. Atopobium parvulum GUH 160323
4. A. odontolyticus ATCC 17929 5. A. vaginae GUH 010535
5. C. gracilis ATCC 33236 6. B. ureolyticus GUH 080189
6. C. rectus ATCC 33238 7. B. biavatii GUH 071026
7. C. showae ATCC 51146 8. Bifidobacterium bifidum GUH 070962
8. Capnocytophaga gingivalis ATCC 33612 9. Bifidobacterium breve GUH 080484
9. C. ochracea ATCC 33596 10. B. longum GUH 180689
10. C. sputigena ATCC 33612 11. Corynebacterium aurimucosum
GUH 071035
11. E. corrodens ATCC 23834 12. Corynebacterium nigricans GUH 450453
12. E. saburreum ATCC 33271 13. Dialister sp. GUH 071045
13a. Fusobacterium nucleatum nucleatum ATCC 25586 14a. E. faecalis GUH 170812
13b. Fusobacterium nucleatum
ATCC 10953 14b. E. faecalis ATCC 29212
13c. F. nucleatum naviforme ATCC 49256 15. E. coli GUH 070903
14. Fusobacterium periodonticum ATCC 33693 16. G. vaginalis GUH 080585
15. L. acidophilus ATCC 11975 17. H. influenzae ATCC 49247
16. L. buccalis ATCC 14201 18. H. pylori ATCC 43504
17. N. mucosa ATCC 33270 19. L. crispatus GUH 160342
18. P. intermedia ATCC 25611 20. L. gasseri GUH 170856
19. P. micra ATCC 19696 21. Lactobacillus iners GUH 160334
20. P. melaninogenica ATCC 25845 22. L. jensenii GUH 160339
21. P. nigrescens ATCC 33563 23. Lactobacillus vaginalis GUH 0780928
22. P. acnes (type I +II) ATCC 11827/28 24. M. curtisii GUH 070927
23. P. gingivalis ATCC 33277 25. Mobiluncus mulieris GUH 070926
24. S. noxia ATCC 43541 26. Peptoniphilus sp. GUH 550970
25. S. aureus ATCC 25923 27. P. anaerobius GUH 160362
26. S. anginosus ATCC 33397 28. P. endodontalis ATCC 35406
27. S. constellatus ATCC 27823 (M32b) 29. Prevotella bivia GUH 450429
28. S. gordonii ATCC 10558 30. P. disiens GUH 190184
29. S. intermedius ATCC 27335 31. P. mirabilis GUH 070918
Natural Experimental Gingivitis Volume 80 • Number 5
presented in Figures 4 through 6, respectively. Anal-
ysis by Wilcoxon signed-sum rank test demonstrated
that higher bacterial counts at baseline (P<0.001)
were found for 20 species, including Actinomyces
neuii,Atopobium vaginae,A. actinomycetemcomi-
tans (serotype a), Actinomyces naeslundii,Campylo-
bacter rectus,Eubacterium saburreum,Leptotrichia
buccalis,Parvimonas micra (previously Peptostrepto-
coccus micros or Micromonas micros), Peptoniphilus
sp., Pseudomonas aeruginosa,Selenomonas noxia,
Staphylococcus aureus,S. gordonii,Streptococcus
intermedius,Streptococcus mitis,Streptococcus
Table 1. (continued)
Bacterial Species and Subspecies Included in the DNA-DNA Checkerboard Kit
Species Panel 1 Collection Species Panel 2 Collection
30. S. mitis ATCC 49456 32. P. aeruginosa ATCC 33467
31. S. oralis ATCC 35037 33a. S. aureus (yellow) GUH 070921
32. S. sanguinis ATCC 10556 33b. S. aureus (white) GUH 070922
33. S. mutans ATCC 25175 34. Staphylococcus epidermidis GUH 130381
34. T. forsythia ATCC 43037 (338) 35. Staphylococcus haemolyticus GUH 071047
35. T. denticola ATCC 35405 36. S. agalactiae GUH 230282
36. T. socranskii D40DR2 37. Varibaculum cambriense GUH 070917
37. Veillonella parvula ATCC 10790
ATCC =AmericanType Culture Collection;D =sample fromForsyth Institute, Boston,Massachusetts; GUH=Ghent University HospitalCollection, Ghent, Belgium.
Ta b l e 2 .
Subject Characteristics at Baseline (BL) and Week 4 (W4)
Subject Age (years) Teeth (N) Time PI
(% sites)
(mm; mean)
(mm; SD)
Father family 1 46 28 BL 0.2 35.7 2.5 0.7
W4 0.8 35.7 2.1 0.7
Mother family 1 45 26 BL 0 34.6 1.7 0.6
W4 0.9 0.0 2.2 0.6
Older child (A) family 1 (female) 18 28 BL 0 17.9 2.1 0.5
W4 0.2 3.6 1.9 0.5
Younger child (B) family 1 (male) 8 23 BL 0.8 47.8 2.1 0.4
W4 0.2 17.4 1.7 0.8
Father family 2 44 28 BL 0.1 10.7 2.6 0.6
W4 0.1 10.7 2.1 0.7
Mother family 2 44 26 BL 0.8 75.0 2.4 0.6
W4 0.5 14.3 2.5 0.6
Older child (C) family 2 (female) 12 26 BL 0.1 0.0 2.4 0.8
W4 0.4 11.5 2.2 0.6
Younger child (D) family 2 (female) 11 23 BL 0 27.3 1.8 0.6
W4 0.2 4.4 1.8 0.7
Young male 1 25 28 BL 0.8 27.3 2.0 0.6
W4 1.5 17.9 2.0 0.6
Young male 2 21 28 BL 0.31 71.4 2.7 0.6
W4 0.53 10.7 2.4 0.5
J Periodontol • May 2009 Baumgartner, Imfeld, Schicht, Rath, Persson, Persson
mutans,Streptococcus oralis,T. forsythia,Treponema
denticola,Treponema socranskii, and for the total
bacterial count. Trends (P<0.01) for higher bacterial
counts at baseline were found for Lactobacillus acid-
ophilus,S. oralis,Campylobacter gracilis,Campylo-
bacter showae,Streptococcus constellatus,S.
