Arrest – Fluoride and plaque control

Fluoride and plaque control
Arrest of enamel carious lesions is a reality, as shown in the studies by Backer-Dirks (1966) and von der Fehr et al (1970). In vitro as well as in vivo studies have shown that carious lesions in enamel can successfully be arrested by plaque control or topical use of fluoride. The most efficient means is a combination of both, as exemplified in Fig 156. On the left is an active, noncavitated enamel lesion on the mesiolingual surface of a mandibular second molar. Fluoride accumulates in the plaque fluid and as calcium fluoride on the enamel surface. During the acid challenge, calcium fluoride is dissolved. The enamel surface acts as a micropore filter and F- and H+- ions (HF) diffuse into the subsurface lesion, increasing the amount of fluoride in the active lesion compared to the surrounding intact enamel. Within the lesion, the F- ions retard demineralization of the enamel crystals during acid challenge and enhance remineralization by crystal growth and accumulation of fluorapatite on the crystal surfaces when the pH rises. Such a lesion can successfully be arrested if the patient maintains a high standard of approximal plaque control and uses fluoride toothpaste. 
Remineralization of the lesion is usually incomplete. “Continuous” access to a low concentration of fluoride results in more complete remineralization than does a high concentration of fluoride, which induces more rapid remineralization of the outer surface of the lesion (sealing of the micropore filter). As a result, the remineralized enamel surface will be less caries prone than the original intact surface. The total amount of fluoride is greater in the arrested lesion. 
At the subclinical, microscopic level, repeated cycles of acid challenge, followed by a rise in pH, combined with frequent (daily) access to low concentrations of fluoride from water and toothpaste, will result in so-called secondary maturation, and the tooth enamel will gradually become more caries resistant. In vivo studies on the development of experimental carieslike lesions have shown that lesions in extracted, unerupted teeth with mature enamel could be induced to depths about 1.5, 2, and 3 times greater than in extracted teeth that had been exposed to the oral environment for 0 to 3 years, 4 to 10 years, and more than 30 years, respectively (Kotsanos and Darling, 1991). 
Figure 157 shows a cross section of an in vitro experimentally developed, noncavitated, enamel carious lesion in polarized light. There is an outer surface zone (the micropore filter), and the inner so-called lesion body has more extensive mineral loss. Figure 158 illustrates successful arrest of such a lesion in vitro, through the use of low concentrations of fluoride. Only at the base of the lesion body is there some residual net loss of minerals. Clinically such an arrested enamel lesion would have a smooth, hard, translucent surface like that of intact enamel, but the inner part of the enamel would tend to be somewhat whiter. 
Applying the orthodontic band technique by Hals and Simonsen (1972) described earlier, Holmen et al (1987) created areas of undisturbed plaque on the buccal surfaces of premolars that were scheduled for extraction for orthodontic indications, inducing active carious lesions in enamel over a period of 4 weeks. Figure 159 shows the typical white-spot appearance of such an active enamel lesion on removal of the orthodontic band after 4 weeks of undisturbed plaque accumulation. After only 1 week of regular plaque control and exposure to the oral environment, including
fluoride from fluoride toothpaste, the inactive or arrested lesion appears less whitish, because of remineralization, wear, and polishing of the external, partly dissolved surface (Fig 160). 
Figure 161 shows another active enamel lesion, less white on removal of the orthodontic band after plaque accumulation. After 2 weeks of plaque control and exposure to the oral environment, the arrested lesion is not as readily discernible clinically. The surface has a glossy appearance (Fig 162). 
On the basis of these experiments, it was concluded that local elimination of oral
mechanical disturbance of plaque accumulation enhanced lesion progression and that
reexposure to mechanical disturbance, including oral hygiene procedures, not only
arrested further progression of lesions, but also resulted in partial regression of
lesions. The gradual enhancement of microwear in relation to time supports the
concept that mechanical removal of the cariogenic biomass has been responsible for
the observed arrest (Holmen and Thylstrup, 1986).
In orthodontic patients with poor and irregular oral hygiene and limited use of topical
fluoride, caries is a frequent complication. The lesions typically associated with the
direct-bonding technique develop on the cervical enamel because of plaque retention.
In children who had undergone routine orthodontic treatment for about 2 years, Artun
and Thylstrup (1986, 1989) monitored such lesions at the time of debonding, at 1, 2,
3, 4, 8, and 12 weeks.
The demineralized areas on the maxillary incisors, adjacent to the bonded brackets,
were examined in detail: (1) clinical examination of plaque distribution, the extent
and surface texture of the lesions, and clinical estimation of enamel opacity; (2) color
slides at each appointment, before and after removal of microbial deposits, the latter
preceded by air-drying for 20 seconds; and (3) SEM examination of replicas made at
each appointment, after the tooth surfaces had been pumiced and washed with a
solution of 5% vol/vol hypochlorite for 30 seconds. As a reference for SEM
examinations, at the time of debonding, a furrow was made in the bonding area with a
sharp hand instrument.
Heavy accumulations of dental plaque were observed in all areas gingival to the
brackets at the time of debonding. After cleaning, the cervical region of the labial
enamel showed the characteristic chalky white appearance of active enamel caries.
The border between the lesion and the sound enamel that had been covered by the
bonding material was very distinct (Fig 163).
From being chalky and soft at the time of debonding, a gradual change was noted
during the ensuing 2 to 8 weeks: The surface of the lesions became glossy, and gentle
probing disclosed a gradual improvement in hardness, to the level of the adjacent
