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pdf
When we breathe through the mouth, there is loss of saliva and dryness of the mouth and this
can increase the risk of tooth decay and inflammation of the gums.

amj CLINICAL NUTRI
Results of this study suggest that mild to modcrate
undernutrition during enamel formation is causally linked
to the formation of LEHs.
Developmental ages at LEH development
The estimated peak age at formation of a LEH on the upper
central incisor is ---24-36 mo developmental age in both groups,
with a slightly earlier mean age at formation (2.03-2.17 y) in
the supplemented vs the control groups. This small mean difference
in developmental age may be somewhat less than the
actual difference in chronological age because developmental
timing may be relatively delayed in the control group individuals
with poorer nutritional status (42). Whereas poor nutritional
status can significantly delay eruption times, less is known of its
effect on the timing of matrix formation. It is, however, likely
to be less significant, especially for a highly canalized tooth.
The peak age at formation ofa LEH in both groups is similar
to that found in another study in Mexico (26) and in a number
ofstudies ofprehistoric and historical populations (3). This peak
also follows closely after the median age at completion of weaning
(-20-24 mo) in this community (28) and is congruent with the
age at which the incidence of illness is greatest (28, 30).
The greatest relative difference in frequency of LEH between
supplemented and control groups occurs before I .5 y and after
3.0 y, or before and after weaning and the time ofgreatest illness.
It is as if all children are at great risk of LEH immediately after
weaning, but the supplemented individuals are afforded greater
protection before and after weaning. These data also support
the hypothesis that common respiratory and gastrointestinal illnesses
are an immediate cause of LEH, especially in individuals
with compromised nutritional status.

Extensive- hypoplasia-
Aberrations in the function of tooth forming cells lead to
permanent morphological consequences. DDE (Developmental
defects of Enamel) present in a spectrum of severity ranging from a
change in translucency, also known as enamel opacity to reduction or
loss of enamel known as enamel hypoplasia. Injury encountered during
the early stages of enamel formation are thought to result in Enamel
Hypoplasia (EH) where as those resulting during later or more mature
stages cause Enamel Opacity (EO) [5,6]. The extent of enamel defects
varies from accentuated incremental lines of Retzius to complete
absence of enamel and depends upon the intensity and duration of
etiological factors
The childs sibling and parents reported a
normal dentition without any evidence of enamel hypoplasia or enamel
opacities. Birth history revealed normal delivery; mother denied any
use of medication during pregnancy. The child was weaned by 6
months of age.
However in our case Amelogenesis imperfecta was ruled out as
the primary dentition was unaffected. That the dental manifestation
was due to exposure to excessive fluoride also could not have been a
possibility as childs sibling who was 1 year younger showed a healthy
dentition and the family resided in low fluoride region. Moreover
clinically, the defects of fluorosis are evident through out the enamel as
diffuse opacities whereas environmental hypoplasia affects a localised
thickness of enamel presenting as demarcated opacities.

Crombe [9] in their study evaluated the exposure to environmental
contaminants such as PCBs and dioxins, peri- and neonatal problems,
fluoride exposure as causative factors for MIH but found insufficient
evidence to reach conclusive etiology.
PCBs (polychlorinated biphenyls ) and dioxins could not have
contributed much to the etiology in our case as the child was weaned
off by 6 months of age. Alaluusua [10] found a correlation between
prolonged breast feeding and hypo mineralisation of first molars and
claimed that environmental contaminants like dioxin were interfering
with tooth development. In their study the median duration of breast
feeding was 12 months; and no child with defects had been breast fed
for less than eight months.
8. Jalevik B, Noren JG (2000) Enamel hypomineralisation of permanent first
molars: a morphological study and survey of possible aetiological factors. Int J
Paed Dent 10: 278-289.
5. Suckling GW (1989) Developmental defects of enamel: Historical and present
day perspectives of their pathogenesis. Adv Dent Res 3: 87-94.
6. Den Besten PK (1999) Mechanism and timing of fluoride effects on developing
enamel. J Public Health Dent 59: 247-251.
9. Crombie F, Manton D, Kilpatrick N (2009) Aetiology of molar-incisor
hypomineralistaion: a critical review. Int J Paed Dent 19: 73-83.
10. Alaluusua S, Lukinamaa PL, Koskimies M, Pirinem S, Holta P, et al. (1996)
Development dental defects associated with Long breast feeding. European J
Oral Sci 104: 439-447.


