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Publication date: Aug. 2012
Expiration date: July 2015
Abstract
Periodontitis is a disease that is more serious from a health perspective
than previously known. Peri-implant diseases are prevalent: They not only
present risk for implant failure but may also present systemic risk. The
doctors ability to determine an accurate diagnosis for both of these diseases
is critical. Ideally, the diagnostic capacity should be able to accomplish fve
important goals:
Ie eeterm|ae |l t|e r|.| ler e|.e+.e |. jre.eat |a +a |.ea j+t|eat
Ie eeterm|ae |l t||. r|.| |. ||| er |ew |a e+c| j+t|eat
Ie eeterm|ae |l +cta+| e|.e+.e |. jre.eat +t +a |e.e| el e|.e+.e (e+r|,
moderate, or late stages)
Ie eelae w||c| tre+tmeat |. me.t +e.|.+||e ler t|e .jec|lc j+t|eat.
Ie eeterm|ae |l ce-m+a+emeat |. +jjrejr|+te ler e+c| j+t|eat.
||.ter|c+||, er+| mee|c|ae (eeat|.t.) |+. at|||tee + meee| t|+t c+a ea|
identify disease after it has become clinically apparent by the loss of or
e+m+e te +a+tem|c+| .tractare.. (|0|, jec|et eejt|, r+e|er+j||c |m+e.,
etc.) While this legacy model can determine a history of past disease, it does
not fll any specifc goal of an ideal diagnostic model for the two diseases in
|ae.t|ea. Iee+, c||a|c+| |+| te.t. t|+t at|||te .+||.+ jre.|ee |alerm+t|ea ler
accomplishing the important goals of diagnosis, risk assessment, treatment
planning, and monitoring for periodontal and peri-implant diseases.
Learning Objectives:
After completion of this course, the clinician
will be able to:
1. Apply the scientifc data that
underscores the need for more
accurate diagnosis for periodontitis and
peri-implant diseases.
2. Understand the clinical utility of saliva to
identity patients at risk for periodontal
disease and peri-implant diseases.
3. Understand the shift in concentration of
specifc oral pathogens, and a specifc
genetic trait, that provide important
biological information regarding these
two diseases.
4. Understand that patients may display
similar clinical profles but have diferent
diseases.
!. t|||te + .+||.+ .+mj|e te jer.ea+||te
treatment of periodontitis and
peri-implant diseases.
Author Profile
Thomas W. Nabors, DDS, FACD
|r. N+|er. rece|.ee ||. eeree lrem t|e a|.er.|t 0l Ieaae..ee te||ee 0l |eat|.tr. |e .er.ee
in the U.S. Navy as a dentist and rotated through all of the dental specialties including oral
surgery, periodontal surgery, endodontic therapy, prosthetic dentistry and general dentistry.
|ar|a ||. teaare |a jr|.+te jr+ct|ce, |e .er.ee ea t|e mee|c+| .t+ el |+jt|.t Memer|+| |e.j|t+|
|a t|e 0r+| :arer +ae |eat+| ||.|.|ea ler +jjre\|m+te| z! e+r..
|a z1, |e ce-leaaeee +ae .er.ee +. t|0 ler |e.+acee |eat+| ||+ae.t|c., ||t.
|a z, |e leaaeee 0r+||N| |+|.. + .+||.+r e|+ae.t|c. c||a|c+| |+|er+ter.
In 2009, Dr. Nabors worked with a dedicated team to validate saliva as a suitable molecular
analyte for detection of HPV in the oral cavity.
Dr. Nabors is a frequent lecturer for both dental and medical groups on the subject of molecular
genetics in the feld of oral medicine: Including the role that periodontal disease contributes to
systemic infammation and this relationship to heart disease, stroke and diabetes. His lectures
also include the role that HPV plays in the development of certain forms of oropharyngeal
cancer.
Today, Dr. Nabors serves as president and leaaeer el |ater+tee |e+|t|t+re tea.a|t+at., ||t.
|e |+. ja|||.|ee aamerea. +rt|c|e. w|t||a + .+r|et el jeer re.|ewee ja|||c+t|ea.. |e |. + ||le
Mem|er el t|e |mer|c+a |eat+| |..ec|+t|ea, +a +..ec|+te mem|er el t|e |||, + |e||ew el t|e
|mer|c+a te||ee el |eat|.t., + mem|er el t|e ||erre |+ac|+re |eaer+r :ec|et, +ae .er.e.
within numerous dental associations.
He can be reached at: drtomnabors@gmail.com
Author Disclosure
The author of this course has no commercial ties with the sponsors or providers of the
unrestricted educational grant for this course. The author serves as executive consultant to
0r+||N| |+|..
This course has been made possible through an unrestricted educational grant.
Supplement to PennWell Publications
This course was written for dentists, dental hygienists and assistants, from novice to skilled.
Educational Methods: This course is a self-instructional journal and web activity.
Provider Disclosure: PennWell does not have a leadership position or a commercial interest in any
products or services discussed or shared in this educational activity nor with the commercial supporter.
