Close
About
FAQ
Home
Collections
Login
USC Login
Register
0
Selected
Invert selection
Deselect all
Deselect all
Click here to refresh results
Click here to refresh results
USC
/
Digital Library
/
University of Southern California Dissertations and Theses
/
The utility of bleeding on probing and 0.25% sodium hypochlorite rinse in the treatment of periodontal disease
(USC Thesis Other)
The utility of bleeding on probing and 0.25% sodium hypochlorite rinse in the treatment of periodontal disease
PDF
Download
Share
Open document
Flip pages
Contact Us
Contact Us
Copy asset link
Request this asset
Transcript (if available)
Content
1
THE UTILITY OF BLEEDING ON PROBING AND
0.25% SODIUM HYPOCHLORITE RINSE IN THE
TREATMENT OF PERIODONTAL DISEASE
By
Stephanie Gonzalez
1
____________________________________________________
A Thesis Presentation to the
FACULTY OF THE USC GRADUATE SCHOOL
UNIVERSITY OF SOUTHERN CALIFORNIA
In Partial Fulfillment of the
Requirements for the Degree
MASTER OF SCIENCE
(CRANIOFACIAL BIOLOGY)
December 2013
Copyright 2013 Stephanie Gonzalez
This work was supported in part by a grant from the Clorox Company ®.
1
Department
of
Periodontology
Contact:
gonza47@usc.edu
University
of
Southern
California
Herman
Ostrow
School
of
Dentistry
Los
Angeles,
CA
90089-‐0641
USA
2
Table of Contents
Summary 3
Highlights 4
Introduction 5
Results 9
Discussion 15
Experimental Procedures 22
Acknowledgments 29
Bibliography 30
Figure and Table Legends 34
Figures and Tables 36
3
Summary
It is important to understand the relationship of bleeding on probing (BOP) to
other traditional measurements of periodontal disease. The purpose of the present study
was to determine if there is a correlation between BOP and plaque score, pocket depth
(PD), or subgingival microbiota. A clinical and microbiological examination was
performed on 30 adults, diagnosed with periodontitis, at baseline (Visit 1), two weeks
(Visit 2) and 3 months (Visit 3). The results indicate that there was a statistically
significant positive correlation between BOP and plaque score, between BOP and PD,
and between BOP and the PD’s >4 mm within each group at all study times (p<0.0001).
No statistically significant differences were found in the microbiota between Visit 1 and
Visit 2 or between test and control groups (p>0.05). It can be concluded that BOP is a
clinical measurement that is strongly correlated to other key indicators of periodontal
disease.
4
Highlights
• Statistically significant positive correlation between BOP and plaque score
• Statistically significant positive correlation between BOP and PD
• Statistically significant positive correlation between BOP and PD of ≥4 mm
• As PD increased, the incidence of BOP also increased
5
Introduction
Periodontitis is an infectious disease of the periodontium that is defined as loss of
the periodontal ligament and alveolar bone. Since painless inflammation and bleeding are
initial signs of periodontitis, the condition may progress unnoticed by an affected
individual. Some types of periodontitis are known to arrest spontaneously; however, if
the disease persists, it can lead to tooth mobility, abscesses, and major tooth loss
(Armitage et al., 2010). The cause of periodontitis involves a combination of putative
periodontal pathogens, usually gram-negative anaerobic rods and herpes viruses, and the
inflammatory response of the host defense (Slots, 2010).
The successful prevention and treatment of periodontal disease involves early
intervention that is safe and efficacious, and instituted by the dental professional in
collaboration with the patient. Treatment of periodontal infection entails removal of
biofilm and subgingival calculus that harbor offending organisms. Periodontal therapy
may range from non-surgical scaling and root planing to various surgical approaches.
Tooth brushing and flossing may provide effective self-care, but these procedures
can be difficult to implement for many patients. The use of chemotherapeutics has
increased with the acknowledgement of microbial specificity in periodontology, and
regimens that involve topical and/or systemic antimicrobials are being increasingly
prescribed in periodontics. In two different clinical studies, oral rinses with dilute sodium
hypochlorite were found to decrease dental plaque by nearly 50% compared to that
detected in water rinse control groups (De Nardo et al., 2010; Lobene et al., 1972).
Sodium hypochlorite, diluted with water, may provide a highly affordable antiseptic rinse
6
that is self-applied, easy-to-use and safe, and which may greatly assist in the control of
periodontal infections.
Periodontitis undergoes periods of exacerbation and remission. While the disease-
active period is of utmost concern, there is uncertainty and lack of precision with current
periodontal diagnostics for identifying real-time presence of the destructive phase.
Investigators have shown some evidence that disease-active periodontitis occurs rather
infrequently.
Lindhe et al. reported that, over a six-year period, attachment loss was identified
in only 12% of untreated periodontitis lesions with most breakdown occurring in 8% of
the study participants (Lindhe et al., 1983). Renvert et al. identified intraosseous
periodontal defects with probing depths of >6 mm. The lesions had been treated with
scaling and root planing alone or by periodontal flap surgery with no subsequent
subgingival treatment. Five years later, non-surgical and surgical sites showed similar
attachment gain, and relapses were first beginning to occur at the end of the 5-year study
(Renvert et al., 1990).
The inability of periodontal diagnostics to avoid errors in determining active
disease, coupled with a low incidence of a destructive phase, may indicate need for
judiciousness in treatment planning and for a “wait and see” attitude after nonsurgical
therapy. Surgical intervention may be needed only if the patient exhibits signs of high
risk or if there is new, clear evidence of advancing periodontal disease.
An active and dependable periodontal maintenance program is a necessity for
assuring proper follow-up care after initial periodontal therapy. Recall intervals are
generally determined by taking into account the periodontal diagnosis along with an
7
estimation of the motivation and capability of the patients to care for their teeth. Rules or
guidelines for recall intervals between periodontal debridement sessions are to a great
extent patient-specific (Beirne et al., 2007). Ideally, the recall intervals should be
established by the healthcare provider based on risk of future periodontal breakdown.
However, reliable tests for predicting disease-active periodontitis have not yet been
developed or tested. A consideration ought to be that, if patients are maintaining
appropriate oral self-care or harbor low levels of periodontal pathogens, the usual 3-6
month periodontal maintenance recall may be prolonged (Listgarten et al., 1989).
Periodontal disease progression has been studied by several investigators who
have sought data on parameters that might be used with predictive value in relation to
active and quiescent phases of periodontitis. Lang et al. determined that periodontal sites
with bleeding on probing (BOP) at four consecutive visits bore a 30% risk of attachment
loss, while those with BOP at only one of four visits had a 3% risk of breakdown (Lang
et al., 1996). Additionally, patients with bleeding in less than 10% of tooth sites have a
generally low risk of disease, while those with bleeding in more than 25% of tooth sites
may require shorter recall intervals for more frequent professional maintenance care
(Lang et al., 1996).
Rams et al. conducted a series of investigations and found some predictive
parameters on which to base decisions for recall intervals (Rams et al., 1996). Low
sextant scores (0-2) with the Community Periodontal Index of Treatment Need (CPITN)
screening system provided data for plausible identification of non-progressive disease.
On the other hand, high sextant scores were not predictive of active, progressive disease
(Rams et al., 1996). With use of Ramfjord’s six index teeth (numbers: 3, 9, 12, 19, 25,
8
28), they determined a lack of disease progression, indicative of low disease risk for the
dentition as a whole (Rams et al., 1993). Furthermore, essentially no risk of periodontal
disease progression for 2 years (predictive value equal to 100%) was noted when
periodontitis sites radiographically exhibited intact crestal lamina dura (Rams et al.,
1994).
Despite that BOP has shown promise as a predictor of future periodontal disease
status, and is frequently used in the dental office to guide future therapy, only sparse
information is available on how BOP relates to dental plaque scores and degree of past
periodontal breakdown. The association between BOP and specific periodontopathic
bacteria is also not clear. The aim of this study was to determine the relationship
between BOP and supragingival plaque, between BOP and periodontal pocket depth, and
between BOP and subgingival periodontal pathogens. The effect on PI and BOP of
twice-weekly oral rinse with 0.25% sodium hypochlorite was studied as well.