7. Goodman AH, Martinez C, Chavez A. Nutritional Supplementation and the Development of
Linear Enamel Hypoplasias in Children from Tezonteopan, Mexico. American Journal of
Clinical Nutrition 1991;53(3):773-781.
8. Zhou L, Corruccini R. Dental enamel hypoplasia and historical famine in China (1954-1961)
(Abstract). Am J Phys Anthropol 1994;Supplement 18:214.
9. Zhou LM, Corruccini RS. Enamel hypoplasias related to famine stress in living Chinese. Am J
Hum Biol 1998;10(6):723-733.
10. Seow W. A study of the development of the permanent dentition in very low birthweight
children. Pediatr Dent 1996;18:379-384.
11. Psoter WJ, Reid BC, Katz RV. Malnutrition and dental caries: A review of the literature.
Caries Res 2005;39(6):441-447.


Behavioral guide
It is possible to communicate with the child patient briefly
at the beginning of a dental appointment to establish rapport
and trust. However, once a procedure begins, the dentists ability
to control and shape behavior becomes paramount, and information
sharing becomes secondary. The 2-way interchange
of information gives way to 1-way manipulation of behavior
through commands. This type of interaction is called requests
and promises.19 When action must take place to reach a goal
(eg, completion of the dental procedure), the dentist assumes the
role of the requestor. Requests elicit promises from the patient
that, in turn, establish a commitment to cooperate. The dentist
may need to frame the request in a number of ways in order to
make the request effective. For example, reframing a previous
command in an assertive voice with appropriate facial expression
and body language is the basis for the technique of voice
control. While voice control is classified as one of the means of

The dentist should include an evaluation of the childs cooperative
potential as part of treatment planning. Information
can be gathered by observation of and interacting with the child
and by questioning the childs parent. Ideal assessment methods
are valid, allow for limited cognitive and language skills, and
are easy to use in a clinical setting. Assessment tools that have
demonstrated some efficacy in the pediatric dental setting, along
with a brief description of their purpose, are listed in Appendix
1.24,27,29,30,36-44 No single assessment method or tool is completely
accurate in predicting a child patients behavior for dental treatment,
but awareness of the multiple influences on child behavior
may aid in treatment planning for the pediatric patient.


To alleviate these barriers, the dentist should become a teacher.
The dentists methods should include assessing the patients
developmental level and comprehension skills, directing a message
to that level, and having a patient who is attentive to the
message being delivered (ie, good communication). To deliver
quality dental treatment safely and develop an educated patient,
the teacher-student roles and relationship must be established
and maintained.

AAPD fluoride use
As the Environmental Protection Agency/Department of Health and Human Services
recommendation9 for opti-mizing community water supplies to 0.7 ppm F is instituted, fluorosis
due to reconstituting infant formula with fluoridated water will be less of an issue.