mutans,Propionibacterium acnes, Prevotella melani-
nogenica,Streptococcus anginosus,Anaerococcus
vaginalis,Bacteroides ureolyticus,Bifidobacterium
biavatii,Lactobacillus gasseri, and Mobiluncus
curtisii. Higher bacterial counts at week 4 (P<0.001)
were found for Helicobacter pylori and Lactobacillus
crispatus. Trends (P<0.01) for higher bacterial counts
at week 4 were found for Porphyromonas gingivalis
and Enterococcus faecalis.
Subgingival samples. The total bacterial count of
all 74 species was significantly higher at 4 weeks
(P<0.001). The bacterial counts were specifically
higher (P<0.001) for 24 of 74 species, including Ac-
tinomyces odontolyticus,A. vaginae,B. ureolyticus,
Eikenella corrodens,L. acidophilus,Capnocytophaga
ochracea,Dialister sp., Escherichia coli,Fusobacte-
rium nucleatum naviforme,Gardnerella vaginalis,
Haemophilus influenzae,H. pylori,L. crispatus,
Lactobacillus jensenii,N. mucosa,Peptoniphilus
sp., Porphyromonas endodontalis,Prevotella disiens,
Figure 1.
BOP at baseline (BL) and at week 4 for each subject. Data for the
children are given after their parents.
Figure 2.
Anterior clinical image for one of the subjects at baseline.
Figure 3.
Anterior clinical image for the same subject in Figure 2 at 4 weeks.
Figure 4.
Counts of T. forsythia in tongue samples from baseline and week 4.
Only one sample was taken at each time point.
Figure 5.
Counts of A. actinomycetemcomitans (a) in tongue samples from
baseline and week 4. Only one sample was taken at each time point.
Natural Experimental Gingivitis Volume 80 • Number 5
Prevotella mirabilis,Staphylococcus aureus (two
strains), Streptococcus agalactiae,S. anginosus,and
S. mitis and illustrated for three selected species with
significant differences between baseline and week 4
and based on bacterial distributions among the 10
subjects (Figs. 7 through 9). Trends of higher counts
(P<0.01) at week 4 were also noted for the following
species: Capnocytophaga sputigena,Peptostrepto-
coccus anaerobius,Prevotella intermedia,Prevotella
nigrescens,S. oralis,andStreptococcus sanguinis.
At week 4, lower counts (P<0.001) were found for A.
naeslundii,Bifidobacterium longum,andL. buccalis.
Through daily television broadcastings it became ob-
vious that the participating subjects were mainly oc-
cupied by tasks such as searching for and preparing
food, as well as conserving energy. The lack of access
to detergents and water was obvious. They had been
provided a stock supply of cereals, wild fruits, nuts,
herbs, wild mushrooms, honey, some salt, and dried
meat. They had no access to refined sugars or modern
kitchen utensils and had to prepare food over an open
Figure 6.
Counts of S. gordonii in tongue samples from baseline and week 4.
Only one sample was taken at each time point.
Figure 7.
Box plot diagram illustrating the distribution of subgingival samples of
P. endodontalis at baseline (BL) and P. endodontalis at week 4 (W4)
as calculated from all sites examined in each subject (=outlier value;
*=extreme outlier value). Unit of measure for y axis 10
Figure 8.
Box plot diagram illustrating the distribution of subgingival samples of
F. nu c l e a t um nav i f o r m e at baseline (BL) and at week 4 (W4) as
calculated from all sites examined in each subject (=outlier value; * =
extreme outlier value). Unit of measure for y axis 10
bacterial cells.
Figure 9.
Box plot diagram illustrating the distribution of subgingival samples of
H. pylori at baseline (BL) and at week 4 (W4) as calculated from all
sites examined in each subject (=outlier value; * =extreme outlier
value). Unit of measure for y axis 10
bacterial cells.
J Periodontol • May 2009 Baumgartner, Imfeld, Schicht, Rath, Persson, Persson
fire. Some of the subjects used twigs to clean their
teeth. The data demonstrated that the use of such oral
hygiene tools was highly insufficient to prevent further
accumulation of supragingival dental plaque, as il-
lustrated by an increase in PI. Although some of
the clinical measurements were taken only from the
mesio-buccal aspects, the use of twigs was also insuf-
ficient at these sites, which might have been the easi-
est ones to clean.