9
Results
A total of 36 participants were enrolled in the study. Ten participants were lost to
attrition. Twenty-six patients were included for analysis,14 patients in the test group and
12 patients in the control group. The proportion of male to female subjects was 17:13,
and the mean age of the group was 41.2 years. A total of 26 participants completed Visits
1 and 2, and 11 subjects completed Visit 3. Due to time limitations, the rest of the
participants have not yet completed the study
Plaque
The presence or absence of visible plaque on facial and lingual tooth surfaces of
all teeth within each of the test and control patients were recorded at baseline, Visit 2, and
Visit 3. Next, test and control groups were pooled together, and the plaque score was
calculated for the pooled group at each time point.
In the test group, there were 891 sites (41.0%) that had dental plaque at baseline,
719 sites (33.2%) that had plaque at Visit 2, and 215 sites (20.7%) that had plaque at
Visit 3 (Table 1). There was a decrease in the amount of plaque within the test group at
the second visit and again at the third visit.
In the control group, there were 654 sites (34.0%) that had plaque at baseline, 582
sites (30.2%) that had plaque at Visit 2, and 306 sites (45.1%) that had plaque at Visit 3
(Table 1). There was an increase in the percentage of sites with dental plaque over time
within the control group.
10
In the pooled group there were 654 sites (37.7%) that had plaque at baseline, 1301
sites (31.8%) that had plaque at Visit 2, and 521 sites (30.4%) that had plaque at Visit 3
(Table 1). The number of sites with positive plaque within the pooled cohort decreased
over time.
BOP
The presence or absence of BOP on facial and lingual tooth surfaces of each
patient within the test and control groups were recorded at baseline, Visit 2, and Visit 3.
Next, test and control groups were pooled together, and the percentage of BOP score was
calculated for the pooled group at each time point.
In the test group, there were 1340 sites (61.7%) that had BOP at baseline, 919
sites (42.3%) that had BOP at Visit 2, and 351 sites (33.8%) that had BOP at Visit 3
(Table 1). The percentage of sites exhibiting BOP, in the test group, decreased from
baseline to Visit 3 at 3 months.
In the control group, there were 963 sites (50.0%) that had BOP at baseline, 849
sites (44.1%) that had BOP at Visit 2, and 263 sites (38.8%) that had BOP at Visit 3
(Table 1). The percentage of sites exhibiting BOP decreased over time within the control
group.
In the pooled group, there were 2303 sites (56.2%) that had BOP at baseline, 1768
sites (43.1%) that had BOP at Visit 2, and 614 sites (35.8%) that had BOP at Visit 3
(Table 1). Within the pooled group, there was an overall decrease in the percentage of
sites that were positive for BOP over time.
11
Plaque and BOP
The data were analyzed according to the presence of BOP at sites exhibiting
dental plaque. In the test group, there were 618 sites that were positive for dental plaque
and BOP at baseline, 389 sites positive for dental plaque and BOP at Visit 2, and 120
sites at Visit 3. Tables 2 and 3 shows that within the test group, the percentage of sites
exhibiting dental plaque and BOP decreased over time from 28.5% at baseline to 11.7%
at the 3
rd
visit. Within the test group, the correlation between plaque and BOP was found
to be statistically significant at baseline, Visit 2 and Visit 3 (p<0.0001).
In the control group there were 425 sites that were positive for dental plaque and
BOP at baseline, 393 sites positive for dental plaque and BOP at Visit 2, and 154 sites at
Visit 3. Tables 2 and 4 shows that within the control group, the percentage of sites
exhibiting dental plaque and BOP increased over time from 22.1% at baseline to 22.7% at
the 3
rd
visit. Within the control group, the correlation between plaque and BOP was found
to be statistically significant at all time points throughout the study (p<0.0001).
In the pooled group there were 1043 sites that were positive for dental plaque and
BOP at baseline, 782 sites positive for dental plaque and BOP at Visit 2, and 274 sites at
Visit 3. Tables 2 and 5 shows that within the pooled group, the percentage of sites
exhibiting dental plaque and BOP decreased over time from 25.5% at baseline to 15.9%
at the 3
rd
visit. Within the pooled group, the correlation between plaque and bleeding on
probing was found to be statistically significant at all time points evaluated in the study
(p<0.0001).
12
Pocket Depth and BOP
The data were analyzed according to the presence or absence of BOP at different
pocket depths. There was a statistically significant correlation between pocket depth and
BOP within the test group at baseline, Visit 2 and Visit 3 (p<0.0001). Figures 1-3 show
that as the pocket depth increased, the number of sites with BOP also increased.
The correlation between BOP and pocket depth was also statistically significant
for the control group (p<0.0001). The correlation remained statistically significant
throughout all time points. Figures 4-6 show that as the pocket depth increased, the
number of sites exhibiting BOP also increased.
Finally, when test and control groups were pooled together, the correlation
between pocket depth and BOP was also found to be statistically significant (p<0.0001).
This relationship remained statistically significant throughout all visits. Figures 7-9 show
that as pocket depth increased for all sites within the groups, the number of sites that are
positive for BOP also increased.
Pocket Depth >4 mm and BOP
The data were dichotomized according to pocket depth, using a measurement of 4
mm as the point of interest. In the test group there were 287 sites that measured >4 mm
and were also positive for BOP at baseline, 282 sites that measured >4 mm and were also
positive for BOP at Visit 2, and 86 sites at Visit 3. Within the test group, the correlation
between pocket depth of > 4mm and bleeding on probing was found to be statistically
significant at all time points evaluated in the study (p<0.0001) (Table 2 and 6).
13
In the control group there were 343 sites that measured >4 mm and were also
positive for BOP at baseline, 343 sites that measured >4 mm and were also positive for
BOP at Visit 2, and 159 sites at Visit 3. Within the control group, the correlation between
pocket depth of > 4mm and bleeding on probing was found to be statistically significant
at all time points evaluated in the study (p<0.0001) (Table 2 and 7).
In the pooled group there were 631 sites that measured >4 mm and were also
positive for BOP at baseline, 625 sites that measured >4 mm and were also positive for
BOP at Visit 2, and 245 sites at Visit 3. Within the pooled group, the correlation between
pocket depth of > 4mm and bleeding on probing was found to be statistically significant
at all time points evaluated in the study (p<0.0001) (Table 2 and 8).
Microbiology at Sites Exhibiting BOP
The patients were grouped into two separate cohorts according to presence or
absence of BOP in the sites that were sampled, and the microbiota present at these sites
were analyzed within each group. The average number of bacteria for each strain
analyzed was calculated for the BOP-positive and BOP-negative sites within both groups
at each time point (Tables 9-10). The total percentage of bacteria was calculated for each
patient within the 2 cohorts, by adding the percent score for each bacterium within the
sample.
Within the BOP-positive group, the median value for the total percentage of
bacteria was calculated for 9 control and 11 test subjects at the baseline visit, for 8
control and 10 test subjects at visit 2, and for 3 control and 3 test subjects at visit 3 (Table
11). Within the BOP-positive group, the difference between median values, for the total
14
percentage of bacteria, at baseline and at visit 2 were analyzed for 10 patients in the test
group and for 7 patients in the control group. The difference between median values, for
the total percentage of bacteria, at baseline and visit 3 was not analyzed for either test or
control groups because there were only 3 subjects available for analysis within these
groups (n=3).
Within the BOP-positive group, there was no statistically significant difference
between the median total percentage of bacteria at baseline and visit 2 for either the test
or control subjects (p>0.05) (Table 12). Additionally, no statistically significant
differences were found for the median total percentage of bacteria between the test and
control groups at either baseline (p>0.05), or visit 2 (p>0.05) (Table 13). The analysis to
compare the difference in total percentage of bacteria between test and control group at
visit 3 could not be performed due to the low number of subjects within this group (n=3).