G_FLOURIDE THERAPY
PROFESSIONAL APPLICATION OF FLUORIDE
The efficacy of fluoride varnish in permanent teeth, applied atthree or six month intervals, also
has been reported in atleast four randomized controlled trials.19-22 Meta-analyses of 14
placebo-controlled trials show that fluoride gels, applied
at three month to one year intervals, are efficacious in permanent teeth.23 Some topical fluoride
gel and foamproducts are marketed with recommended treatmenttimes of less than four minutes,
but there are no clinicaltrials showing efficacy of shorter than four-minuteapplication times.14
There also is limited evidence thattopical fluoride foams are efficacious.24,25 Children
atincreased caries risk should receive a professional fluor-ide treatment at least every six
months.14 As the risk categories may change over time, the type and fre-quency of preventive
interventions should be adjusted.1
Other topical fluoride products, such as 0.2 percent sodium fluoride (NaF) mouthrinse (900
ppm F)26,27,28 and brush-on gels/pastes (eg, 1.1 percent NaF; 5,000 ppm F) also have been
shown to be effective in reducing dental caries in permanent teeth.29,30 Home use of fluoride
products for children should focus on regimens that maximize topical contact, in lower-dose
higher-frequency approaches.31 Meta-analyses of more than 70 randomized or quasi-
randomized controlled clinical trials show that fluoride toothpaste is efficacious in reducing
prevalence of dental caries in permanent teeth, with the effect increased in children with
higher baseline level of caries and by higher concentration of fluoride in the toothpaste, greater
frequency of use, and super-vision of brushing.32,33 A meta-analysis of eight clinical trials on
caries increment in preschool children also shows that tooth brushing with fluoridated
toothpaste significantly re-duces dental caries prevalence in the primary dentition.34 A smear
of fluoridated toothpaste for children less than two years of age at risk for dental caries may
decrease risk of fluorosis. A pea-size amount of toothpaste is appropriate for children aged
two through five years (see Figure).35,36 To maximize the beneficial effect of fluoride in the
toothpaste, rinsing after brushing should be kept to a minimum or eliminated altogether.34,37

P_DIETARY RECOMMENDATION
USDA and DHHS published Dietary Guidelines for Ameri-cans.
9,32
These guidelines include:
eating a variety of nutrient-dense foods and beverages;
balancing foods eaten with physical activity to maintain a healthy body mass index;
maintaining a caloric intake adequate to support normal growth and development and to reach
or maintain a healthy weight;
choosing a diet with plenty of vegetables, fruits, and whole grains and low in fat, saturated
(especially trans-saturated) fat, and cholesterol; and
using sugars and salt (sodium) in moderation.9,32

bLEACHING
Policy statement
The AAPD encourages:
the judicious use of bleaching for vital and nonvital teeth;
patients to consult their dentists to determine appropriate methods for and the timing of dental
whitening within the context of an individualized, comprehensive, and sequenced treatment
plan;
dental professionals and consumers to consider side effects when contemplating dental
bleaching for child and adolescent patients;
further research of dental whitening agents in children.
The AAPD discourages full-arch cosmetic bleaching for patients in the mixed dentition.
RESTORATIVE

SSCs can be indicated to restore anterior teeth in cases where multiple surfaces are
carious, where there is incisal edge involvement,
following pulp therapy, when hypoplasia is present, and when there is poor moisture
control.92 One study suggests that "extent of caries" is
the main factor that influences pediatric dentists' choice to use anterior veneered
SSCs.93 Where esthetics are a concern, the facing of SSCs
can be removed and replaced with a resin-based composite (open-faced technique).
Another option when esthetic concerns predominate is
primary SSCs with preformed tooth-colored veneers. Although these veneered crowns
can be more difficult to adapt (due to their limited
crimping area) and are subject to fracture or loss of the facing, in some cases veneered
SSCs possess a major advantage over conventional
SSCs due to their superior esthetics and high parental satisfaction.94-98
Recommendations:
1. Children at high risk exhibiting anterior tooth caries and/or molar caries may be
treated with SSCs to protect the remaining atrisk
tooth surfaces.
2. Children with extensive decay, large lesions, or multiple-surface lesions in primary
molars should be treated with SSCs.
3. Strong consideration should be given to the use of SSCs in children who require
general anesthesia.90

Association between development
enamel hypoplasia is a quantitative defect involving a reduced enamel thickness.20 It has been
demonstrated that in deciduous teeth, the area of enamel affected by defects
(hypomineralization) has a lower mineral content compared to sound enamel and could be
compared to the mineral content in white spot lesions.21 It has been suggested that these
characteristics can allow additional plaque accumulation,11,12 and colonization by
Streptococcus mutans and Lactobacilli,22 facilitating greater caries onset and progress than
seen in non-defective enamel.11

