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Aus der Abteilung für präventive Zahnmedizin und Kinderzahnheilkunde
(Leiter: Prof. Dr. med. dent. Ch. H. Splieth)
im Zentrum für Zahn-, Mund- und Kieferheilkunde
(Geschäftsführender Direktor: Prof. Dr. med. habil. G. Meyer)
der Medizinischen Fakultät der Ernst-Moritz-Arndt-Universität Greifswald

Therapeutic Sealing of Proximal Tooth Surfaces:
Two-Year Clinical and Radiographic Evaluation

Inaugural – Dissertation zur Erlangen des Akademischen Grades
Doktor der Zahnmedizin (Dr. med. dent)
der Medizinischen Fakultät
der Ernst-Moritz-Arndt-Universität Greifswald

Vorgelegt von
Mohammad Alkilzy
Geb. am 27.1.1974 in Albab / Syrien


Dekan: Prof. Dr. rer. nat. Heyo K. Kroemer

1. Gutachter: Prof. Dr. Christian H. Splieth

2. Gutachter: OA PD Dr. H. Meyer-Lückel,

Ort, Raum: Greifswald, Hörsaal ZZMK, Walter-Rathenaustr. 42

Tag der Disputation: 6.7.2009

2 Table of Contents
1 Introduction and literature review 5
1.1 Definition of dental caries 5
1.2 History of dental caries 5
1.3 Epidemiology of dental caries 6
1.4 Etiology of dental caries 6
1.5 Histology of dental caries 8
1.5.1 Enamel changes during early caries lesion formation 8
1.5.2 Dentine changes during early caries lesion formation 10
1.6 Diagnosis of dental caries 11
1.6.1 Clinical caries diagnosis 12
1.6.2 Radiographic caries diagnosis 13
Bite-wing x-rays 13
Digital x-rays 14
1.6.3 Assessment of caries risk 15
1.6.4 Assessment of caries activity 15
1.7 Prevention of dental caries 15
1.7.1 Nutrition and diet 16
1.7.2 Oral hygiene (tooth brushing, flossing) 17
1.7.3 Fluoride 18
1.7.4 Antimicrobial agents 19
1.8 Treatment of dental caries 20
1.8.1 Making treatment decision 20
1.8.2 Operative treatment 21
1.8.3 Non-invasive treatment, de- and re-mineralization 21
1.8.4 Minimal invasive treatment 22
1.8.5 Sealants 22
2 Aim of the study 25
3 Material and methods 26
3.1 Sample 26
3.2 Material and study design 26
3 Baseline examination 26
Proximal sealing 27
Recall and evaluation 30
X-ray evaluation 31
Statistical analysis 32
4 Results 33
4.1 Baseline data 33
4.1.1 Distribution of sample with respect to gender and age 33
4.1.2 Distributions of proximally sealed teeth 33
4.1.3 Distribution of control teeth 34
4.1.4 Medical history 34
4.1.5 Dental examination 35
DMFT/S and dmft/s Indices 35
Vitality tests of test, control, and adjacent teeth 35
Distribution of plaque and bleeding in the sample 35
4.2 Changes in medical history, DMFT/S, plaque, gingival bleeding
and tooth vitality through out the study 36
4.3 Clinical results throughout the study 39
4.4 Radiographic evaluation after 2 years 41
4.5 Drop-out analysis 42
5 Discussion 44
6 Summary 48
Zusammenfassung (Deutsch) 49
7 References 50
8 Appendixes 59
Appendix 1 Study’s consent 59
Appendix 2 Data sheet: Baseline 63
Appendix 3 Recall sheet 65
Eidesstattliche Erklärung 67
Lebenslauf 68
Danksagung 71
4 1 Introduction and Literature Review