Within the BOP-negative group, the median value for the total percentage of
bacteria was calculated for 3 control and 2 test subjects at the baseline visit, for 4 control
and 4 test subjects at visit 2, and for 2 control and 3 test subjects at visit 3 (Table 14).
Within the BOP-negative group, the difference between median values, for the total
percentage of bacteria, could not be analyzed at any time point due to the small amount
of subjects within this group (n≤4).
15
Discussion
There is a worldwide, urgent need to develop effective and low-cost self-care
techniques for prevention and treatment of periodontal disease. The current methods for
removing dental plaque are cumbersome, provide limited benefits, and perform poorly
for most individuals (Slots, 2012). Toothbrushing reduces the average plaque scores only
by about half and plaque is left behind on 85% of interdental surfaces; interdental
brushes, toothpicks and dental floss fail to eliminate all interdental plaque and are only
used by 5-10% of the population; toothpastes are expensive and do not significantly
enhance the plaque-removal by toothbrushing alone; and most commercial mouthwashes
are expensive and, with the exception of chlorhexidine, essentially only serve a cosmetic
purpose (Slots, 2012). High prices and low performance of self-care devices and
treatments may be some of the biggest issues in periodontal healthcare.
Sodium hypochlorite represents potentially an efficacious, safe, inexpensive and
widely available complement or alternative to current periodontal self-care techniques. A
highly diluted sodium hypochlorite solution (0.05%), used twice daily as an oral rinse in
an experimental gingivitis design study, was able to reduce dental plaque index scores by
48%, gingival Index score by 52%, and BOP sites by 39% compared with water rinse (De
Nardo et al., 2012). However, as the twice-daily use of a freshly made sodium
hypochlorite solution may be impractical for most individuals, we sought to examine if a
biweekly regimen of 5 times higher sodium hypochlorite oral rinse solution (0.25%)
would provide similar clinical improvements.
16
We found that the sodium hypochlorite oral rinse group showed marked
improvements from baseline to 3 months in plaque-free facial surfaces (P=0.02), plaque-
free lingual surfaces (P=0.07), and BOP-free teeth (P=0.002), whereas the water-rinse
control group showed no significant clinical improvements. The sodium hypochlorite-
rinse group and the water-rinse group, respectively, showed increases of 94% and 29%
(3.2 fold difference) in plaque-free facial surfaces, of 195% and 30% (6.5 fold difference)
in plaque-free lingual surfaces, and of 421% and 29% (14.5 fold difference) in number of
teeth with no BOP. The sodium hypochlorite-rinse group, but not the water-rinse group,
demonstrated continued clinical improvements up to the 3-month endpoint of the study,
suggesting that the difference between the sodium hypochlorite test group and the water
control group would widen even further with a longer study period. The biochemical
basis for the remarkable decrease in dental plaque after only twice-a-week sodium
hypochlorite rinse is unknown, but substantivity to the tooth surface is an intriguing
possibility.
Oral rinses penetrate only 0.1-0.2 mm into periodontal pockets (Pitcher et al.,
1980; Boyd et al., 1992), however, the present study found marked clinical improvements
in periodontitis lesions as well. The most likely explanation relates to the sustained
absence of supragingival plaque, which is known to affect the subgingival ecology and
reduce periodontopathogen counts in pockets up to 5 mm in depth (Dahlen et al., 1992;
Hellstrom et al., 1996; Ximenez-Fyvie et al., 2000).
There also is a pressing, though unrealized, need for objective clinical indices that
the clinician can use to differentiate between healthy/normal sites and those with active
periodontal disease. Many of the indices used today involve a visual assessment of the
17
clinical condition and as a result, are wrought with subjectivity. Historically, the indices
involving the determination of the presence or absence of gingival bleeding have been
hailed as a highly objective method of clinical assessment. This is due to the dichotomous
nature of this type of clinical examination measurement.
In order to further evaluate the clinical utility of BOP, this study examined the
relationships between BOP and plaque score and between BOP and periodontal pocket
depth, using the data from the sodium hypochlorite study. We found that there was a
statistically significant correlation between BOP and the presence or absence of dental
plaque at a site. We also identified a statistically significant correlation between sites
measuring > 4 mm of probing depth and BOP.
Studies on the relationship between BOP and periodontal variables are
surprisingly few, and more information is needed to establish the correlation between
BOP and dental plaque or periodontal pocket depth. The earliest type of investigations on
BOP focused on correlations with gingival crevicular fluid (GCF) levels. Hancock et. al
studied the relationship between the histologic and clinical condition of the gingiva and
GCF levels. They grouped patients according to the Loe and Silness Gingival Index and
measured BOP and the GCF levels before taking a biopsy for histologic evaluations.
There were strong correlations found between the histological appearance of the inflamed
gingiva and the clinical signs of inflammation such as BOP. However, there were only
weak correlations found between clinical and histologic signs of inflammation and the
GCF levels (Hancock et al., 1979). Nowicki et al. formulated a bleeding time index
based on the amount of time that it took for bleeding to occur after probing. They found a
18
statistically significant correlation between GCF levels and the bleeding time index
(Nowicki et al., 1981).
Several studies have looked at the relationship between the BOP status and the
histologic appearance of inflammation. Greenstein et al. found that BOP was associated
with inflammatory changes in the gingiva, such as an increase in the percentage of cell-
rich and collagen poor connective tissue. Their study found that BOP might be able to
detect inflammation earlier than visual indices (Greenstein et al., 1981). Davenport et al.
studied the histologic appearance of advanced periodontitis lesions that were classified as
active or inactive based on the presence of absence of BOP. The study found the
percentage of infiltrated connective tissue, plasma cells, and mononuclear cells to be
markedly larger in bleeding sites than in non-bleeding sites. The authors concluded that
BOP is a good indicator of the presence of histopathologic changes in a site affected by
periodontitis (Davenport et al., 1981). Polson et al. found that sites with BOP had
significantly less epithelium and more connective tissue than sites, which did not bleed,
due to a significant increase in the amount of inflamed connective tissue present (Polson
et al., 1981).
The most recent studies have focused on the BOP status as a predictor of future
periodontal breakdown. Lang et al. evaluated the usefulness of BOP as a prognostication
tool for identifying sites at risk for future periodontal breakdown. The study found that
pockets measuring more than 5 mm had a significantly greater incidence of BOP. Also,
patients that had more than 16% of sites exhibiting BOP, were at increased risk of losing
attachment. They concluded that BOP was a valuable tool for identifying patients at risk
for future breakdown in the maintenance phase of therapy, if used appropriately (Lang et
19
al., 1986). Lang et al. suggested that, although the presence of BOP was not a good way
to predict disease progression at sites, the absence of BOP was an excellent indicator of
periodontal stability and health. The positive predictive value for disease progression was
6%; however, the negative predictive value was 98%. This indicates that absence of BOP
is a reliable tool for prognostication of periodontal health (Lang et al., 1990).
Claffey et al. followed 17 patients after initial therapy and found BOP to be
valuable tool for predicting probing attachment loss at specific sites. The predictive value
of BOP was greatest when combined with other indicators of periodontal disease
progression, such as increased probing depth of the BOP sites (Claffey et al., 1990).
Badersten also found an association between BOP and probing attachment loss. After
performing multiple regression analyses, she found that the predictive value of BOP for
future periodontal breakdown was about 30% (Badersten et al., 1990). Joss et al. found
that the majority of the sites which lost attachment during the maintenance phase
occurred in the cohort of patients that had a mean BOP score of >30%. In contrast, only
1/5 of the sites which lost attachment were found in the group of patients who exhibited a
mean BOP score of >20%. The investigators concluded that patients with a BOP score of
less than 20% have a significantly reduced risk for future probing attachment loss (Joss et
al., 1994).
However, a study by Vanooteghem found partly disparate results. Nineteen patients
diagnosed with periodontitis were monitored for 24 months after a single treatment of
root debridement. The BOP scores were analyzed to determine if they could be used
diagnostically as indicators of probing attachment loss. Of the sites that had BOP at 7 or
more of the 8 post-op examinations, only 23% demonstrated probing attachment loss.