No manufacturer or third party has had any input into the development of course content.
Requirements for Successful Completion: Ie e|t+|a z t| cree|t. ler t||. eeac+t|ea+| +ct|.|t ea ma.t j+
the required fee, review the material, complete the course evaluation and obtain a score of at least 70%.
CE Planner Disclosure: |e+t|er |eee., t| teere|a+ter eee. aet |+.e + |e+eer.||j er cemmerc|+| |atere.t
with products or services discussed in this educational activity.
Educational Disclaimer: temj|et|a + .|a|e ceat|aa|a eeac+t|ea cear.e eee. aet jre.|ee eaea| information
to result in the participant being an expert in the feld related to the course topic. It is a combination of many
educational courses and clinical experience that allows the participant to develop skills and expertise.
Registration: I|e ce.t el t||. t| cear.e |. ;1. ler z t| cree|t..
Cancellation/Refund Policy: Any participant who is not 100% satisfied with this course can request a
full refund by contacting PennWell in writing.
Go Green, Go Online to take your course
PennWell designates this activity for 2 Continuing Educational Credits
2 www.ineedce.com
Educational Ojectives
After completion of this course, the clinician will be able to:
1. Apply the scientifc data that underscores the need
for more accurate diagnosis for periodontitis and peri-
implant diseases.
2. Understand the clinical utility of saliva to identity
patients at risk for periodontal disease and peri-implant
diseases.
3. Understand the shift in concentration of specifc oral
pathogens, and a specifc genetic trait, that provide
important biological information regarding these two
diseases.
4. Understand that patients may display similar clinical
profles but have different diseases.
5. Utilize a saliva sample to personalize treatment of
periodontitis and peri-implant diseases.
Abstract
Periodontitis is a disease that is more serious from a health
perspective than previously known. Peri-implant diseases
are prevalent: They not only present risk for implant failure
but may also present systemic risk. The doctors ability to
determine an accurate diagnosis for both of these diseases is
critical. Ideally, the diagnostic capacity should be able to ac-
complish fve important goals:
To octcrminc if thc risk for oiscasc is prcscnt in any
given patient
To octcrminc if this risk is high or low in cach paticnt
To octcrminc if actual oiscasc is prcscnt at any lcvcl of
disease (early, moderate, or late stages)
To ocfnc which trcatmcnt is most aovisallc for thc
specifc patient.
To octcrminc if co-managcmcnt is appropriatc for cach
patient.
Historically, oral medicine (dentists) has utilized a
model that can only identify disease after it has become
clinically apparent by the loss of or damage to anatomi-
cal structures. (BOP, pocket depth, radiographic images,
etc.) While this legacy model can determine a history of
past disease, it does not fll any specifc goal of an ideal
diagnostic model for the two diseases in question. Today,
clinical lab tests that utilize saliva provide information
for accomplishing the important goals of diagnosis, risk
assessment, treatment planning, and monitoring for peri-
odontal and peri-implant diseases.
The Medical Model
General medicine has for decades utilized a different
model for diagnosis and treatment of disease than has
oral medicine / dentistry. This model is oft referred to as
the Medical Model: the traditional approach to the di-
agnosis and treatment of illness as practiced by physicians in
the Western world since the time of Koch and Pasteur. The
clinical decisions made by the physician are based upon
an accurate diagnosis that requires the clinical exam,
medical history, and the results from specifc lab tests.
1, 2

Clinical lab tests and lab values become the cornerstone of
the medical exam and record. These tests represent the major-
ity of clinical data for each patient. Physicians rely heavily on
this information and interpretations to make critical decisions
that govern patient diagnosis and treatment. To put the value
of lab tests in perspective, laboratory fndings affect 60 to 70
percent of all clinical decisions in medicine.
3
Current data supports the benefts for using saliva
within the clinical lab model for both periodontal and
implant dentistry for several reasons:
Improved diagnosis and risk assessment
Genetic risk assessment
Improved patient treatment outcomes
Monitoring patient improvement post-treatment
Assessing the potential need for systemic antibiotics
Risk for bacterial contamination of implant and bone
grafting procedures.
Saliva as an important analyte within
periodontics and implant dentistry
Saliva, the most accessible and noninvasive biofuid of our
body, harbors a wide spectrum of biological analytes infor-
mative for clinical diagnostic applications.
4
Saliva contains
gingival crevicular fuid (GCF), sloughed oral epithelial
cells, and pathogenic bacteria and their products among
other elements.
5
Saliva is a representative diagnostic
specimen for an overall view of the oral microbiota since
bacteria from various sites and surfaces of the oral cav-
ity are found in saliva and mouth rinse samples. Salivary
sampling and polymerase chain reaction (PCR) technique
allow rapid and accurate identifcation of pathogenic bac-
teria and viruses, as well as human mucosal cells. The de-
tection of multiple pathogenic bacterial species in saliva is
closely associated with periodontal infections.