The consequence of having no access to modern
oral hygiene methods is reflected by the increase in
supragingival plaque scores. However, this increase
was not accompanied by an anticipated increase in
the severity of gingival inflammation. The insignifi-
cant increases in the subjects’ mean GI from 0.38 to
0.43, with a decrease in BOP scores as well as a slight
decrease in PDs, was not expected.
Different patterns of bacterial changes were ob-
served between the tongue and subgingival samples.
For tongue samples, higher bacterial counts of S.
gordonii and S. mitis were found at baseline, whereas
higher counts at week 4 compared to baseline in sub-
gingival samples were found only for S. mitis. This dif-
ference may have to do with differences in nutrition
and the requirement for sugars between these two
bacteria. In contrast, P. endodontalis was found at higher
levels in tongue and subgingival samples at week 4
compared to baseline. S. oralis was found at higher
counts at baseline samples from the tongue, but at
higher counts at week 4 in subgingival samples. This
may also have to do with differences in access to
nutrients as an effect of diet changes among the sub-
jects. Counts of A. actinomycetemcomitans (Y4) and
T. denticola were higher at baseline than at week 4 in
samples from the tongue; they did not undergo
changes in the subgingival samples. S. mutans and
S. gordonii were found at higher counts in samples
from the tongue at baseline, but no changes were
noted in subgingival samples. The reductions of T.
forsythia (Fig. 4) and S. gordonii (Fig. 6) in the tongue
samples were consistent among all subjects. The
changes in the levels of A. actinomycetemcomitans
(a) were not as obvious. The adolescent and children
in the study (subjects 3, 4, 7, and 8) did not seem to
differ from the adults in terms of bacterial changes.
The fact that a more pathogenic microbiota, com-
monly found in tooth decay and gingivitis/periodonti-
tis, was not present may have several explanations.
The lack of access to refined sugars could have had
an impact on sugar-fermenting bacteria and biofilm
development associated with disease. Honey was
the primary source of sugar. The findings reported
here are consistent with earlier studies
on car-
bohydrate restriction. Dietary sugar restriction seems
to be an appropriate measure to reduce the extent of
gingivitis, whereas a carbohydrate-rich diet increases
the severity of gingivitis.
A diet rich in sucrose
seems to enhance plaque accumulation, whereas a
glucose-rich diet seems to have marginal effects.
The assessment of dietary habits was difficult be-
cause an analysis of the percentage or weight of car-
bohydrates, fat, proteins, and calories for the specific
stock supply of dried fruits, nuts, grains, mushrooms,
dried meat, and so forth was not possible. The sub-
jects lost between 1 and 5 kg of body weight and a re-
duction in blood pressure was noted (data not shown)
during the 1-month period.
These subjects had been eating a normal Swiss diet
prior to enrollment in the project. The Swiss diet is
commonly rich in carbohydrates and fat. We hypoth-
esized that the changes in the clinical and microbio-
logic parameters were the effects of diet and life
conditions in general.
Although honey contains glucose and sucrose, it
seems to have antibacterial properties against viri-
dans streptococci.
Phenolic compounds in honey
may exert antibacterial activity.
Through its capac-
ity to reduce levels of reactive oxygen species, honey
seems to have antibacterial properties against P.
However, in the present study, counts
of P. aeruginosa increased in subgingival samples.
P. aeruginosa has been associated with periodonti-
Data have also shown that honey reduces blood
lipids, homocysteine, and C-reactive protein in nor-
mal and hyperlipidemic subjects.
Reductions in sys-
tolic and diastolic blood pressures were found among
the participating subjects (data not shown).
Dog rose, sour cherries, blackberries, strawberries,
raspberries, and blueberries are high in antioxi-
Flavonoids are commonly found in fruit,
vegetables, nuts, seeds, stems, flowers, tea, wine,
and honey. For centuries, preparations containing
these compounds have been used to treat human dis-
eases. Various structures of flavonoids may possess
antifungal, antiviral, and antibacterial activity.
Cereals and berries were primary food sources for
the subjects. Cereals and berries are rich in polyphe-
nols with anti-inflammatory properties.
found in nature and cereals were sought by the sub-
jects. They also consumed mushrooms. Data suggest
that mushrooms can modulate immune responses,
resulting in more enhanced innate and acquired dis-
ease resistance.
It was not assessed whether psychologic stress was
a major component during the 4 weeks. The 4 weeks
away from daily life might have been a positive factor
for the participants. The current level of stress and
psychosocial variables indicative of stress suscepti-
bility do not seem to account for variability in plaque
accumulation and gingival inflammation during ex-
perimental gingivitis in young adults.
The impact
of stress on experimental or persistent gingivitis might
Natural Experimental Gingivitis Volume 80 • Number 5
also be very different.
Furthermore, the impact on
inflammation in experimental gingivitis may be differ-
ent from that of persistent gingivitis.
The design of experimental gingivitis usually in-
cludes an initial phase in which subjects are provided
instruction about oral hygiene to reduce gingival in-
flammation, followed by a period of no hygiene.
jects entered into the present study without an initial
phase of attempting oral hygiene improvements to re-
duce gingival inflammation. This was reflected by an
average BOP score of 34.8%. Therefore, in our first
hypothesis, prior to the initiation of the study, we an-
ticipated that abstinence or further insufficient oral hy-
giene measures would result in a significant increase
in PD, BOP, GI, and PI. The data demonstrated that this
was only true for PI. Therefore, we believe that other fac-
tors compensated for the lack of access to toothbrushes,
toothpaste, dental floss, toothpicks, and mouthrinses.