sound enamel. Concomitantly, the pronounced whiteness of the lesion at the time of
the debonding changed to a more diffuse opacity (Fig 164).
At the end of the 3-month observation period, only some residual enamel opacity
persisted. In some cases, small surface microcavities had developed during the first
weeks of observation: These areas regained normal enamel translucency relatively
rapidly. In the SEM, there was a marked ledge at the border between the surface of
the active lesion and the adjacent sound enamel (Fig 165).
After 3 months, the difference in levels between the lesion surface and the sound
surface became more marked, indicating somewhat greater wear of the “soft” lesion
surface than of the sound enamel (Fig 166). The furrow in the bonding area could not
be discerned, but the ledge at the border between the lesion and the bonding area was
still distinct. The 3-month observations generally revealed marked wear, and the
surface microcavities were either leveled out or barely discernible.
From this study, it was concluded that long periods of undisturbed plaque, associated
with orthodontic banding, result in more pronounced carious dissolution than was
revealed in previous short-term studies. The direct dissolution of the outer surface
became much more evident, with a visible difference in surface levels between the
lesion and the sound enamel. The clinical impression of a less white, arrested lesion
was therefore predominantly a result of wear and polishing of the partly dissolved,
“chalky” surface of the active lesion. This phenomenon also explained the clinical
impression of regained surface hardness. The study again demonstrated that removal
of cariogenic plaque resulted in arrest of lesion progression and that the clinical
impression of lesion regression is related to remineralization and intraoral wear,
including oral hygiene procedures.
Progression can be arrested by plaque control and either short-term use of high
fluoride concentration or long-term use of low fluoride concentration. To date, the
long-term effect of rapid arrest at the enamel surface has not been compared with a
slow but more complete arrest throughout the entire enamel lesion.
In toothbrushing populations of children and young adults, the approximal surfaces of
the posterior teeth, particularly from the mesial surfaces of the second molars to the
distal surfaces of the second premolars, are the sites commonly susceptible to caries.
In the permanent dentition, the mesial surfaces of the first molars are usually the first
approximal surfaces to decay, because of the relatively wide contact with the distal
surfaces of the second primary molars and limited accessibility for the toothbrush.
Figure 167 shows an active enamel lesion on the mesial surface of a maxillary first
molar. The surface has been exposed by exfoliation of the primary second molar.
Note the location of the gingival margin at the cervical border of the opaque lesion.
The contact area is located above the lesion.
Figure 168 shows an SEM of an initial surface dissolution (a micropore filter) cervical
to the contact facet in such an active enamel lesion. Details of the surface dissolution
patterns are shown in Fig 169. These figures clearly illustrate that approximal enamel
lesions of the molars are initiated apical to, and sometimes subgingival to, the contact
facet. To prevent the development of such lesions, or to arrest early lesions,
cariogenic plaque apical to the contact facet must therefore be removed.
During the relatively short interval of about 2 months, from exfoliation of the primary
second molars to full eruption of the second premolars, the mesial surfaces of the
permanent first molars are readily accessible for plaque control as well as for topical
fluoride application, offering an excellent opportunity for arrest of carious lesions in
enamel (Figs 170 and 171).
If there is caries on the distal surface of the primary second molar, the grinding
technique (Figs 172 and 173) is recommended, to prolong exposure of the mesial
surface of the permanent first molars, allowing prevention of enamel lesions and
arrest of established lesions in enamel and noncavitated lesions in dentin. The
exposed dentin of the primary second molar (with caries excavated where necessary)
should be semipermanently restored with glass-ionomer cement. This material acts as
a slow-release fluoride reservoir, which can be recharged by application of topical
fluoride agents, such as fluoride varnish.
Carvalho et al (1989) reported that, 48 hours after PMTC, plaque reaccumulation is
almost five times greater on the occlusal surfaces of erupting permanent first molars
than it is on fully erupted molars. This explains why almost all fissure caries in molars
is initiated during the extremely long eruption time (12 to 14 months for first molars
and 14 to 18 months for second molars) and why fissure caries seldom occurs in
premolars, which have an eruption time of only 1 to 2 months.
Carvalho et al (1992) taught the parents of children with erupting or recently erupted
permanent first molars to brush the fissures with a special technique. In a selected
high-risk group, this was supplemented, at needs-related intervals, by PMTC and
application of sodium fluoride solution until the molars were fully erupted and in
chewing function. Figure 174 shows the number of enamel lesions at the baseline
examination that were subsequently arrested in the different sites of the occlusal
surfaces, and the very limited number of new noncavitated enamel lesions that
developed during the 3-year longitudinal study. This study showed that even occlusal
enamel lesions could be successfully arrested by plaque control and topical use of
In another study, similar results have been achieved in first and second molars
(Kuzmina, 1997). These studies support the contention that application of fissure
sealants to fully erupted, caries-free teeth is costly overtreatment. However, in
populations with high caries prevalence, the earliest possible use of fluoride-releasing
fissure sealents (glass-ionomers) in the erupting permanent first and second molars is
still a very efficient method of fissure caries control.
Views: 1612 | Comments: 4 Send reply
Aren’t the lockets beiuuaftl? They’re $98.00. We’re sold out of a couple colours, but still have the brighter blue, dusty rose, grey, caramel and pistachio. Let me know if you need anything else! Cheers, Sarah