1.1 Definition of Dental caries
Dental caries is the medical term for tooth decay (Latin: caries = putrescence,
rottenness) (Dorland, 1985). Through the history of medicine and dentistry the
definition of dental caries is changing relating to the progress in understanding this
disease. Till now there is no unity about the definition of dental caries but many
describing definitions, and that is understandable and acceptable in such a multi-
factorial disease. Still a sufficient definition of a disease is important to deal with it
Clinically, dental caries is a chronic disease, a process that progresses very slowly in
most individuals. The signs of the disease can be arranged on a scale ranging from
initial loss of mineral at the ultra structural level to total tooth destruction.
thIn the late 19 century, Miller (1890) implicated bacteria as the cause of human
thdental caries. Then at the turn of the 20 century, Black (1908) recognized that
certain areas of the teeth are less prone to caries than others. The works and
concepts of Miller and Black established dentistry and provided the impulse for
important and continuing work in the fields of basic caries research.
Biologically, dental caries is an infectious and transmissible disease caused by
bacteria colonizing the tooth surfaces. Unlike most infectious diseases affecting
humans, caries is the result of an imbalance of the indigenous oral biota rather than a
non indigenous, exogenous pathogen (Caufield and Dasanayake, 2005).
But actually, dental caries reflects symptoms of ongoing and past disease not the
disease itself, there are patho-physiological processes leading to net loss of mineral,
which occurs through imbalance between de- and re-mineralization (Steinberg,

1.2 History of dental caries
In the most ancient hominids, the incidence of caries was less than 1%. Although
many Neandertal specimens have been discovered, no carious lesions have been
described except for a single root lesion in some Neandertal teeth (Koca et al.,
2007). In European material, there is a gradual increase from very low rates through
the Paleolithic, Neolithic, Bronze and Iron Age, to a rapid rise through Medieval and
5 modern times. There has been sporadic, but generally increasing caries prevalence
over the past 5,000 years. During the first 4,000 years there is a gradual increase in
caries prevalence ranging from 2 to 10 carious teeth per 100 teeth, followed by a
sharp rise at about the year 1000 A.D. to 24 carious teeth per 100 for 3 out of 4
populations. The year 1000 A.D. is the approximate date for the introduction of sugar
cane to the Western world. The introduction of refined sugar into modern society diet
has tipped the balance from health to disease (Caufield and Dasanayake, 2005).

1.3 Epidemiology of dental caries
An epidemiological description of a given health problem usually includes its
prevalence, severity (morbidity, mortality) and age-adjusted distribution in the
population. To understand the disease process and how caries presents in different
groups in society, one needs to know about the disease in various populations or
communities, as opposed to just at the individual patient level which normally
concerns the clinician providing dental care.
To obtain epidemiological caries data some instrument are needed such as indexes,
diagnosis methods, and statistical analyses.
It should be remembered that dental caries is a disease of lifestyle with strong
regional differences.
In the last four decades epidemiological studies demonstrated a remarkable
decrease in caries severity in schoolchildren and adolescences in most industrialized
societies (Petersen, 2003; Marthaler, 2004). This has been attributed to several
factors such as a change in the understanding of the caries process, a slower
progression rate of the carious lesions (Pitts et al., 2003), and a spread of oral
hygiene procedures and fluoridated toothpaste (NIH, 2001).
The epidemiological data suggest that in the permanent dentition of children dental
caries continues to be seen, mainly on occlusal surfaces, particularly of first and
second permanent molars (Dummer et al. 1988; Chestnut et al., 1996). In adults,
approximal lesions are more common (Dummer et al. 1988; Chestnut et al., 1996;
Marthaler et al. 1996; Mejare and Mjör, 2003), while in elderly root caries is a
problem (Beck, 1990).