Among the volunteers who participated in the
4-week experiment that qualifies as a modified exper-
imental gingivitis study, there was no clinical evi-
dence of increased gingival inflammation, despite
increasedsupragingival plaquelevels. Despite increas-
ing plaque scores, PD and BOP values decreased over
Four of the participants were children or adoles-
cents. Thus, it is possible that the impact of transition
from deciduous teeth to permanent teeth or hormonal
effects in young individuals had an impact on the
measurements. However, we found no trends of differ-
ences that specifically suggested that changes in con-
ditions among these four subjects were different from
the older subjects.
The subgingival microbiota did not change with an
enhanced bacterial colonization; increases in the
counts of bacteria associated with periodontitis or
tooth decay were not found. The primary explanation
for why these subjects did not develop evidence of in-
creased gingivitis must be the sugar intake restriction
and the intake of food items rich in antibacterial and
anti-inflammatory components. Thus, the traditional
experimental model published in hundreds of studies
may only be applicable if the subjects maintain a
Western diet rich in sugar and low in anti-inflamma-
tory foods. These data are based on a small sample,
however. Nevertheless, the findings are worthy of fur-
ther research to assess how diet restriction in experi-
mental gingivitis studies influences the results. The
presented hypothesis that sugar restriction and the
supplemental intake of antioxidants and flavonoids
are important dietary guidelines for subjects with gin-
givitis and periodontitis may be extremely important.
Studies of indigenous populations with regard to gin-
gival inflammation and oral bacterial colonization
may be crucial to understand the development of gin-
givitis and its progression to periodontitis.
The present observations support the concept that di-
etary factors are important in the control or develop-
ment of gingivitis, in the absence of oral hygiene
measures, over 4 weeks. Therefore, the experimental
gingivitis model commonly used without dietary con-
trol may have significant limitations. Although plaque
levels increased, decreases in BOP and PDs were
found. Diet restriction, coupled with abstinence from
oral hygiene, did not result in increased gingival in-
flammation; however, it did result in increases in bac-
terial counts in subgingival samples and decreases in
counts in samples from the tongue. The increase in
subgingival samples did not include species commonly
associated with periodontitis. Specifically, counts of
Streptococcus species decreased in tongue samples
over time.
The Clinical Research Foundation, University of Bern,
supported this study. The authors express their ap-
preciation to Ms. Marianne Weibel and Ms. Regula
Hirschi-Imfeld, Laboratory of Oral Microbiology,
University of Bern, for their dedicated laboratory
processing of the study material. The authors report
no conflicts of interest related to this study.
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Correspondence: Dr. Thomas Imfeld, Department of Pre-
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Medicine, University of Zu
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Submitted July 10, 2008; accepted for publication De-
cember 19, 2008.
Natural Experimental Gingivitis Volume 80 • Number 5
... While for several decades, the destruction of bacterial biofilms has been the major focus of periodontal therapy and is still the proposed as the treatment of choice 3 , there is growing evidence that dental plaque may not be the true cause of gingivitis 4 . In this context, a landmark study conducted under stone-age conditions (simulated from archeological findings between 4000-and 3500 BC) found that gingival inflammation decreased due to stone-age dietary pattern, even in the absence of any plaque control measures and higher dental plaque values 5 . Available nutrition during this stone-age setting included whole grains from resident grain like barley, wheat and spelt, herbs, honey, milk, salt and meat from goats and hens. ...
... Available nutrition during this stone-age setting included whole grains from resident grain like barley, wheat and spelt, herbs, honey, milk, salt and meat from goats and hens. The authors concluded that the relation between plaque and gingival inflammation might not be valid under a diet omitting processed foods, in particular refined sugars 5 . Meanwhile, it has been found that the gingivitis-associated biofilm (predominantly represented by anaerobic, proteolytic bacteria) is highly depended on inflammatory processes resulting in a higher exudation of gingival crevicular fluid 6 . ...
... The experimental group was placed on an AID for 4 weeks after 2 transitional weeks, whereas the control group was instructed to continue their habitual PID for another 6 weeks. The duration of 4 weeks for the experimental group was chosen based on other comparable studies 5,12 . The recommended diet for the experimental group was low in processed carbohydrates and animal products, and rich in fibers, omega-3 fatty acids (by a daily portion of fish or an omega-3 supplement), vitamin C and D, antioxidants, and plant nitrates 10 . ...
Full-text available
A previous randomised controlled trial showed that an anti-inflammatory diet (AID) significantly reduced gingival inflammation despite constant plaque values. This exploratory study investigated the role of serum fatty acids in relation to the observed clinical effects. Therefore, data of thirty participants with gingivitis, following either a pro-inflammatory dietary pattern (PID) rich in saturated fat, omega 6 fatty acids, and refined carbohydrates or an AID for 4 weeks, were correlated with corresponding serum samples for a variety of fatty acids. Changes in the fatty acid profile and effects on clinical periodontal parameters were analysed. Results showed that the polyunsatured:saturated fatty acids ratio (PUFA:SFA ratio) and nervonic acid level were significantly higher in the AID group than in the PID group at the end of the study. Significant intragroup differences were seen only in the AID group. Diverse fatty acids showed heterogeneous relations to clinical parameters. This study demonstrated that the serum fatty acid profile was not fundamentally associated with the clinical gingivitis-lowering effects of an AID in short-term, although some fatty acids showed individual relations to clinical parameters with respect to inflammation. Hence, short-term effects of dietary therapy on gingivitis may be rather based on carbohydrate-related effects and/or micronutrients.