6

Traditional clinical data vs. The clinical
laboratory using saliva in conjunction with
clinical data
In 2009, Giannobile, et al. stated the following: In periodon-
tics and implant dentistry, traditionally clinical criteria are often
insuffcient for determining sites of active disease, for monitoring
quantitatively the response to therapy or for measuring the degree
of susceptibility to future disease progression. Saliva as a mirror
of oral and systemic health is a valuable source for clinically
relevant information because it contains biomarkers specifc for
the unique physiological aspects of periodontal / peri-implant
disease, and qualitative changes in the composition of these
biomarkers could have diagnostic value by identifying patients
with enhanced disease susceptibility, identifying sites with ac-
tive disease, predicting sites that will have active disease in the
future and/ or serving as surrogate end points for monitoring the
effectiveness of therapy.
7
www.ineedce.com 3
The authors continued to state that, [today, the prin-
cipal focus on both periodontal disease and peri-implant
disease is directed toward late stage or end-stage disease.
Thus, there is a need for earlier disease detection. Having
predictable biomarkers that can be measured within sa-
liva can provide a valuable dimension to preventing both
of these diseases as well as a more targeted strategy in the
treatment of these diseases.]
5
Aimetti et al., recently published data to show that
the desirability to measure clinical signs plus the resident
bacteria before periodontal treatment and after treatment
provided valuable information regarding treatment ob-
jectives as well as treatment success or failure in the One
Stage Full Mouth Disinfection model of therapy.
8
A recent article by Zia, et al., stated that clinical
measurements used in diagnosis of periodontal disease
are often of limited usefulness in that they are indications
of previous periodontal diseases rather than the present
disease activity. Biochemical mediators in oral fuids such
as saliva and gingival crevicular fuid (GCF) are highly
benefcial in the determination of current periodontal
status.
9
It is important especially for the general practitioner
to understand the pathogenic potential of specifc bacte-
rial species that may reside within the bioflm communi-
ty at the earliest time, and that different infections within
different individuals tend to vary signifcantly based on
bacterial specifcity and dose. When defning periodontal
disease within 774 subjects using six known periodontal
pathogens, Beikler, et al., discovered 46 different combi-
nations or Pathogen Complexes.
10
While the mouth contains hundreds of different
bacterial species and millions of individual bacteria, de-
struction of the periodontal tissues is a complex interac-
tion between specifc pathogenic bacteria, dose/concen-
tration, and the host immune response. Due to unique
pathogenic properties, some oral bacteria possess well
established differences in their ability to excite the host
immune response. It is also known that these specifc
bacteria that proliferate within the bioflm community
exhibit a higher pathogenic potential than health related
bacteria.
8-22
It is the virulence or pathogenic potential
of these specifc bacterial species that increases the host
response toward attachment loss and infammation.
9-14

The initiation and progression of both chronic periodon-
titis, as well as peri-implantitis, have well documented
references to support that when these specifc bacteria in-
crease in volume, a clear and present danger exists within
the host with an infammatory movement toward disease
and bone loss.
13,14
The events associated include the bac-
terial infection, genetic response, metabolic response
with eventual anatomical destruction. The time lag will
be different in individuals based on these events as well
as well documented risk factors.
Paju et al., found that saliva testing supported the role
of specifc bacteria and the traditional clinical signs of
periodontal disease. Per this article, the pathogens that
are considered to create the greatest pathogenic poten-
tial for chronic infammatory periodontal diseases are
Aggregatibacter actinomycetemcomitans, Porphyromonas
gingivalis, Prevotella intermedia, Tannerella forsythia,
Campylobacter rectus, and Treponema denticola. Others,
such as Fusobacterium nucleatum, Eubacterium nodatum,
Eikenella corrodens, and Micromonas micros (Peptostrep-
tococcus micros) also exhibit virulent potential and are of-
ten found in large numbers within the saliva of those with
periodontal diseases.
25

In the Paju, et al. study referenced above, bacterial
DNA from 1,198 subjects from saliva samples was ex-
tracted and PCR detection was performed using spe-
cies-specifc primers for A. actinomycetemcomitans, P.
gingivalis, P. intermedia, T. forsythia, C. rectus, and T.
denticola.
Their fndings are as stated: We investigated whether
certain bacterial species and their combinations in saliva
can be used as markers for periodontitis. In 1,198 subjects,
the detection of multiple species, rather than the presence of
a certain pathogen in saliva was associated with periodon-
titis as determined by the number of teeth with deepened
periodontal pockets.
Kononen, et al published a population based study
of salivary carriage rates of periodontal pathogens in
2007. In this study, the authors stated that saliva
is an easily obtainable and noninvasively collected micro-
biological specimen, containing the microbes which detach
from various oral surfaces. It is a suitable sample material
for large-scale oral microbiological studies utilizing PCR-
based assays, which offer a labor-minimizing technique. In
oral microbiological studies, culture has been appreciated
as the gold standard despite its relatively low sensitivity.
Due to the development of molecular biological methods,
which do not need viable cells for detection, more accurate
data on the presence of target bacteria in the specimen can
be expected.