1.4 Etiology of dental caries
It is interesting to know how hums understood dental caries through its development.
6 According to ancient Sumarian text “The legend of worm” toothache was caused by a
worm that drank the blood of teeth and fed on the root of the jaws. The ancient Greek
believed that a person’s physical and mental constitution was determined by four
elemental humours of the body- blood, phlegm, black bile and yellow bile. An
imbalance in these humours is the cause of all diseases including dental caries. At
the beginning of nineteenth century till the middle of the last century started the first
main subjective caries’ theories. In 1819 Parmly proposed The Chemical (Acid)
Theory. According to this theory, teeth were destroyed by the acids formed in the oral
cavity by the putrefaction of protein which produced ammonia and was subsequently
oxidized to nitric acid. In 1895 Robertson proposed that dental decay was caused by
acids formed by fermentation of food particles around teeth (Ismail et al., 2001).
According to the Chemo-Parasitic Theory by D. W. Miller (1890), microorganisms of
the mouth, by secretion of enzymes or by their own metabolism, degrade
fermentable carbohydrate food materials to form acids which demineralize the
enamel and the disintegrated enamel is subsequently mechanically removed by force
of mastication. Miller summarized his theory as follows: Dental decay is a
chemoparasitic process consisting of 2 stages- decalcification or softening of the
tissue and dissolution of the softened residue (Fejerskov and Kidd, 2003).
The Proteolytic Theory (Gottlieb, 1947) proposed that microorganisms invade the
organic pathways (lamellae) of the enamel and initiate caries by proteolytic action.
Subsequently, the inorganic salts are dissolved by acidogenic bacteria. Pincus
(1950) stated that the initial caries process in dental caries was due to the proteolytic
breakdown of the dental cuticle.
By the middle of twentieth century it was known that dental caries is a multifactorial
disease that is caused by an interplay of three major factors, i.e., teeth, cariogenic
bacteria, fermentable sugars and this process needs the last known factor, time.
Epidemiological studies revealed the relationship between caries prevalence and
sugar consumption (Fejerskov and Thylstrup, 1994).
Microbiologically, dental caries is an infectious and transmissible disease initiated by
mutans streptococci. Mutans streptococci include several different species, including
Streptococcus mutans and S. sobrinus, which are found in human caries. As mutans
streptococci require the tooth surface as a habitat, infants do not harbor these
organisms until sometime after the teeth emerge. The major source of mutans
streptococci is their mothers. The detection rate of mutans streptococci increases
7 with age. Dental plaque is a typical biofilm consisting of micro-organisms and their
products such as adhesive glucan. Plaque bacteria produce a large quantity of acids
such as lactic acid from fermentable carbohydrates. Acids are entrapped between the
tooth surface and plaque biofilm, then the pH of the enamel easily falls below 5.6,
and loss of mineral (demineralization) from enamel is induced (Foods Food
Ingredients, 2005).
Diet, saliva, fluoride and microbial species have been described as tooth and
biological determinants influencing the caries progression rate, resulting in either a
faster or slower progression rate. Various other factors such as behavioral and socio-
economic factors, known as the confounders, influence caries through the
determinants (Fejerskov, 2004).
Currently, it is obvious that for caries lesion to be developed, an interaction, or a
disturbance of the equilibrium, between the plaque and the tooth substance at the
surface and subsurface has to take place (Pitts and Stamm, 2004).
With consideration to the re-mineralization process, the caries occurs when the
imbalance between re- and de-mineralization takes place at the site of loss of
minerals in tooth substance.

1.5 Histology of dental caries
The intact enamel is comprised of 95% by weight (86% by volume) mineral and 5%
by weight (14% by volume) water and organic-matrix. Whereas the dentine is
comprised of 70% by weight (50% by volume) mineral and 20% by weight (50% by
volume) organic matrix (Cate et al., 2003).
Light microscopic examinations showed that the enamel consist of rods. These rods
consist of individual crystals (inorganic portion) separated by minute inter-crystalline
spaces (organic portion). The enamel is considered a micro-porous solid composed
of tightly packed crystals.
Due to this arrangement of enamel structure, light that enters the enamel will in
general pass through.