... A healthy diet was directly associated with lower values of initial periodontitis, suggesting the involvement of systemic mechanisms of the role of diet in periodontal health. Clinical studies have shown that a healthy diet reduces gingival inflammation, regardless of the biofilm and oral microbiome (Baumgartner et al., 2009;Woelber et al., 2017Woelber et al., , 2019. Our findings identified the direct association between a healthy diet and lower values of periodontitis, with a dose-response effect. ...
... Furthermore, while using time-related data, it is noteworthy that the FFQ included data regarding the regular consumption of the past year, and the outcomes included data on gingival bleeding and PD, reflecting a sustained periodontal disease activity at the time of the examination (Lang & Bartold, 2018). Randomized clinical trials have shown that change to a healthier dietary pattern was able to reduce BoP and PPD in 4 weeks (Baumgartner et al., 2009;Woelber et al., 2017Woelber et al., , 2019. Hence, the reverse causality mechanism is improbable in our study because it is unlikely that initial periodontitis has influenced the adolescents' dietary choices, as periodontitis is an asymptomatic disease in its early stages (Tonetti et al., 2017) and tooth loss in the studied sample is trivial (only 0.59% of the sample had <20 teeth) (Naka et al., 2014). ...
Aim: To investigate pathways between unhealthy and healthy dietary patterns with periodontitis in adolescents (18-19 years). Methods: This population-based study (n=2,515) modeled direct and mediated pathways (via biofilm and obesity) from patterns of Healthy Diet (fruits, fiber, vegetables, and dairy) and Unhealthy Diet (sugars, snacks, salty/fast foods) with Initial Periodontitis (bleeding on probing (BoP), probing depth (PD) ≥ 4mm, clinical attachment loss (CAL) ≥ 4mm), Moderate Periodontitis (BoP, PD ≥ 5 mm and CAL ≥ 5 mm) and EFP-AAP Periodontitis definition at, adjusting for sex, socioeconomic status, smoking, and alcohol, through structural equation modeling (alpha=5%). Results: Higher values of Healthy Diet were associated with lower values of Initial [Standardized Coefficient (SC) = -0.160; p< 0.001], Moderate Periodontitis (SC = -0.202; p<0.001), and EFP-AAP periodontitis (p<0.05). A higher value of Unhealthy Diet was associated with higher values of Initial (SC = 0.134; p=0.005) and Moderate Periodontitis (SC = 0.180; p<0.001). Biofilm mediated the association between higher values of Unhealthy Diet and all periodontal outcomes (p<0.05). Conclusion: Our findings suggest healthy and unhealthy dietary patterns may contribute to reduced or increased extent and severity of periodontitis by local and systemic mechanisms, preceding the effect of other established causes, like smoking and obesity, in younger.
... A 2014 study indicated that refined sugar intake among adults in the United States has risen by more than 30% over the past three decennia [71]. Recent evidence suggests that consumption of high-glycemic foods alone might increase gingival and periodontal inflammation and bleeding as well, while a diet abundant in complex carbohydrates, with no increase in total energy intake, may lower the risk of gingivitis and periodontitis [72][73][74][75][76][77]. A seminary investigation has indicated that refined carbohydrates are a risk factor for both caries and periodontal disease. ...
Full-text available
Over the last few decades, studies on the oral microbiome have increased awareness that the balance between the host and the microbial species that coexist in it is essential for oral health at all stages of life. However, this balance is extremely difficult to maintain, and many factors can disrupt it: general eating habits, sugar consumption, tobacco smoking, oral hygiene, and use of antibiotics and other antimicrobials. It is now known that alterations in the oral microbiota are responsible for developing and promoting many oral diseases, including periodontal disease. In this context, diet is an area for further investigation as it has been observed that the intake of particular foods, such as farmed animal meat, dairy products, refined vegetable oils, and processed cereals, affects the composition of the microbiota, leading to an increased representation of acid-producing and acid-tolerant organisms and periodontal pathogens. However, little is known about the influence of diet on the oral microbiome and the creation of a suitable microenvironment for the development of periodontal disease. The aim of the present study is to evaluate current knowledge on the role of diet in the oral dysbiosis underlying periodontal disease.
... Distinguishing the existing evidence on caries and periodontitis prevention with regard to evolutionary dentistry, there is already significant evidence for the efficacy of causal therapies: -Dietary patterns focusing on a higher intake of non-processed (fibrous and antioxidantrich) and an avoidance of processed foods were consistently shown to reduce gingival inflammation-even despite constant or higher plaque values [99][100][101][102]. Whole-food diets were shown to reduce periodontal pathogens without any additional mechanical therapy [103,104]. ...