20
Results from this study demonstrated that the diagnostic accuracy of BOP was low
(Vanooteghem et al., 1987).
The possible involvement of specific periodontal bacteria in BOP needs to be
studied further. There may be a correlation between BOP and spirochetes and motile
forms of bacteria. Armitage studied the correlation between clinical indices of disease
and the percentage of motile bacteria in the subgingival microbiota. He found that there
was a larger increase in the relative percentage of subgingival spirochetes when there was
BOP observed at a specific site (Armitage et al., 1981). However, other investigators
have failed to show an association between components of the subgingival microflora and
the BOP status. Although our data pointed to a positive association between
Porphyromonas gingivalis and BOP, perhaps due to the relatively small sample size, we
were unable to identify a statistically significant correlation between any specific bacteria
and BOP.
In conclusion, the increasing costs of periodontal health-care combined with a
growing number of underserved populations worldwide underscores the need for finding
alternative ways of managing periodontal disease. We propose that patients ought to be
able to prevent and control most types of periodontal disease, and replace a significant
part of current professional therapy, by using an effective antiseptic agent capable of
reaching the disease-producing plaque. In this study, we used BOP to evaluate the
periodontitis preventive and curative potential of sodium hypochlorite. Our study found
that 0.25% sodium hypochlorite oral rinse twice-weekly for 3 months dramatically
reduced BOP in periodontitis sites that had not been subjected to subgingival scaling and
root planing. The study, based mainly on data from the control group, also showed that
21
BOP was positively correlated to plaque scores and pocket depths greater than 4 mm.
However, in spite of the encouraging findings of sodium hypochlorite oral rinse being
able to reduce BOP in pocket of moderate-sized depth, controlled studies are still needed
to determine the periodontal benefit of sodium hypochlorite rinse with long-term usage.
Also, although the concept of antimicrobial periodontal therapy is simple, studies are
needed to identify the most successful way of introducing sodium hypochlorite treatment
to the public.
22
Experimental Procedures
Study Participants
A total of 36 adults with periodontitis, who presented to USC Ostrow School of
Dentistry clinics for periodontal therapy were enrolled in the study. Of the total number
of patients enrolled in the study, 10 were lost to attrition. A total of 26 patients completed
the protocol and were included for analysis.
The proportion of male to female study participants was 17:13 and the mean age
was 41.2 years. Patients had an average of 27 teeth. After careful review of the medical
history, none of the participants were found to have any systemic conditions that would
affect their periodontal status or contraindicate participation in the study. The patients
each exhibited at least one periodontal pocket probing 6 mm or more in each quadrant of
the dentition and tested positive for one or more known periodontal pathogens. Non-
emergency restorative dental needs were postponed until after the completion of the
study.
In order to participate in the study, the patients were required to have a diagnosis
of periodontitis and have at least 4 teeth with periodontal pockets of 6 mm or more.
They should have current full mouth radiographs on record and have been treatment
planned to undergo, or are undergoing, standard periodontal therapy including scaling
and root planing.
The subjects must not have received periodontal therapy or systemic antibiotics
for at least 6 months prior to entering the study. Subjects cannot be medically
compromised, pregnant, immunocompromised, unable to comply with the protocol, have
23
a smoking habit of >10 cigarettes/day, or require emergency dental care indicated for
dental caries or periodontitis. A diagnosis of diabetes, HIV or other forms of
immunosuppression were all considered reasons for exclusion from the study. The study
was approved by the University of Southern California Health Sciences Campus
Institutional Review Board (HSCIRB) (#HS-10-00509). All patients understood and
signed informed consent and HIPAA documents prior to enrolling in the study.
Study Design
This study was performed as a randomized, controlled, single-blinded, clinical
trial in parallel groups according to the CONSORT criteria. (Schulz et al., 2001; Altman
et al., 2010) The study patients were randomly divided into 2 groups. The test group
received sodium hypochlorite rinses (15 test participants), and the control group received
water rinses (15 control participants). The clinical examination was performed by a single
blinded examiner.
Participant Selection
Inclusion criteria:
Participants of either sex and of any race, 18 years of age or older were included, in the
study.
Inclusion criteria were:
1. Diagnosed with periodontitis,
2. Current full mouth radiographs on record
3. At least 4 teeth with periodontal pockets of 6mm or more
24
Exclusion criteria were:
1. Medically compromised and unable to comply with protocol, including the
immunocompromised and pregnant
2. Smoking habit of >10 cigarettes/day
3. Emergency dental care indicated for dental caries or periodontitis
4. Periodontal abscesses and/or acute periodontitis
5. At least 3 months since last periodontal treatment was performed (Prophylaxis, Scaling
and root planing, subgingival irrigation with antimicrobials, local antibiotics, pocket
reduction surgery)
6. At least 3 months since patient took systemic antibiotics
Clinical Procedures
All study participants received a comprehensive clinical examination. The
following clinical variables were completed/assessed in each participant, according to the
standard treatment of periodontitis patients: (1) medical questionnaire and general oral
examination (2) existing full-mouth dental radiographs, (3) number of teeth, (4) plaque
index, (5) gingival index, (6) gingival bleeding on probing, (7) periodontal pocket depth
in mm, (8) gingival recession in mm, (9) furcation involvement, (10) mobility. (1) - (10)
were assessed at Baseline (Visit 1), at Day 14 (Visit 2) and at Month 3 (Visit 3).
After careful review of the medical history, none of the participants were found to
have any systemic conditions that would affect their periodontal status or contraindicate
participation in the study. Each patient had a full mouth series of radiographs (FMX)
25
taken before starting the study. These radiographs were used to assess the patient’s
overall dental condition and identify any emergency conditions that would require
immediate attention. Also, the FMX was used to assess bone loss and provide a guide for
estimating the deepest pockets in the mouth for microbial sampling. The number of teeth
was counted for each patient and teeth were identified using the Universal numbering
system, whereby the teeth are numbered from 1-32, starting with the 3
rd
molar on the
maxillary right quadrant.
The presence or absence of supragingival plaque was assessed by visual
inspection of the facial and lingual surfaces of the teeth. No other methods of plaque
identification were employed. A value of “0” was assigned to those surfaces with absence
of plaque and a value of “1” was assigned to those surfaces with any presence of plaque.
The bleeding on probing (BOP) was assessed as any evidence of bleeding from the
pocket after probing to the full depth. The bleeding was observed for approximately 30
seconds after the probing was completed for the facial or lingual surfaces of the teeth in
the quadrant. The presence or absence of BOP was marked on 6 surfaces on each tooth,
facial, lingual, mesiofacial, distofacial, mesiolingual and distolingual. A value of “0” was
assigned for the absence of BOP, and a value of “1” was assigned for the presence of
BOP on any of the six sites evaluated on the teeth.
The pocket depth was measured in millimeters using a Marquis CP 12 probe. The
pockets were measured at 6 sites on each tooth, facial, lingual, mesiofacial, distofacial,
mesiolingual and distolingual. The probing force used was roughly 0.75 Ncm, or the
weight of the probe itself. The measurements were made with the probe as parallel as
possible to the long axis of the teeth, and the same angulation was carried out throughout
26
the entire examination. The recession was measured in millimeters, using a Marquis CP
12 probe, as the distance from the natural cemento-enamel junction of the tooth to the
free gingival margin. A recording was taken at 6 sites on each tooth, facial, lingual,
mesiofacial, distofacial, mesiolingual and distolingual.
Furcation involvement was measured using a Naber’s probe and Hamp’s
classification was employed to assess the level of periodontal destruction present. A score
of Class I was assigned if there was a horizontal loss of periodontal support of less than 3
mm. A score of Class II was assigned if there was a horizontal loss of support exceeding
3 mm, but not encompassing the entire width of the furcation area. A score of Class III
was assigned if there was horizontal destruction of periodontal support through the entire
width of the furcation area.
Mobility was evaluated by placing the blunt end of the handle of 2 instruments on
the facial and lingual surfaces of the teeth and applying pressure while attempting to rock
the tooth. The teeth that moved less than 1 mm were assigned a score of Class 1 mobility.