26
In the discussion, the authors stated: Periodontitis-
associated organisms colonize not only subgingival sites, but
also supragingival sites, and appear in saliva. According
to Umeda et al,
27
whole saliva was even superior to pooled
subgingival samples to detect P. gingivalis, P. intermedia,
and T. denticola in the oral cavity, and reasonably good de-
tection rates were obtained also for A. actinomycetemcomi-
tans and T. forsytheis.
Umeda, et al., made a signifcant statement regard-
ing the presence or absence of specifc pathogens. While
carriage rates were high within their study population
(88.2%), subjects without any pathogens were typically fe-
male, young, with higher education, married, non-smok-
ing, and having full dentition, and no pockets around teeth.
4 www.ineedce.com
This is a signifcant fnding and is also consistent with
other laboratory fndings. Subjects with clinical signs of
attachment loss tend to carry multiple pathogenic spe-
cies in higher concentration than those within healthy
subjects. However, subjects without clinical signs of
disease (healthy subjects), do not tend to have patho-
genic species. Or if present, they are at very low con-
centration.
In concluding remarks, the authors stated There is
abundant evidence that the prevalence of major periodon-
tal pathogens in oral (saliva) specimens varies between
individuals due to differences in their periodontal health
status. In pathogen carriers, the proportion of pathogens
increases in saliva due to deteriorating periodontal status,
an indication that a subject with advanced periodontitis
can serve as a potential source of pathogens to his/her close
contacts. Monitoring the carriage pattern of periodontal
pathogens at the general population level may help in
designing preventive strategies to attempt to control the
acquisition of less benefcial members of the human oral
microbiota.

Boutaga, et al. studied the comparison of subgingival
bacterial detection with oral mouth wash samples (oral
lavage) to detect and quantify periodontal pathogens.
The study was used to compare saliva with site specifc
testing via subgingival detection and also the abilities
of anaerobic culture technique compared to the use of
real-time PCR technique to detect and quantify bacte-
rial pathogens.
28
The aim of the study was to compare the presence
and numbers of Actinobacillus actinomycetemcomitans,
Porphyromonas gingivalis, Tannerella forsythia, Prevotella
intermedia, and Micromonas micros in subgingival plaque
and mouth wash samples.
The conclusions included: Both qualitatively and
quantitatively, saliva detected Aa, Pg, Tf, Pi, & Mm
more successfully than subgingival samples. The highest
detection frequencies were found in mouth wash samples
with real-time PCR.
Rapid detection and quantifcation of periodontal
pathogens in mouth wash samples are possible by real-time
PCR. The procedure is signifcantly less time-consuming
than subgingival sampling with paper points. This ap-
proach to detect major periodontal pathogens in mouth
wash samples may simplify microbial diagnosis in peri-
odontitis patients and may be used to monitor periodontal
treatment.
Per a host of literary reviews, the diagnosis of peri-
odontal disease as well as the progression of periodontal
destruction cannot be predicted by traditional clinical
signs of disease. However, the progression of chronic
periodontal disease can be predicted by the levels of spe-
cifc bacterial pathogens that can be accurately measured
within a salivary sample.
Saliva testing and genetics
The role of genetic susceptibility to periodontal infections has
been a topic of much research during the past decade.
29-34
Periodontitis is considered as a complex genetic
disease whose phenotype is determined by both the ge-
netic makeup and the environmental infuences on the
affected individual.
29
Clinical studies have demonstrated that cytokine neu-
tralization was able to inhibit alveolar bone loss. There are
several reasons to believe IL-1 is an important mediator
of connective tissue destruction in the gingiva and peri-
odontal ligament and in the resorption of alveolar bone.
IL-1 is a potent stimulator of bone resorption in vitro and
in vivo as well as a potent stimulator of matrix metallopro-
teinase expression. It is also the most potent stimulator of
bone resorption in vitro of all the cytokines and hormones
and a strong stimulator of prostaglandin E2 formation
which fosters bone resorption mediated by RANKL ex-
pression in perio tissues.
Along with periodontal disease, there are clinical
studies showing the importance of IL-1 for joint in-
fammation and destruction in RA and osteoarthritis.
Saliva, Implants and bone grafts
Infections are a signifcant concern for both the time of
surgical placement of osseointegrated dental implants as
well as their long term survivability. Both the optimal
placement time as well as survivability may be predicted
more effectively by knowing specifc oral bacterial pres-
ence and concentration than by observation of clinical
signs. Increased occurrence of Porphyromonas gingiva-
lis, Prevotella intermedia, Treponema denticola, and Ag-
gregatibacter actinomycetemcomitans are considered risk
factors for further attachment loss around implants and
bone grafts.
35-38
Charalampakis

et al., from July, 2011, clearly demon-
strates that a history of periodontitis increases the risk for
mucositis and peri-implantitis.
37
This study included the
following:
Cohort stuoy from 1996-2006
N=736 subjects
Mean follow-up 35.6 months
Scvcrc chronic inammation status turnco out to lc a
signifcant risk factor for implant failure after 50 months
HR=8.06 (Greater risk than smoking)
Smoking inoicatcs a signifcant cffcct aftcr 30 months
HR=2.76
Fcriooontal status ano smoking arc signifcant risk
factors for late implant failures.