Full-text available
Plaque control is one of the most recommended approaches in the prevention and therapy of caries and periodontal diseases. However, although most individuals in industrialized countries already perform daily oral hygiene, caries and periodontal diseases still are the most common diseases of mankind. This raises the question of whether plaque control is really a causative and effective approach to the prevention of these diseases. From an evolutionary, biological, and nutritional perspective, dental biofilms have to be considered a natural phenomenon, whereas several changes in human lifestyle factors during modern evolution are not "natural". These lifestyle factors include the modern "Western diet" (rich in sugar and saturated fats and low in micronutrients), smoking, sedentary behavior, and continuous stress. This review hypothesizes that not plaque itself but rather these modern, unnatural lifestyle factors are the real causes of the high prevalence of caries and periodontal diseases besides several other non-communicable diseases. Accordingly, applying evolutionary and lifestyle medicine in dentistry would offer a causative approach against oral and common diseases, which would not be possible with oral hygiene approaches used on their own.
... Furthermore, this field is still quite uninvestigated, with a lot of unknown helpful knowledge which could empower everyone's lives in regard to oral and overall health. This also applies to the pathogenicity of oral biofilms (dental plaque) and the corresponding host resistance, whereby initial nutritional studies no longer see any or only a very weak correlation between plaque and oral diseases, like caries and periodontal inflammation, in natural or optimized dietary environments [9][10][11]. Future studies will also have to consider the application and development of new statistical methods in order to deliver a sufficient picture of the connections [20,30]. ...
Full-text available
Nutrition is, like oxygen, one of the basic requirements for animals and, accordingly, Homo sapiens to live [...]
... Sporcu içecekleri, sporcuların ağız sağlığını olumsuz etkileyebilecek başlıca besin öğesi olarak görülmektedir.53 Bu içeceklerin, yüksek karbonhidrat içeriğinin proinflamatuar etki göstererek dişeti hastalıklarına neden olabileceği ifade edilmiştir.70 2.2.7. ...
Full-text available
Aim: The purpose of this study is to analyse the results of some skiers from some cities (Bursa, Erzurum, İstanbul, Kars and Kayseri) in the Turkey Championship who competed in the branch of Alpine Skiing between 2005 and 2013. Material and method: The data of this study was taken from the competition results section of official website of Turkish ski federation ( tr). Race results were analysed according to years, cities, athlete categories and the type of the race. SPSS 15 packet program was used while analysing the data. Results: There was a decrease in the number of athletes who attended to The Turkey Championship from Bursa 0.9%, Erzurum 40.84%, Kars 75.71%, Kayseri 71.5% while İstanbul was the only city that saw an increase by 65,31 percent. When looking at the numbers of athletes who were in the top ten , Bursa, Erzurum, Kars and Kayseri had the most athletes in 2006 season while İstanbul had the most in 2011 with 71 athletes. When looking at the numbers of medals Istanbul has the most gold and silver medals while Erzurum has the most bronze medals. According to the race results in children categories İstanbul, has a considerable superiority. In junior and senior categories Erzurum and bursa have the superiority. Conclusion: Istanbul, which is the only city that does not have a ski resort among these cities has the superiority in substructure in comparison to other cities thanks to the planning and a full year of training with both skiing and not skiing. However, atlhletes’ quitting sports in the following years and continuing their education abroad shows a nonsustaining success. In other cities, athletes’’ success especially after gençler category is because of their acceptance of sport as a profession. Key Words: Alpine Discipline, Ski, Turkish Championship
... Future studies should try to confirm the correlation of easy evaluation screening tools such as the MEDAS with oral inflammatory parameters to provide adherence evaluation tools for use in clinical research and clinical practice. Although the diet affects inflammation [9][10][11][12][13], the common dental therapeutic goal of low plaque values may be oversimplified because it does not address possible malnutrition, which can also lead to other nonoral diseases. Plaque scores are regularly discussed with patients and are used to motivate patients to increase oral hygiene procedures. ...
Full-text available
This study aimed to evaluate the Mediterranean Diet Adherence Screener (MEDAS) in a study investigating the anti-inflammatory effect of a 6-week Mediterranean diet intervention on periodontal parameters. Data from a randomized clinical trial were analyzed for correlations between the MEDAS score and oral inflammatory parameters (bleeding on probing (BOP), gingival index (GI), and periodontal inflamed surface area (PISA)) and select nutrient intakes estimated by a food frequency questionnaire (FFQ) and a 24-h dietary recall (24dr). A mixed model, calculations of Spearman ρ, Lin’s Concordance Coefficient (CC), and Mann–Whitney U test were used for the statistical analyses. The MEDAS score was significantly negatively correlated with periodontal inflammation (BOP: CoE −0.391, p < 0.001; GI −0.407, p < 0.001; PISA −0.348, p = 0.001) and positively correlated with poly unsaturated fatty acids/total fat, vitamin C, and fiber intake estimates obtained from the FFQ and 24dr (ρ 0.38–0.77). The FFQ and 24dr produced heterogeneously comparable intake results for most nutrients (CC 0–0.79, Spearman ρ 0.16–0.65). Within the limitations of this study, the MEDAS was able to indicate nutritional habits associated with different levels of periodontal inflammation. Accordingly, the MEDAS can be a sufficient and useful diet screener in dental studies. Due to its correlation with oral inflammatory parameters, the MEDAS might also be useful in dental practice.