The teeth that moved 1 mm or more but less than 2 mm were assigned a score of Class 2
mobility. The teeth that moved 2 mm or more and can be depressed into its socket were
assigned a score of Class 3 mobility.
On the first visit, the participants received professional subgingival irrigation with
either 0.25% sodium hypochlorite (test) or water (control). Following the clinical
examination, subgingival irrigation was performed with a 3cc Monoject
®
Endodontic
Syringe with a 23 gauge cannula (metal w. side port). The syringe was placed at the
bottom of the pockets of all teeth in the dentition, and sodium hypochlorite or water was
applied for a total of 5 minutes.
27
After subgingival irrigation, the subjects in the test group were asked to mix the
0.25% sodium hypochlorite bleach at home as per our study directions. The procedure for
rinsing was explained and practiced under the supervision of the investigator. The
patients were asked to rinse their mouth every Wednesday and Sunday for 30 seconds
with either 0.25% sodium hypochlorite or water. Oral hygiene instructions were given to
participants for home care. Patients were to brush twice a day, using the Modified Bass
Technique, and floss once per day. Participants were provided with a manual Oral B
tooth brush and dental floss samples.
The mouth rinse for home use was made up as follows. Participants in the test
group were provided with Clorox Bleach (6%) and asked to mix 5 ml (one teaspoonful)
of the Clorox Bleach solution with 120 ml (one half-glass) of water. The test group
participants were asked to rinse with 5 ml of the study solutions for 30 seconds and then
spit out. They were asked to abstain from subsequent rinsing with water for at least 10
minutes after rinsing. The control group was instructed in the same manner, but will be
using a water rinse only. In an effort to ensure patient compliance, the patients were
given a rinse log, where they could record the exact date and time that they rinsed. The
patients were instructed to bring this rinse log with them to the final visit, so that we
could assess their compliance. Additionally, an attempt was made to call the patients and
remind them to rinse and inquire about their success with the rinsing protocol.
Each subject received the standard periodontal therapy for periodontitis at the
conclusion of the study, including explanation of the cause of the disease, instruction in
oral hygiene, scaling and root planing, supragingival polishing, and recall schedule to
prevent recurrence of the disease.
28
Statistical Methods
The data was recorded at each visit. The presence of PI and BOP were recorded as
dichotomous variables. Pocket depth was recorded as a discrete variable in mm and was
further dichotomized into >4 and ≤ 4 mm. Descriptive statistics were calculated at each
visit. Pearson χ
2
and correlation coefficient tests were used to assess the relationship
between BOP and PI as well as BOP and PD. The significance level was set at α =0.05.
Data analysis was performed using STATA
©
statistical software (StataCorp, College
Station, Texas, USA)
Additionally, the patients were grouped into two separate cohorts according to
presence or absence of BOP in the sites that were sampled, and the microbiota present at
these sites were analyzed within each group. The total percentage of bacteria was
calculated for each patient within the 2 cohorts, by adding the percent score for each
bacterium within the sample. Medians and range were calculated for each set of data. As
the sample size was small and data values were not normally distributed, and the sample
size was almost reduced to half at the 3rd visit, the analysis was performed using non-
parametric statistics. Differences within the groups between the data at baseline, visit 2
and whenever possible, visit 3, were compared using Wilcoxon signed-rank sum test.
Comparisons between test and control group at each of the 3 time points were
accomplished using Wilcoxon Mann-Whitney's U test. All analyses were performed
using SAS v9.3. A two-sided alternative hypothesis and a 0.05 significance level were
assumed in all testing. No adjustment on the p-values were made for the multiple testing.
29
Acknowledgments
I would like to express my deepest gratitude to the professors who have been
friends and mentors throughout this arduous process.
Thank you Dr. Jorgen Slots for the knowledge that you have imparted and for the
example of hard work and diligence that you have set for us. The help and
encouragement you offered to help me reach my goal will never be forgotten.
Thank you Dr. Sandra Rich for all of your guidance and excellent advice. Our
success is due largely in part to your leadership and expertise.
Thank you Dr. Homa Zadeh for your patience, advice and mentorship. I
appreciate all of the work you have put into helping your seniors attain their goals.
Thank you Dr. Mahvash Navazesh for your support and care throughout these
years.
Thank you Dr. Kian Kar and Dr. Alon Frydman for being an unwavering source
of sound advice, endless encouragement, and true mentorship.
Finally, thank you Dr. Maria Galvan and Dr. Chloe Cohen for your
professionalism and collaboration in this study.
This work was supported in part by a grant from the Clorox Company ®.
30
Bibliography
1. Altman DG, Schulz KF, Moher D. (2001). The revised CONSORT statement
for reporting randomized trials: explanation and elaboration. Ann Intern Med.
134: 663–694.
2. Armitage GC, Dickinson WR, Jenderseck RS, Levine SM, Chambers DW. (1982).
Relationship between the percentage of subgingival spirochetes and the severity of
periodontal disease. J Periodontol. 53(9): 550-556.
3. Armitage GC, Cullinan MP, Seymour GJ. (2010). Comparative biology of
chronic and aggressive periodontitis: introduction. Periodontol 2000. 53: 7–11.
4. Badersten A, Nilvéus R, Egelberg J. (1990). Scores of plaque, bleeding, suppuration
and probing depth to predict probing attachment loss. 5 years of observation following
nonsurgical periodontal therapy. J Clin Periodontol. 17(2): 102-107.
5. Beirne P, Clarkson JE, Worthington HV. (2007). Recall intervals for oral health
in primary care patients. Cochrane Database of Systematic Review. 4:
CD004346.
6. Boyd RL, Hollander BN, Eakle WS. (1992). Comparison of a subgingivally
placed cannula oral irrigator tip with a supragingivally placed standard irrigator
tip. J Clin Periodontol. 19: 340-344.
7. Claffey N, Nylund K, Kiger R, Garrett S, Egelberg J. (1990). Diagnostic predictability
of scores of plaque, bleeding, suppuration and probing depth for probing attachment
loss. 3 1/2 years of observation following initial periodontal therapy. J Clin
Periodontol. 17(2): 108-114.
31
8. Dahlén G, Lindhe J, Sato K, Hanamura H, Okamoto H. (1992). The effect of
supragingival plaque control on the subgingival microbiota in subjects with
periodontal disease. J Periodontol. 19: 802–809.
9. Davenport RH Jr., Simpson DM, Hassell TM. (1982). Histometric comparison of
active and inactive lesions of advanced periodontitis. J Periodontol. 53(5): 285-295.
10. De Nardo R, Chiappe V, Gomez M, Romanelli H, Slots J. (2012). Effect of
0.05% sodium hypochlorite oral rinse on supragingival biofilm and gingival
inflammation. Int Dent J. 62: 208–212.
11. Greenstein G, Caton J, Polson AM. (1981). Histologic characteristics associated with
bleeding after probing and visual signs of inflammation. J Periodontol. 52(8): 420-425.
12. Hancock EB, Cray RJ, O'Leary TJ. (1979). The relationship between gingival
crevicular fluid and gingival inflammation. A clinical and histologic study. J
Periodontol. 50(1): 13-19.
13. Hellström MK, Ramberg P, Krok L, Lindhe J. (1996).The effect of
supragingival plaque control on the subgingival microflora in human
periodontitis. J Clin Periodontol. 23: 934–940.
14. Joss A, Adler R, Lang NP. (1994). Bleeding on probing. A parameter for monitoring
periodontal conditions in clinical practice. J Clin Periodontol. 21(6): 402-408.
15. Lang NP, Joss A, Orsanic T, Gusberti FA, Siegrist BE. (1986). Bleeding on probing. A
predictor for the progression of periodontal disease? J Clin Periodontol. 13(6): 590-
596.
16. Lang NP, Adler R, Joss A, Nyman S. (1990). Absence of bleeding on probing. An
indicator of periodontal stability. J Clin Periodontol. 17(10): 714-721.
32
17. Lang NP, Joss A, Tonetti MS. (1996). Monitoring disease during supportive
periodontal treatment by bleeding on probing. Periodontol 2000. 12: 44–48.