Sara,Just reading this makes me so inedcribly sad because I know how frightened you must be having to go into surgery and worrying about how this might affect your life. You can look at the positive side of things which is thankfully they found the tumor and are removing it. I will pray for you and keep you continuously in my thoughts. When my sister was in her accident and in a coma I prayed for her at church and I prayed fervently that she would get better. I will do the same for you because you are such a unique person and a dear friend of mine. I know you will pull through this. You just have to have faith and trust in God. Your friends and family will always be there to love and support you through the thick and thin, and you will find your peace of mind once again. Hope will pull you through these difficult times. I know you will find the inner strength you need. I look forward to seeing you again and catching up this weekend. It has been way too long. Love you!!!!

First of all, I am so sorry. That must be terrifying. I can toltaly understand your fears about brain surgery; I would worry about all those things too.I think Eileen is right, this si not your time to be strong, which is not to say that you can’t handle it it is just not about being strong. Take your time and panic for a bit. Kick, scream, cry, get all your worries out. Feel whatever you have to feel. Then calm down, compose yourself, and do what you have to do get that sucker out of there!I also think you will come out as Sara. Who knows, maybe you will even remember a few things you thought you had forgotten!We will be thinking of you.

I feel like we’ve become real frdenis through our blogs over the past months (year?) not just blog frdenis . I cannot even begin to say I understand what you’re feeling because I clearly do not. Just know that we’re all thinking of you. I think it’s normal to be scared, but I also know that living in that fear is draining. I’ll be praying not only for your physical well being (for the surgery, recovery, etc.) but also that you have the mental and emotional courage you need, as well as being able to feel that fear lift off, leaving peace in its place. [url=]rcpbzjvvf[/url] [link=]jjpwqewl[/link]

Send reply


Pleas enter the code on picture:
Enter this code 

Articles for theme “caries”:
Development of Carious LesionsEnamel cariesDevelopmentThe physicochemical integrity of dental enamel in the oral environment is entirely dependent on the composition and chemical behavior of the surrounding fluids: saliva and plaque fluids. The main factors governing the stability of enamel apatite are pH and the free active concentrations of calcium, phosphate, and fluoride in solution.  The development of a carious lesion in enamel involves a complicated interplay among a number of factors in the oral environment and the dental hard tissues.
Development and Diagnosis of Carious LesionsIntroductionA carious lesion should be regarded not as a disease entity, but as tissue damage or a wound caused by the disease dental caries. The coronal lesion begins as clinically undetectable subsurface demineralization of enamel, visible only at microscopic level, and gradually progresses, first to visible demineralization of the enamel surface and to cavitation of the dentin, and finally to complete destruction of the tooth crown despite restoration, but without prevention (Fig 145).
ConclusionsCaries riskFrom a cost-effectiveness aspect caries-preventive measures should be applied strictly according to predicted caries risk. In populations with very high caries prevalence and caries incidence (where almost everyone develops new lesions every year) the traditional whole population strategy would be cost effective. The number of such populations is dwindling, however, particularly in the industrialized countries where caries prevalence was high 20 to 30 years ago.
Cariogram ModelA new model, the Cariogram, was presented in 1996 by Bratthall for illustration of the interactions of caries-related factors. The model makes it possible to single out individual risk or resistance factors. A special interactive version for the estimation of caries risk has been developed.The original Cariogram was a circle divided into three sectors, each representing factors strongly influencing carious activity: diet, bacteria, and susceptibility. The development of the model was based on a need to explain why, in certain individuals, carious activity could be low in spite of, for example, high sucrose intake, poor oral hygiene, high mutans streptococci load, or nonuse of fluorides.
Detailed risk profiles for dental cariesIf a patient is at high risk predominantly for either caries or periodontal disease, a more detailed risk profile is available for the specific disease. Box 19 shows a list of abbreviations for the most important variables related to caries risk.  Figure 138 illustrates how a high-risk patient (C3) has been transformed to a low-risk patient (C1) by improved self-care supplemented by professional preventive measures. The greater the difference between the solid line and the dotted line, the greater the improvement.