Since most implant benefciaries have a history of
periodontitis, it would be helpful to know how signif-
cant this is on a patient to patient basis. When observ-
www.ineedce.com 5
ing the fndings, chronic infammation around remain-
ing teeth resulted in a signifcantly greater risk factor for
implant failure after 50 months than smoking.
With respect to surgical grafts and contamination
with saliva:
Verdugo et al., recently published an article
38
en-
titled: Periodontopathogen and Epstein-Barr Virus
Contamination Affects Transplanted Bone Volume in
Sinus Augmentation. The odds ratio (OR) of having
bone microbial contamination in patients with a history
of periodontitis was 37.5 times higher than in individu-
als without periodontitis.
Additionally, the likelihood of having moderate to
pronounced bone volume loss 6 months post augmenta-
tion was 7.5 times greater in those patients presenting
with 3 specifc pathogens (Porphyromonas gingivalis,
Aggregatibacter actinomycetemcomitans, Tannerella
forsythia, or Prevotella intermedia) versus those with
only one (P <0.05).
The following are the salient features of this article:
Hackground:
Bone microbial contamination can impair osteogen-
esis. Human herpes viruses-associated vasculitis
can cause vascular damage within the osseous graft
and host.
This study was conducted to substantiate specifc
contamination and assess the impact 6 months after
sinus augmentation.
Xcthods:
Culture and PCR-based identifcation were per-
formed on harvested bone particles and unstimulated
whole saliva in a group of 30 patients undergoing
maxillary sinus augmentation.
Thirty patients were divided into two groups: those
with and those without a history of periodontitis.
Radiographic evaluation was done to assess and
compare bone healing and volume gain at baseline
and 6 months post-transplantation.
HcsuIts:
Seventeen patients had a history of periodontitis, and
13 did not.
Ten showed culture- and PCR-negative results and
belonged to the periodontally healthy group.
The 17 patients with periodontitis showed culture
or PCR-positive results for the targeted periodontal
pathogens.
Patients with periodontitis were 2.3 times more likely
to have positive salivary Epstein-Barr virus type 1
(EBV-1) than those with no history of periodontitis.
HcsuIts:
The likelihood of having moderate to pronounced
bone volume loss 6 months post augmentation was
7.5 times greater in those patients presenting with
3 specifc pathogens (Forphyrononas gingivaIis,
Aggrcgatibactcr actinonycctcnconitans,
JanncrcIIa forsythia, or FrcvotcIIa intcrncdia)
versus those with only one (P <0.05).
The odds ratio (OR) of pronounced volume loss
was 16.3 times higher in those contaminated with a
combination of salivary EBV-1 and 3 of the previ-
ously mentioned species versus only EBV-1 (P <0.05).
Individuals showing positive salivary EBV-1 had
bone bacterial contamination associated 57% of the
time.

The odds ratio of having bone microbial contamina-
tion in patients with a history of periodontitis was
37.5 times higher than in individuals without
periodontitis.
Conclusions
The medical model of utilization of clinical lab tests has
proven for the past 100 years the value of biological in-
formation in patient care. Periodontal diseases are serious
infections that deserve the same degree of urgency that is
provided for the prevention and treatment of all human
diseases and infections. If each periodontal infection was
the same, then the treatment of all infections the same
way would make sense. However, since periodontal infec-
tions differ widely based on etiological agents, genetic
factors, and additional risk factors, the use of clinical lab
tests has signifcant value for both diagnosis and therapy.
Perhaps, the greatest value lies within the general dentist
offce as the widest variety of periodontal diseases may be
expected. Upon identifcation of specifc infections and
consideration of risk elements, the GP may choose to treat
the disease, refer the patient to a specialist, or co-manage
the patient based on additional information received from
saliva testing.
The etiological agents of periodontal disease are well
established with a multitude of scientifc articles that
clearly state the relationship between specifc bacteria
and concentration are related to both periodontitis and
peri-implant infections. Plus, the ability to detect a spe-
cifc genetic variation appears to make signifcant differ-
ences in certain individuals as to their risk for disease as
well as the severity of their disease.
6 www.ineedce.com
The referenced articles within this course support
the use of specifc bacteria and specifc genetics to more
accurately defne both periodontal infections and peri-
implant diseases. The use of saliva as a valuable, predict-
able, and accurate analyte in conjunction with clinical
signs is proving to add great value to periodontal and im-
plant dentistry for diagnosis, treatment and monitoring
of periodontal disease.
Today, saliva and the clinical lab model exist for ev-
eryday use. The future, really, is today.