18. Lindhe J, Haffajee AD, Socransky SS. (1983). Progression of periodontal
disease in adult subjects in the absence of periodontal therapy. J Clin
Periodontol. 10: 433- 442.
19. Listgarten MA, Sullivan P, George C, Nitkin L, Rosenberg ES, Chilton NW,
Kramer AA. (1989). Comparative longitudinal study of 2 methods of
scheduling maintenance visits: 4-year data. J Clin Periodontol. 16: 105–115.
20. Lobene RR, Soparkar PM, Hein JW, Quigley GA. (1972). A study of the
effects of antiseptic agents and a pulsating irrigating device on plaque and
gingivitis. J Periodontol. 43: 564–568.
21. Nowicki D, Vogel RI, Melcer S, Deasy MJ. (1981). The gingival bleeding time index.
J Periodontol. 52(5): 260-262.
22. Pitcher GR, Newman HN, Strahan JD. (1980). Access to subgingival plaque by
disclosing agents using mouthrinsing and direct irrigation. J Clin Periodontol.
7: 300-308.
23. Polson AM, Greenstein G, Caton J. (1981). Relationships between epithelium and
connective tissue in inflamed gingiva. J Periodontol. 52(12): 743-746.
24. Rams TE, Oler J, Listgarten MA, Slots J. (1993). Utility of Ramfjord index
teeth to assess periodontal disease progression in longitudinal studies. J Clin
Periodontol. 20: 147–150.
25. Rams TE, Listgarten MA, Slots J. (1994). Utility of radiographic crestal lamina
dura for predicting periodontitis disease activity. J Clin Periodontol. 21: 571–
33
576.
26. Rams TE, Listgarten MA, Slots J. (1996). Efficacy of CPITN sextant scores for
detection of periodontitis disease activity. J Clin Periodontol. 23: 355–361.
27. Renvert S, Nilveus R, Dahlen G, Slots J, Egelberg J. (1990). 5-year follow up
of periodontal intraosseous defects treated by root planing or flap surgery. J
Clin Periodontol. 17: 356–363.
28. Slots J. (2010). Herpes viral-bacterial interactions in periodontal diseases. Periodontol
2000. 52(1): 117-140.
29. Slots J. (2012). Low-cost periodontal therapy. Periodontol 2000. 60: 110-137.
30. Vanooteghem R, Hutchens LH. (1987). Bleeding on probing and probing depth as
indicators of the response to plaque control and root debridement. J Clin Periodontol.
14(4): 226-230.
31. Ximénez-Fyvie LA, Haffajee AD, Som S, Thompson M,Torresyap G,
Socransky SS. (2000). The effect of repeated professional supragingival plaque
removal on the composition of the supra- and subgingival microbiota. J Clin
Periodontol. 27: 637–647.
34
Figure and Table Legends
Table 1. Percentage of Plaque and BOP
Table 2. Percentage of Plaque and Pockets Measuring >4 mm at BOP (+)/(-) Sites
Table 3. Percentage of Sites Exhibiting Plaque and BOP at Visits 1, 2, and 3 within the
Test Group
Table 4. Percentage of Sites Exhibiting Plaque and BOP at Visits 1, 2, and 3 within the
Control Group
Table 5. Percentage of Sites Exhibiting Plaque and BOP at Visits 1, 2, and 3 within the
Pooled Group
Figure 1. Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-10 mm
within the Test Group at Baseline
Figure 2. Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-10 mm
within the Test Group at Visit 2
Figure 3. Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-9 mm
within the Test Group at Visit 3
Figure. 4 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-12 mm
within the Control Group at Baseline
Figure. 5 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-11 mm
within the Control Group at Visit 2
Figure. 6 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-12 mm
within the Control Group at Visit 3
35
Figure. 7 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-12 mm
within the Pooled Group at Baseline
Figure. 8 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-11 mm
within the Pooled Group at Visit 2
Figure. 9 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-12 mm
within the Pooled Group at Visit 3
Table 6. Percentage of Sites Exhibiting Pocket Depth >4 mm and BOP at Visits 1, 2, and
3 within the Test Group
Table 7. Percentage of Sites Exhibiting Pocket Depth >4 mm and BOP at Visits 1, 2, and
3 within the Control Group
Table 8. Percentage of Sites Exhibiting Pocket Depth >4 mm and BOP at Visits 1, 2, and
3 within the Pooled Group
Table 9. Mean Bacteria Present at BOP (+)/(-) Sites Within the Test Group
Table 10. Mean Bacteria Present at BOP (+)/(-) Sites Within the Control Group
Table 11. Median total percentage of bacteria for the BOP-positive Cohort
Table 12. P-values for an analyses of the difference in median values for the total
percentage of bacteria, between baseline and visit 2, for the test and control subjects
within the BOP-positive cohort.
Table 13. P-values for an analyses of the difference between median values for the total
percentage of bacteria, between test and control groups, at baseline and visit 2, within the
BOP-positive cohort.
Table 14. Median total percentage of bacteria for the BOP-negative Cohort
36
Figures and Tables
Table 1. Percentage of Plaque and BOP
Table 2. Percentage of Plaque and Pockets Measuring >4 mm at BOP (+)/(-) Sites
Items
Sodium
Hypochlorite
(test) Group
Water
(control)
Group
Pooled Group
Study
Visit
Baseline
(Visit 1)
Week 2
(Visit 2)
Month 3
(Visit 3)
Baseline
(Visit 1)
Week 2
(Visit 2)
Month 3
(Visit 3)
Baseline
(Visit 1)
Week 2
(Visit 2)
Month 3
(Visit 3)
Plaque
Index
(%)
41.0 33.2 20.7 34.0 30.2 45.1 37.7 31.8 30.4
BOP
(%)
61.7 42.3 33.8 50.0 44.1 38.8 56.2 43.1 35.8
Items
Sodium Hypochlorite
(test) Group
Water (control)
Group
Pooled Group
Study
visit
Baseline
(Visit 1)
Week 2
(Visit 2)
Month 3
(Visit 3)
P-values*
Baseline
(Visit 1)
Week 2
(Visit 2)
Month 3
(Visit 3)
P-values*
Baseline
(Visit 1)
Week 2
(Visit 2)
Month 3
(Visit 3)
P-values*
BOP
Status
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
Plaque
Index
(%)
28.5 12.6 18 15.2 11.7 9.2 <0.0001 <0.0001 22.1 11.9 20.4 9.8 22.7 22.4 <0.0001 <0.0001 25.5 12.2 19.1 12.7 15.9 14.4 <0.0001 <0.0001
Pocket
Depth
> 4
mm
(%)
13.0 3.4 13.0 3.6 8.3 9.1 <0.0001 <0.0001 18.0 3.2 17.8 3.2 23.5 4.7 <0.0001 <0.0001 15.4 3.3 15.3 3.4 14.3 7.3 <0.0001 <0.0001
37
Table 3. Percentage of Sites Exhibiting Plaque and BOP at Visits 1, 2, and 3 within the
Test Group
Table 4. Percentage of Sites Exhibiting Plaque and BOP at Visits 1, 2, and 3 within the
Control Group
Baseline Visit2 Visit3
% of PI
&BOP
22.1 20.4 22.7
Correlation
coefficient
(p value)
0.22
(p<0.0001)
0.31
(p<0.0001)
0.22
(p<0.0001)
Table 5. Percentage of Sites Exhibiting Plaque and BOP at Visits 1, 2, and 3 within the
Pooled Group
Baseline Visit2 Visit3
% of PI
&BOP
25.5 19.1 15.9
Correlation
coefficient
(p value)
0.17
(p<0.0001)