1.5.1 Enamel changes during early carious lesion formation
The earliest clinical evidence of dental caries appears as a loss of translucency, the
so-called ‘white spot’ lesion. Histologically, by means of polarized light microscopy,
8 four distinguishable areas have been described within the enamel lesion (Silverston,
The first two zones, visible when water is used as imbibition media, are:
1. the surface zone (width 20-50 µm), characterized by a pore volume on about
1% and regarded as apparently relatively intact.
2. the body of the lesion, that contains the greatest mass of the small lesion with
wider pores and a pore volume of 5-25%.
The other two zones are noted when Canada balsam or quinoline (identicate
refractive index compared to enamel) are used.
3. the dark zone, a demineralized zone below the body of lesion with pore
volume of 2-4%
4. the translucent zone of a width of 5-100 µm is a structure-less translucent
zone at the advanced front of the lesion, which is not always apparent.
The increased pore volume corresponds to loss of minerals on the microradiographs.
Micrographs of enamel lesions under constant and high cariogenic challenge confirm
the development of a more pronounced subsurface dissolution, compared to the
dissolution on the surface.
At the electron microscope level, this mineral loss spreads into the enamel following
the rod directions. Under lower cariogenic challenges there is a fluctuation between
remission and recurrence phases. These phenomena can be seen by irregular
patterns of mineral distribution within the lesion on the microradiographs (Silverston,
1973; Thylstrup et al., 1994).
In situ studies (Holmen et al., 1985a,b and 1987a,b; Thylstrup et al., 1994) under
cariogenic circumstances the changes on and under the enamel surface were
recorded using scanning electron microscope and polarized light. After one week, the
outer enamel structure showed dissolution, mainly of the crystal’s peripheries, and
there was an enlargement of the inter-crystalline spaces. At the polarized light level,
the increase in enamel porosity indicated a loss mineral in the order of 20-100 µm
from the surface. At this stage, no clinically visible signs of demineralization were
The initial clinical visible signs were detectable after 2 weeks. An opaque lesion could
be visually detected after thorough air-drying indicating a further loss of minerals.
9 After 14 days it seemed that the dissolution which had taken place had preferentially
been under the surface, confirming that a caries lesion consists of a subsurface zone
which is more demineralized than the surface zone.
After 3-4 weeks with external plaque-protected conditions, the enamel was further
demineralized and eroded, causing loss of translucency and surface shine and giving
rise to a diffuse reflection of light, allowing the visible signs of opacity to be
recognized, even under wet conditions. The outermost microsurface exhibited
complete dissolution of thin perikimata overlapping and more marked dissolution.
The more extensive loss of mineral was constantly increasing beneath the outer
surface. At this stage, at polarized light microscopy level, the classical zones of the
‘white spot’ lesion were identifiable.
The characteristics of approximal white-spot lesion differ slightly. The shape of
approximal white-spot lesion is determined by the distribution of the microbial
deposits between the contact facet and the gingival margin, which result in a kidney-
shaped appearance. The lesion extend buccally and lingually and stops where the
natural cleaning occur. The examination of the surface of an approximal active white-
spot lesion showed irregular fissures and small defects along the periphery of the
facet. In the opaque surface enamel cervical to the facet irregular holes are seen,
which in other areas merge together, forming larger areas of irregularity and minor
fractures of the perikymata edge.
Typically, the lesion appears triangular in sections cut through the central lesion part.
Carious dissolution follows the direction of the rods in a conically shape.
Comparisons of surface-layer thickness within lesions showed that the peripheral part
of the surface layer was always thinner than the central part, probably reflecting a
less advanced stage of lesion progression in the lesion periphery (Cate et al., 2003).

1.5.2 Dentine changes during early caries lesion formation
The most common defense reaction by the pulpo-dentinal organ is tubular sclerosis,
which is deposition of mineral along and within the dentinal tubules, resulting in their
gradual occlusion (Stanley et al., 1983). Caries is a stimulus that accelerates the age-
related tubular sclerosis which is the result of mild stimuli from environment mediated
through the enamel.
With light microscope, caries-related tubular sclerosis is seen corresponding to the
deepest part of the progressing enamel lesion. Initial tubular sclerosis is seen before

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