Full-text available
According to the new classification, periodontitis is defined as a chronic multifactorial inflammatory disease associated with dysbiotic biofilms and characterized by progressive destruction of the tooth‐supporting apparatus. This definition, based on the current scientific evidence, clearly indicates and emphasizes, beside the microbial component dental biofilm, the importance of the inflammatory reaction in the progressive destruction of periodontal tissues. The idea to modulate this inflammatory reaction in order to decrease or even cease the progressive destruction was, therefore, a logical consequence. Attempts to achieve this goal involve various kinds of anti‐inflammatory drugs or medications. However, there is also an increasing effort in using food supplements or so‐called natural food ingredients to modulate patients’ immune responses and maybe even improve the healing of periodontal tissues. The aim of this chapter of Periodontology 2000 is to review the evidence of various food supplements and ingredients regarding their possible effects on periodontal inflammation and wound healing. This review may help researchers and clinicians to evaluate the current evidence and to stimulate further research in this area.
The gut microbiome is critical for overall human health. Many factors can disturb the gut microbiome and create dysbiosis. Both the mucous layer and the gut epithelial lining, which collectively serve as the gastrointestinal mucosal border, can be structurally degraded by gut dysbiosis. Increased intestinal permeability and compromised host resistance can ensue. Since all mucosal tissues in the body participate in cross-talk, other organ systems can be affected according to genetic predispositions and an increase in systemic chronic inflammation. The manifestation of named chronic diseases is the ultimate outcome. In this case, symptoms of various chronic diseases must be addressed. Specifically, periodontal disease, which is a chronic disease, must be understood and treated appropriately because it can become a second nidus of infection along with the primary nidus emanating from gut dysbiosis. However, the mystery of treatment does not only require medical intervention, although medical treatment for acute disease is critical. Essential treatment for this scenario usually includes a dietary and lifestyle solution to restore healthy gastrointestinal tract function. Unraveling the mystery of treatment involves introducing viable probiotics and prebiotics; removing elements of an inflammatory diet; providing necessary nutrients and nourishment for cellular function, eliminating toxic elements and chemicals; and creating a healthy lifestyle of stress reduction, restorative sleep, and efficient exercise.
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Purpose of review To evaluate the impact of healthy dietary patterns compared to the Western diet on periodontal indices in adults, used in the prevention and treatment of periodontal diseases. Recent findings Four RCTs and seven case–control studies were included on a critical appraisal of the evidence using GRADE, based on random effects meta-analysis by methodological subgroups for periodontal indices, and a narrative synthesis. There is a clinically significant reduction on bleeding on probing, Gingival Index and periodontal inflamed surface area, Calculus and Debris Index and incidence of tooth loss on healthy dietary patterns group, with a very low to moderate certainty of the evidence. Methodological complementation between included studies allows to consider “real-world data” that RCTs ignore, which have a significant effect on this association. Although biological plausibility is reported, more studies are required to clarify these results. Summary healthy dietary patterns could impact on periodontal health–disease status, reducing the global burden of periodontal diseases by improving the results of the standard care actions, such as toothbrushing, interdental cleaning and periodontal therapy. Further research is required to improve the quality of the evidence.
It has been recognized for some time that bacterial species exist in complexes in subgingival plaque. The purpose of the present investigation was to attempt to define such communities using data from large numbers of plaque samples and different clustering and ordination techniques. Subgingival plaque samples were taken from the mesial aspect of each tooth in 185 subjects (mean age 51 +/- 16 years) with (n = 160) or without (n = 25) periodontitis. The presence and levels of 40 subgingival taxa were determined in 13,261 plaque samples using whole genomic DNA probes and checkerboard DNA-DNA hybridization. Clinical assessments were made at 6 sites per tooth at each visit. Similarities between pairs of species were computed using phi coefficients and species clustered using an averaged unweighted linkage sort. Community ordination was performed using principal components analysis and correspondence analysis. 5 major complexes were consistently observed using any of the analytical methods. One complex consisted of the tightly related group: Bacteroides forsythus, Porphyromonas gingivalis and Treponema denticola. The 2nd complex consisted of a tightly related core group including members of the Fusobacterium nucleatum/periodonticum subspecies, Prevotella intermedia, Prevotella nigrescens and Peptostreptococcus micros. Species associated with this group included: Eubacterium nodatum, Campylobacter rectus, Campylobacter showae, Streptococcus constellatus and Campylobacter gracilis. The 3rd complex consisted of Streptococcus sanguis, S. oralis, S. mitis, S. gordonii and S. intermedius. The 4th complex was comprised of 3 Capnocytophaga species, Campylobacter concisus, Eikenella corrodens and Actinobacillus actinomycetemcomitans serotype a. The 5th complex consisted of Veillonella parvula and Actinomyces odontolyticus. A. actinomycetemcomitans serotype b, Selenomonas noxia and Actinomyces naeslundii genospecies 2 (A. viscosus) were outliers with little relation to each other and the 5 major complexes. The 1st complex related strikingly to clinical measures of periodontal disease particularly pocket depth and bleeding on probing.
Bacteria that attach to surfaces aggregate in a hydrated polymeric matrix of their own synthesis to form biofilms. Formation of these sessile communities and their inherent resistance to antimicrobial agents are at the root of many persistent and chronic bacterial infections. Studies of biofilms have revealed differentiated, structured groups of cells with community properties. Recent advances in our understanding of the genetic and molecular basis of bacterial community behavior point to therapeutic targets that may provide a means for the control of biofilm infections.