0.23
(p<0.0001)
0.23
(p<0.0001)
Baseline Visit2 Visit3
% of PI
&BOP
28.5 18 11.7
Correlation
coefficient
(p value)
0.13
(p<0.0001)
0.17
(p<0.0001)
0.24
(p<0.0001)
38
Figure 1. Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-10 mm
within the Test Group at Baseline
Figure 2. Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-10 mm
within the Test Group at Visit 2
0
20
40
60
80
100
120
1
2
3
4
5
6
7
8
9
10
Percentage
of
Sites
Exhbiting
BOP
at
Pocket
Depths
ranging
from
1-10
mm
within
the
Test
Group
at
Baseline
Percentage
of
Sites
Exhbiting
BOP
at
Pocket
Depths
raning
from
1-‐10
mm
within
the
Test
Group
at
Baseline
0
20
40
60
80
100
120
1
2
3
4
5
6
7
8
9
10
Percentage
of
Sites
Exhbiting
BOP
at
Pocket
Depths
ranging
from
1-10
mm
within
the
Test
Group
at
Visit
2
Percentage
of
Sites
Exhbiting
BOP
at
Pocket
Depths
raning
from
1-‐10
mm
within
the
Test
Group
at
Visit
2
39
Figure 3. Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-9 mm
within the Test Group at Visit 3
Figure. 4 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-12 mm
within the Control Group at Baseline
0
20
40
60
80
100
120
1
2
3
4
5
6
7
8
9
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-9
mm
within
the
Test
Group
at
Visit
3
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-‐9
mm
within
the
Test
Group
at
Visit
3
0
20
40
60
80
100
120
1
2
3
4
5
6
7
8
9
10
11
12
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-12
mm
within
the
Control
Group
at
Baseline
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-‐12
mm
within
the
Control
Group
at
Baseline
40
Figure. 5 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-11 mm
within the Control Group at Visit 2
Figure. 6 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-12 mm
within the Control Group at Visit 3
0
20
40
60
80
100
120
1
2
3
4
5
6
7
8
9
10
11
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-11
mm
within
the
Control
Group
at
Visit
2
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-‐11
mm
within
the
Control
Group
at
Visit
2
0
20
40
60
80
100
120
1
2
3
4
5
6
7
8
9
10
11
12
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-12
mm
within
the
Control
Group
at
Visit
3
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-‐12
mm
within
the
Control
Group
at
Visit
3
41
Figure. 7 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-12 mm
within the Pooled Group at Baseline
Figure. 8 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-11 mm
within the Pooled Group at Visit 2
0
20
40
60
80
100
120
1
2
3
4
5
6
7
8
9
10
11
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-12
mm
within
the
Pooled
Group
at
Baseline
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-‐12
mm
within
the
Pooled
Group
at
Baseline
0
20
40
60
80
100
120
1
2
3
4
5
6
7
8
9
10
11
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-11
mm
within
the
Pooled
Group
at
Visit
2
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-‐11
mm
within
the
Pooled
Group
at
Visit
2
42
Figure. 9 Percentage of Sites Exhibiting BOP at Pocket Depths ranging from 1-12 mm
within the Pooled Group at Visit 3
Table 6. Percentage of Sites Exhibiting Pocket Depth >4 mm and BOP at Visits 1, 2, and
3 within the Test Group
Baseline Visit2 Visit3
% of PD >4
mm &BOP
13.0 13.0 8.3
Correlation
coefficient
(p value)
0.45
(p<0.0001)
0.47
(p<0.0001)
0.33
(p<0.0001)
Table 7. Percentage of Sites Exhibiting Pocket Depth >4 mm and BOP at Visits 1, 2, and
3 within the Control Group
0
20
40
60
80
100
120
1
2
3
4
5
6
7
8
9
10
11
12
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-12
mm
within
the
Pooled
Group
at
Visit
3
Percentage
of
Sites
Exhibiting
BOP
at
Pocket
Depths
ranging
from
1-‐12
mm
within
the
Pooled
Group
at
Visit
3
Baseline Visit2 Visit3
% of PD >4
mm &BOP
18.0 17.8 23.5
Correlation
coefficient
(p value)
0.52
(p<0.0001)
0.61
(p<0.0001)
0.49
(p<0.0001)
43
Table 8. Percentage of Sites Exhibiting Pocket Depth >4 mm and BOP at Visits 1, 2, and
3 within the Pooled Group
Baseline Visit2 Visit3
% of PD >4
mm &BOP
15.4 15.3 14.3
Correlation
coefficient
(p value)
0.47
(p<0.0001)
0.53
(p<0.0001)
0.44
(p<0.0001)
Table 9. Mean Bacteria Present at BOP (+)/(-) Sites Within the Test Group
GROUP
Sodium Hypochlorite (Test) Group
VISIT # Baseline (Visit 1) Week 2 (Visit 2) Month 3 (Visit 3)
BOP
STATUS
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+) BOP (-)
BACTERIA
(MEAN) A. actinomycetemcomitans 0 0 0 0.15 0 0
P. Gingivalis 1.19 0.55 0.83 0.8 0.73 0.27
P. Intermedia 0.05 0.3 0.4 0.55 0.53 0.73
T. Forsythia 0.17 0.55 0.13 0.55 0 0.37
Campylobacter spp 1.99 2.6 2.29 0.83 0.33 0.77
Eubacterium spp 0 0 0.06 0.5 0.2 0
Fusobacterium spp 4.32 3.4 4.46 4.13 4.17 2.87
P. Micros 0.82 0 1.11 0.43 1.7 1.07
Enteric gram - rods 1.41 0.5 0.99 0.35 1.6 0.27
Beta Hemolytic
streptococci 0 0 0 0.98 0 0
Yeast 0 0 0.06 0 0.43 0
Eikenella corrodens 0 0 0.19 0 0 0
Staphylococcus spp 0 0 0 0 0 0
D. Pneumosintes 0.3 0.75 0 0 0 0
PLATE COUNT TOTAL 30000000 38000000 29800000 32000000 28000000 20766666.67
44
Table 10. Mean Bacteria Present at BOP (+)/(-) Sites Within the Control Group
Table 11. Median total percentage of bacteria for the BOP-positive Cohort
GROUP
Water (control) Group
VISIT # Baseline (Visit 1) Week 2 (Visit 2) Month 3 (Visit 3)
BOP
STATUS
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BOP
(+)
BOP
(-)
BACTERIA
(MEAN) A. actinomycetemcomitans 0.07 0 0.08 0 0 0
P. Gingivalis 1.4 0 1.5 0.28 1.43 0
P. Intermedia 0.66 0.63 0.6 0 0.87 0
T. Forsythia 0.21 0.43 0.24 0 0 0
Campylobacter spp 1.68 2.77 2.14 2.08 0 0
Eubacterium spp 0 0 0 0 0 0
Fusobacterium spp 3.22 3.5 3.24 2.78 3.77 0.6
P. Micros 1.04 1.47 1.71 1.03 1.67 0
Enteric gram - rods 0.97 2.8 1.2 0.2 1.1 0
Beta Hemolytic
streptococci 0 0 0.31 0 0 0
Yeast 0.4 0.2 0.24 0 0 0
Eikenella corrodens 0.77 0.2 0 0 0 0
Staphylococcus spp 0 0 0 0 0 0
D. Pneumosintes 0.26 0 0.31 0 0 0
PLATE COUNT TOTAL 29111111.11 34666666.67 34000000 24500000 32000000 20000000
BOP-POSITIVE
COHORT VISIT 1 VISIT 2 VISIT 3
TEST
(med)
CONTROL
(med)
TEST
(med)
CONTROL
(med)
TEST
(med)
CONTROL
(med)
TOTAL
PERCENTAGE
OF BACTERIA 10.10 10.70 10.65 11.60 9.00 8.3
45
Table 12. P-values for analyses of the difference in median values for the total percentage
of bacteria, between baseline and visit 2, for the test and control subjects within the BOP-
positive cohort.
Table 13. P-values for an analyses of the difference between median values for the total
percentage of bacteria, between test and control groups, at baseline and visit 2, within the
BOP-positive cohort.