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signifcance and clinical validity: Periodontol 2000, Vol. 39,
2005, 40 52: Arie J, van Winkelhoff, Winkel
14. Microbial complexes in subgingival plaque; J Clin Periodontol
Vol. 25, 134 144; 1998; Socransky, Haffajee, Cugini
15. Microbiological goals of periodontal therapy; Teles, Haffajee,
Socransky; Periodontol 2000, Vol 42, 2006, 180 218
16. Anne Haffajee, Sigmund S. Socransky; Microbial etiological
agents of destructive periodontal disease: Periodontol 2000,
Vol. 5; 1994, 78 111
17. The effect of periodontal therapy on the composition of the
subgingival microbiota: Periodontol 2000, Vol . 42, 2006, 219-
258
18. Role of bacteria in health and disease of periodontal tissues:
Feng, Winberg; Periodontol 2000, Vol. 40, 2006, 50 76
19. Dental Bioflms: diffcult therapeutic targets: Socransky,
Haffajee; Periodontol 2000, Vol. 28, 2002, 9 12
20. Etiology of Periodontal Diseases: Susam Kinder Haake;
Carranzas Clinical Periodontology: Ninth Edition; 2002; 95-
112
21. Rose LF, Steinberg BJ, Minsk L. The relationship between
periodontal disease and systemic conditions. Compend
Contin Educ Dent. 2000 Oct;21(10A):870-7;quiz 878.
22. I. B. Darby, G. G. Adams, B. Hoffmann, E. C. Reynolds, S.
J. Byrne, S. G. Dashper; Progression of chronic periodontitis
can be predicted by the levels of Porphyromonas gingivalis
and Treponema denticola in subgingival plaque : Molecular
Oral Microbiology, 12 OCT 2009, 469-477
23. Beikler, et al., Specifc Antibiotics in the Treatment of
Periodontitis-A Proposed Strategy; J Periodontology, Jan.
2004, Vol 75, #1, 169-175
24. J. Slotts, DMD, PhD, The Search for Effective, Safe, and
Affordable Periodontal Therapy; Periodontology 2000, vol.2,
2002
25. Paju, Pussinen, Suominen-Taipale, Hyvonen, Knuuttila,
Kononen; Detection of Multiple Pathogenic Species in Saliva
Is Associated with Periodontal Infection in Adults: J Clin
Micro Jan. 2009, 235-238
26. Kononen, Paju, Pussinen, Hyvonene, Di Tella, Suominen-
Taipale, Knuuttila; Population-Based Study of Salivary
Carriage of Periodontal Pathogens in Adults: J Clin Miro, Aug.
2007, 2446-2451
27. Umeda, M., A. Contreras, C.Chen, I. Bakker, J. Slotts;
The Utility of Whole Saliva to detect the oral presence of
periodontopathic bacteria; J Periodontology. 69: 828-833
28. Boutaga, Savelkoul, Winkel, van Winkelhoff; Comparison
of Subgingival Bacterial Sampling With Oral Lavage for
Detection and Quantifcation of Periodontal Pathogens by
Real-Time Polymerase Chain Reaction: J Perio Jan. 2007; 79-
86
29. Yoshe, Kobyashim, Tai, Galicia; The role of genetic
polymorphisms in periodontitis; Perio 2000, Vol. 43, 2007,
102-132
30. Dana Graves; Cytokines that Promote Periodontal Tissue
Destruction: J Periodontol. August 2008; 1585-91 (Suppl.)
31. Yen-Chun, G. Liu, Ulf H. Lerner, Yen-Tung A.Teng;
Periodont 2000, Vol. 52, 2010, 163-206
32. Ahmed Abd El-Meguid Mostafa Hamdy, DDS*Mohamed
Abd El-Moniem Ebrahem, DDS, Journal of Oral
Implantology, Faculty of Dentistry, Minia University, Minia,
Egypt., July, 2011; Interleukin 1 Genotype in Peri-implantitis
33. Cytokines that Promote Periodontal Tissue Destruction:
Dana Graves, J Periodontol. August 2008; 1585-91 (Suppl.)
34. Higashi MK, Veenstra DL, del Aguila M, Hujoel P. The cost-
effectiveness of interleukin-1 genetic testing for periodontal
disease. J Perodontolo 2002: 73: 1474-1484
35. Schwarz, F., Becker, J., PERI-IMPLANT INFECTION:
Etiology, Diagnosis, and Treatment; Quintessence
Publishing;

2010; 113
36. Liran Levin1, Ronen Ofec2,3, Yoav Grossmann4, Rachel
Anner; 2 JUN 2011; Periodontal Disease as a Risk Factor for
Implant Failure; Clin Perio Vol. 38, Isssue 8, 732-737; August
2011
37. Georgios Charalampakis1, Per Rabe2, sa Leonhardt1,3,
Gunnar Dahln A follow-up study of peri-implantitis cases
after treatment; 1Article frst published online: 19 JUL 2011
38. Verdugo et al; Periodontopathogen and Epstein-Barr Virus
Contamination Affects Transplanted Bone Volume in Sinus
Augmentation; 2012, Vol. 83, No. 2, J Periodont 162-173 ,
DOI 10.1902/jop.2011.110086
www.ineedce.com 7
Author Profile
Thomas W. Nabors, DDS, FACD
Dr. Nabors received his degree from
the University Of Tennessee College
Of Dentistry. He served in the U.S.