矯正治療で便宜抜歯した第一小臼歯のプラーク形成過程での唾液タンパクの推移を1週間にわたって免疫組織学的に検索した。グルタール・アルデハイドで固定した歯を頬舌的に2分割し, パラフィンまたはLR whit eresin包理した後, EDTAで脱灰した。抗全唾液タンパク抗体と抗耳下腺タンパク抗体を用いたstre上ptavidin-biotin染色で, 1日後の菲薄な皮膜中や, それ以後の菌増殖部に唾液タンパクの局在を認めた。免疫電顕法では, その皮膜のdendritic networkを伴うsubsurface layerにも唾液タンパクを認め, その表面の球菌の付着部にも, 線毛で付着しているものを除いて金粒子の介在を認めた。2日以降の著しい細菌増殖に伴って, 唾液タンパクはそれらの細菌間物質中にも局在した。以上から, 唾液タンパクは獲得皮膜の形成に加えて, 同部への細菌付着や細菌凝集に際して, 付着因子や凝集素として機能することが示唆された。
The presence and levels of complement factors C3, C4, C5, and C3 proactivator, were determined by electroimmuno assay in gingival crevice material from five individuals with healthy gingiva and from six patients with chronically inflamed gingiva. Higher concentrations of C3 and C4 were found in samples from chronically inflamed gingiva when compared to those from healthy gingiva. The amount of C3 in material from healthy as well as from inflamed gingiva was related to that in plasma, when the albumin in plasma and gingival crevice material was used as a reference. The same was found for C4 in samples from healthy gingiva but in those from inflamed gingiva, the values were significantly lower when related to plasma levels. C5 could not be found in material from healthy gingiva but was present in material from inflamed gingiva. C3 proactivator was present in material from inflamed gingiva in the converted form. No C3 proactivator was found in material from healthy gingiva with the methods used.Analysis of C3 in samples from inflamed gingiva, using crossed immunoelectrophoresis, showed that C3 was converted in these samples.The results indicate that the complement system may be activated in gingival crevice material from inflamed gingiva.
The periodontal status of a Scottish mediaeval population was studied. No individual over the age of 11 years had an entirely healthy periodontium. While gingivitis was widespread in the younger age groups, it was essentially a “contained” gingivitis which appeared to progress towards a periodontitis at a fairly constant but slow rate. The pattern of prevalence and distribution of gingivitis and periodontitis was similar to many modern epidemiological studies on natural dentitions but did not support the view that the prevalence of periodontitis in historic material was high. A small proportion of individuals appeared to be either susceptible or resistant to periodontal disease. It was concluded that the study of historic material provides valuable information with regard to the natural history of human periodontal disease.
The purpose of the present investigation was to study the sequential stages in the development of a periodontal lesion starting from a healthy periodontium. Twenty inbred Beagle dogs 10 months of age and weighing 10–12 kilos were used. The animals were equally divided into one experimental and one control group. Throughout the experiment all dogs were given a diet containing 400 gm pellets and 25 gm soya flower. From day zero the teeth (in the left jaws) of the control dogs were twice dally subjected to a careful but gentle brushing with tooth brush and dentifrice. The teeth of the experimental group animals were not cleaned. The dogs were examined at regular intervals during an 18 month period. The results show that it is possible in young dogs to induce gingivitis which gradually develops into periodontitis simply by allowing plaque to accumulate on teeth. The cleaned teeth did not show signs of gingivitis or periodontitis during the entire experiment. It is proposed that in the Beagle dog the progression of the lesion during an 18 month period may occur in three stages: I) subclinical gingivitis, II) clinical gingivitis and III) periodontal breakdown. Subclinical gingivitis was characterized by a rapidly increasing gingival exudation and migration of crevicular leukocytes, i. e. signs off acute inflammation. Clinical gingivitis was characterized by changes in gingival colour, texture and bleeding tendency but only minor alterations of the number of crevicular leukocytes. Periodontal breakdown, characterized by loss of subgingival fiber attachment, occurred only in areas of clinical gingivitis.
We first assessed the association of caregiving with gingival symptom reports. We then assessed whether the observed relationship was mediated by psychophysiologic host factors. Caregivers of spouses with Alzheimer's disease (n = 123) were compared with demographically similar noncaregiver spouses (n = 117). The percentage of caregivers (17%) who reported gingival symptoms was twice that of noncaregivers (8.5%) (p < .05), despite the fact that caregivers and noncaregivers did not differ in oral health care. The relationship between caregiving and gingival symptom reports was mediated by psychophysiologic variables. Caregivers were higher on hassles (p < .05), depressed mood (p < .05), and metabolic risk (insulin, glucose, obesity; p < .05) than were noncaregivers. Greater gingival symptom reports were also associated with greater hassles (p < .01), depressed mood (p < .001), and metabolic risk (p < .001). Measures of subcutaneous fat, inflammation, and frank diabetes were related to gingival symptom reports but not to caregiver status. A higher percentage of caregivers reported gingival symptoms than noncaregivers. These results have implications for research on aging, psychophysiology, and chronic stress.