Table 14. Median total percentage of bacteria for the BOP-negative Cohort
BOP-POSITIVE COHORT V1 vs. V2
TEST
(p-value)
CONTROL
(p-value)
TOTAL PERCENTAGE OF
BACTERIA 0.56 0.94
BOP-POSITIVE COHORT VISIT 1 VISIT 2
TEST vs. CONTROL
(p-value)
TEST vs. CONTROL
(p-value)
TOTAL PERCENTAGE OF
BACTERIA 0.45 0.56
BOP-
NEGATIVE
COHORT VISIT 1 VISIT 2 VISIT 3
TEST
(med)
CONTROL
(med)
TEST
(med)
CONTROL
(med)
TEST
(med)
CONTROL
(med)
TOTAL
PERCENTAGE
OF BACTERIA 8.65 11.90 9.50 7.65 8.90 0.60
Abstract (if available)
Abstract
Background ❧ Objective clinical indices used to differentiate between healthy sites and those with active periodontal disease are of great importance to the clinician. Due to the dichotomous nature of the clinical response, indices involving the determination of the presence or absence of bleeding have been regarded as an unbiased type of clinical assessment. It is important to understand the relationship of bleeding on probing (BOP) to other traditional measurements of the severity of periodontal disease. The purpose of the present study was to determine if there is a correlation between BOP and plaque score, pocket depth, or subgingival microbiota present in study participants with periodontitis. ❧ Materials and Methods ❧ Thirty otherwise healthy adults, diagnosed with periodontitis, were included in the study. The following clinical variables were evaluated at baseline (Visit 1), two weeks post-baseline (Visit 2) and 3 months post-baseline (Visit 3): medical history, dental radiographs, number of teeth, presence or absence of plaque, presence or absence of bleeding on probing, pocket depth, gingival recession, mobility and furcation involvement. Participants randomly received professional subgingival irrigation with either sodium hypochlorite 0.25% (test) or water (control) at visit 1 and visit 2 and rinsed at home twice-a-week with either sodium hypochlorite 0.25% (test) or water (control) throughout the course of the study. ❧ The presence of plaque and BOP were recorded as dichotomous variables. Pocket depth was recorded as a discrete variable in mm and was further dichotomized into >4 and ≤ 4 mm. Descriptive statistics were calculated at each visit. Pearson χ² and correlation coefficient tests were used to assess the relationship between BOP and plaque score as well as BOP and pocket depth. The significance level was set at α =0.05. Additionally, the patients were grouped into two separate cohorts according to presence or absence of BOP in the sites that were sampled, and the microbiota present at these sites were analyzed within each group. The difference within the groups between the data at baseline, Visit 2 and whenever available, Visit 3, were compared using Wilcoxon signed-rank sum test. Comparisons between test and control group at each of the 3 time points were accomplished using Wilcoxon Mann-Whitney's U test. A two-sided alternative hypothesis and a 0.05 significance level were assumed in all testing. Data analysis was performed using SAS v9.3 and STATA© statistical software (StataCorp, College Station, Texas, USA). ❧ Results ❧ The results indicate that there was a statistically significant correlation between BOP and plaque score within each group (test, control and pooled) at all study times (p<0.0001). There was a statistically significant correlation between BOP and pocket depth within each group at all study times (p<0.0001). Pocket depth and the incidence of BOP were positively correlated. A statistically significant correlation was found between BOP and the pocket depths >4 mm within each group at all study times (p<0.0001). Due to the small number of BOP positive sites that were sampled, no statistically significant differences were found in the microbiota between Visit 1 and Visit 2 or between test and control groups (p>0.05). ❧ Conclusions ❧ The present study showed a high statistical correlation between the presence of BOP and the plaque score. Moreover, a statistically significant positive correlation was observed between pocket depth and BOP
Linked assets
University of Southern California Dissertations and Theses
Conceptually similar
PDF
Effect of 0.25% sodium hypochlorite oral rinse and subgingival irrigation on periodontal clinical parameters
PDF
Technological advancements in microbial analyses of periodontitis patients: focus on Illumina® sequencing using the Miseq system on the 16s rRNA gene: a clinical and microbial study
PDF
Periodontal regeneration utilizing antibody mediated osseous regeneration (AMOR): supra-alveolar critical sized defect model
PDF
Metagenomic analysis of the microbial changes following non-surgical periodontal therapy in aggressive periodontitis
PDF
3D volumetric changes of tissue contour after immediate implant placement with and without xenograft in the horizontal gap: a randomized controlled clinical trial
PDF
A randomized controlled clinical trial evaluating the efficacy of grafting the facial gap at immediately placed implants in the anterior maxilla: 3D analysis of bone and soft tissue changes
PDF
Efficacy of fibrin-assisted soft-tissue promotion (FASTP) in treatment of multiple gingival recession defects: a retrospective 3-D volumetric analysis
PDF
Characterization of cytokine/chemokine and microbiology profiles of peri-implant sulci and implant-supported ridge lap pontics
PDF
Maxillary sinus floor and alveolar crest alterations following extraction of maxillary molars: a retrospective CBCT analysis
PDF
The effect of vertical level discrepancy of adjacent dental implants on crestal bone resorption: a retrospective radiographic analysis
PDF
Reporting quality of randomized controlled trials of periodontal diseases in journal abstracts: a cross-sectional survey and bibliometric analysis
PDF
Cone beam computed tomographic measurements of buccal alveolar bone widths overlying the maxillary premolars
PDF
Relationship of buccal bone plate thickness and healing of extraction sockets with or without alveolar ridge preservation: a systematic review
PDF
Detrimental effects of dental encroachment on secondary alveolar bone graft outcomes in the treatment of patients with cleft lip and palate: a cone-beam computed tomography study
PDF
Aggregatibacter actinomycetemcomitans oral infection: in vivo T cell immune responses and a novel bone-targeting conjugate to treat biofilm-mediated osteolytic infection
PDF
Maxillary sinus floor and alveolar crest alterations following extraction of maxillary molars and ridge preservation: a retrospective CBCT analysis
PDF
The effect of crown dimensions & implant dimensions on peri-implant marginal bone loss: a retrospective analysis
PDF
Patient reported outcomes measures (PROMs) and medication count of the three coronal advancement methods for the treatment of multiple gingival recession defects
PDF
Comparison of premolar extraction rates between one-phase and two-phase class II malocclusion
PDF
The performance of light emitting diode (LED) light curing units and dental radiometers
Asset Metadata
Creator
Gonzalez, Stephanie
(author)
Core Title
The utility of bleeding on probing and 0.25% sodium hypochlorite rinse in the treatment of periodontal disease
School
School of Dentistry
Degree
Master of Science
Degree Program
Craniofacial Biology
Publication Date
08/22/2013
Defense Date
07/31/2013
Publisher
University of Southern California
(original),
University of Southern California. Libraries
(digital)
Tag
bleeding on probing,household bleach,mouth rinse,OAI-PMH Harvest,periodontal treatment,plaque score,sodium hypochlorite
Format
application/pdf
(imt)
Language
English
Contributor
Electronically uploaded by the author
(provenance)
Advisor
Slots, Jorgen (
committee chair
), Mahvash, Navazesh (
committee member
), Rick, Sandra K. (
committee member
), Zadeh, Homayoun H. (
committee member
)
Creator Email
steph1478@gmail.com
Permanent Link (DOI)
https://doi.org/10.25549/usctheses-c3-322740
Unique identifier
UC11294894
Identifier
etd-GonzalezSt-2019.pdf (filename),usctheses-c3-322740 (legacy record id)
Legacy Identifier
etd-GonzalezSt-2019.pdf
Dmrecord
322740
Document Type
Thesis
Format
application/pdf (imt)
Rights
Gonzalez, Stephanie
Type
texts
Source
University of Southern California
(contributing entity),
University of Southern California Dissertations and Theses
(collection)
Access Conditions
The author retains rights to his/her dissertation, thesis or other graduate work according to U.S. copyright law. Electronic access is being provided by the USC Libraries in agreement with the a...
Repository Name
University of Southern California Digital Library
Repository Location
USC Digital Library, University of Southern California, University Park Campus MC 2810, 3434 South Grand Avenue, 2nd Floor, Los Angeles, California 90089-2810, USA
Tags
bleeding on probing
household bleach
mouth rinse
periodontal treatment
plaque score
sodium hypochlorite