Navy as a dentist and rotated through
all of the dental specialties including
oral surgery, periodontal surgery, end-
odontic therapy, prosthetic dentistry
and general dentistry. During his tenure in private prac-
tice, he served on the medical staff of Baptist Memorial
Hospital in the Oral Surgery and Dental Division for ap-
proximately 25 years.
In 2004, he co-founded and served as CEO for Advanced
Dental Diagnostics, LLC.
In 2008, he founded OralDNA

Labs: a salivary diag-


nostics clinical laboratory.
In 2009, Dr. Nabors worked with a dedicated team to
validate saliva as a suitable molecular analyte for detec-
tion of HPV in the oral cavity.
Dr. Nabors is a frequent lecturer for both dental and med-
ical groups on the subject of molecular genetics in the feld
of oral medicine: Including the role that periodontal dis-
ease contributes to systemic infammation and this rela-
tionship to heart disease, stroke and diabetes. His lectures
also include the role that HPV plays in the development
of certain forms of oropharyngeal cancer.
Today, Dr. Nabors serves as president and founder of
Integrated HealthCare Consultants, LLC.
He has published numerous articles within a variety of
peer reviewed publications. He is a Life Member of the
American Dental Association, an associate member of
the AAP, a Fellow of the American College of Dentists,
a member of the Pierre Fauchard Honorary Society, and
serves within numerous dental associations.
He can be reached at: drtomnabors@gmail.com
Disclaimer
The author of this course has no commercial ties with the
sponsors or the providers of the unrestricted educational
grant for this course. The author serves as executive
consultant to OralDNA Labs.
Reader Feedback
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course. For your convenience, an online feedback form is
available at www.ineedce.com.
Notes
8 www.ineedce.com
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Questions
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answers. An immediate grade report will be provided and upon receiving a passing grade your Verifcation Form will be provided immediately for viewing and/or printing. Verifcation Forms can be viewed
and/or printed anytime in the future by returning to the site, sign in and return to your Archives Page.
1. The Medical Model is defned by mak-
ing clinical decisions using which of the
following:
a. Medical history
b. Clinical exam
c. Specifc lab tests
d. All of the above
2. Current data supports the use of saliva
within oral diagnosis that will impact
which of the following:
a. Genetic risk assessment
b. Improved diagnosis
c. Specifc pathogenic species
d. All of the above
3. Traditional clinical criteria are often
insuffcient for determining which of the
following:
a. Sites of active disease
b. For monitoring response to therapy
c. Genetic susceptibility
d. All of the above
4. The detection of multiple pathogenic
bacteria species in saliva is
a. Closely associated with periodontal infections.
b. Not signifcant
c. Causes halitosis
d. Is found in all humans
5. Saliva as a mirror of oral and systemic
health is a valuable source for clinically
relevant information because
a. It contains biomarkers unique to periodontal and
peri-implant disease
b. Quality changes in these biomarkers have
diagnostic value
c. It can serve as surrogate end points for monitoring
effectiveness of therapy
d. All of the above
6. Clinical measurements used in diagnosis
today
a. Has limited usefulness
b. Is the best that we have
c. Are indications of previous disease rather than
present disease activity
d. Both a and c
7. Specifc bacteria within bioflm infections
are important because
a. Some bacteria possess virulent properties that
initiate immune responses more than others
b. Concentration of pathogenic species must be taken
into consideration
c. Knowing which bacteria are present helps to
determine how to treat
d. All of the above
8. Specifc bacteria species contained within
saliva can be used as markers for
a. Periodontal disease & peri-implant disease
b. Increased risk for disease
c. Potential risk for both diseases
d. All of the above
9. Some reasons that patients tend to
refract after perio therapy include
which of the following.
a. Major perio pathogens in saliva varies between
individuals
b. Subjects with periodontitis can serve as a carrier to
close contacts
c. Treatment procedures in themselves do not
guarantee that end-point of therapy has been
reached
d. All of the above
10. Saliva samples to detect pathogen groups
and quantify them have been shown to be
a. More successful than subgingival samples.
b. Less successful than subgingival samples
c. A relevant risk assessment model
d. Both a & c
11. All people that have periodontal infec-
tions have
a. An equal degree of susceptibility to infections.
b. Susceptibility may vary based on the IL-1 genotype
c. No need to know this
d. Should brush and foss more
12. Periodontitis is considered to be a
complex disease and differences in disease
activity and appearance is determined by
which of the following
a. Genetic makeup
b. Environmental infuences
c. Specifc bacteria and concentration
d. All of the above
13. Interleukin B (IL-) is
a. An important mediator of connective tissue
destruction
b. A strong stimulator of prostaglandin E2 and bone
resorption
c. Is found only in patients with RA and joint
infammation
d. Found at increased levels in IL-1 genotype
individuals
e. Both a and b
f. A, B, and D
14. Increased occurrence of Pg, Pi, Td, and
Aa are considered risk factors for
a. Attachment loss around implants and bone grafts.
b. Found in all adults
c. Not relative to risk management
d. Dental caries
15. Charalampakis et al. demonstrated that
a history of periodontitis presents
a. No increased risk for implant infections.
b. Signifcant risk for implant infections
c. Should not matter as implants are very successful
d. Patients that want implants dont care
16. As clinical signs are not good predictors
of potential risk of infection, and since a
history of periodontitis increases risk for
implant infections, it seems reasonable
a. To determine the potential risk for implant failure
or infections prior to the placement of an implant.
b. To probe all patients prior to placing implants
c. To determine the potential risk for implant disease
over time
d. All of the above
17. Saliva samples in parallel with clinical
signs to help determine disease or risk for
disease, based on these studies, appears
a. To offer signifcant improvement in diagnosing
periodontal diseases and peri-implant risk over the
traditional model of clinical signs only.
b. Dont improve risk assessment
c. Are becoming standard of care issues
d. Are not available today
18. Saliva contamination of surgical sites can
impair osteogenesis
a. Based on the presence of specifc bacterial and viral
species.
b. Based on surgical expertise
c. Doesnt make signifcant difference in surgical
outcomes
d. Based on patient home-care
19. Saliva has become an important
biofuid due the fact that it harbors a
wide spectrum of
a. Salivary proteins
b. Elements that can be used to detect cancers
c. Biological analytes with information that is
clinically relevant and important.
d. Buffers
20. Laboratory tests and lab values are the
cornerstone of the medical exam and
record. Dentists are the main source of
determining oral disease activity and
genetic susceptibility and lab tests have
become an important addition to the
clinical exam.
a. Adopting the Medical Model is an important
advancement in patient care.
b. Saliva tests are improving diagnosis and risk
management
c. Clinical lab tests for improved patient are using
saliva are available today
d. All of the above
Educational Objectives
1. Apply the scientifc data that underscores the need for more accurate diagnosis for periodontitis and
peri-implant diseases.
2. Understand the clinical utility of saliva to identity patients at risk for periodontal disease and peri-implant diseases.
3. Understand the shift in concentration of specifc oral pathogens, and a specifc genetic trait, that provide important
biological information regarding these two diseases.
4. Understand that patients may display similar clinical profles but have diferent diseases.
5. Utilize a saliva sample to personalize treatment of periodontitis and peri-implant diseases.
Course Evaluation
1. Were the individual course objectives met? Objective #1: Yes No Objective #4: Yes No
Objective #2: Yes No Objective #5: Yes No
Objective #3: Yes No
Please evaluate this course by responding to the following statements, using a scale of Excellent = 5 to Poor = 0.
2. To what extent were the course objectives accomplished overall? 5 4 3 2 1 0
3. Please rate your personal mastery of the course objectives. 5 4 3 2 1 0
4. How would you rate the objectives and educational methods? 5 4 3 2 1 0
5. How do you rate the authors grasp of the topic? 5 4 3 2 1 0
6. Please rate the instructors efectiveness. 5 4 3 2 1 0
7. Was the overall administration of the course efective? 5 4 3 2 1 0
8. Please rate the usefulness and clinical applicability of this course. 5 4 3 2 1 0
9. Please rate the usefulness of the supplemental webliography. 5 4 3 2 1 0
10. Do you feel that the references were adequate? Yes No
11. Would you participate in a similar program on a diferent topic? Yes No
12. If any of the continuing education questions were unclear or ambiguous, please list them.
___________________________________________________________________
13. Was there any subject matter you found confusing? Please describe.
___________________________________________________________________
___________________________________________________________________
14. How long did it take you to complete this course?
___________________________________________________________________
___________________________________________________________________
15. What additional continuing dental education topics would you like to see?
___________________________________________________________________
___________________________________________________________________
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cree|t.. I|e lerm+| ceat|aa|a eeac+t|ea jrer+m el t||. .jea.er |. +ccejtee | t|e |0| ler |e||ew.||j/
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t|e|r .t+te eeat+| |e+re. ler ceat|aa|a eeac+t|ea re|a|remeat.. |eaa\e|| |. + t+||lera|+ |re.|eer. I|e
t+||lera|+ |re.|eer aam|er |. 1!zI. I|e ce.t ler cear.e. r+ae. lrem ;z. te ;..
||0\|||| |N|0|M|I|0N
|eaa\e|| |. +a ||| t||| |ecea|tee |re.|eer. ||| t||| |. + .er.|ce el t|e |mer|c+a |eat+| +..ec|+t|ea
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er/cetecerj/
I|e |eaa\e|| terjer+t|ea |. ee.|a+tee +. +a |jjre.ee ||t| |rer+m |re.|eer
by the Academy of General Dentistry. The formal continuing dental education
jrer+m. el t||. jrer+m jre.|eer +re +ccejtee | t|e |0| ler |e||ew.||j,
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ANSWER SHEET
Saliva and the Clinical Laboratory:
A Data Driven Model for Periodontics and Implant Dentistry
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