In conclusion, enamel hypoplasia can be considered an important factor to the development of dental caries after adjustment for demographic,
socioeconomic and behavioural characteristics. Moreover, it might not only itself render the tooth more prone to caries development, but also
be (in part) a proxy indicator for substandard nutrition and/or childhood infections.16 However, there is a need to carry out investiga-tions to
investigate the influence of childhood life exposures on enamel defects (mainly hypoplasia). Having established a relationship between enamel
defects and dental caries experience, it is important to identify the aetiological risk/ associated factors associated with enamel defects. Recent
report has demonstrated that low birthweight infants were more prone to the occurrence of enamel hypoplasia and should be carefully
monitored because they were at risk to develop early childhood caries.32 This study contributes to the knowledge about relationship between
enamel defects and dental caries, because teeth can be examined for enamel defects (enamel hypoplasia) after eruption, before dental caries
develops.16 This approach can prevent early dental caries when it applied in at-risk children and help to minimise dental pain in childhood and
tooth loss in later life.1 The present findings have also implications in dental treatment, since individuals presenting development enamel
defects (hypoplasia) are more susceptible to caries occurrence, they should be more frequently followed-up. Also, severe cases of enamel
defects may often require comprehen-sive restorative treatment.41,42 In addition, it has been demonstrated that individuals with higher caries
risk are more likely to have failed posterior restoration,43 and therefore restorative treatments in patients with enamel defects could have a
greater chance of failure, but such assumption needs to be investigated in future studies.

KAATTTTHHH 2
Typically, a
local factor can be suspected when the enamel defect
affects a single tooth or a group of neighboring teeth, or
has an asymmetric distribution in the dentition. General
General
symmetric defects are related to the timing of the insult
and thus to the sequence of the development of the teeth
and are called chronological defects. Etiology of general
defects not related to any particular time period during
tooth formation is either genetic or due to nongenetic,
longstanding environmental infl uence.



Enamel hypoplasia is a consequence of defi cient
enamel matrix formation. It appears as a surface defect
resulting from reduced enamel thickness. Hypoplasia
can occur in the form of pits single or multiple, shallow
or deep, or scattered or arranged in horizontal rows; or
grooves single or multiple, narrow or wide, or evident
as partial or complete absence of enamel over a considerable
area of the tooth crown. The enamel of reduced
thickness may be translucent or opaque (9).

THREE PHASES OF TREATMENT
Acute Treatmetn
Enamel hypoplasia is a consequence of defi cient
enamel matrix formation. It appears as a surface defect
resulting from reduced enamel thickness. Hypoplasia
can occur in the form of pits single or multiple, shallow
or deep, or scattered or arranged in horizontal rows; or
grooves single or multiple, narrow or wide, or evident
as partial or complete absence of enamel over a considerable
area of the tooth crown. The enamel of reduced
thickness may be translucent or opaque (9).
Temporary materials as intermediate restorative
material (IRM) may be useful and conventional
glass-ionomer cement (GIC) may also be used as semipermanent
restorations.
OBSERVATIONAL PERIOD
After the acute treatment is taken care of there is a transitional
period when the permanent front teeth and
permanent fi rst molar should be kept under supervision
and restorations are maintained according to the individual
needs. In this period from about 7 to 11 years of
age the major lines in the fi nal treatment are planned. In
complicated cases it is necessary to have contributions
from a multidisciplinary team of specialists
This may include provisional
or permanent fi llings, microabrasion in an attempt
to remove tooth discoloration, insertion of a partial denture
to replace teeth extracted early, or missing due to
hypodontia, tooth retention, or eruption disturbances.
In many cases there is no need for further treatment, but
the teeth with disturbances have to be paid particular
attention at the dental check-ups due to increased risk
for caries, chipping of enamel, or attrition

long term treatment
Long-term treatment
The long-term treatment goals are a combination of a
well-functioning dentition, no pain or sensation from
teeth, and good aesthetics cases with generalized severe
disturbances full crown therapy as early as in teenage

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Basics/Common-Concerns/Bad-Breath/article/What-Causes-My-Bad-Breath.cvsp
Mouth breathing
Dry mouth (xerostomia) This can be caused by salivary gland problems, medications or
by "mouth breathing."

http://www.identalhub.com/article_effects-of-mouth-breathing-179.aspx


Effect on the teeth and the arches
Mouth breathers keep the mouth open so the flaring of the upper teeth is seen. We can see the
open bite that means the upper front teeth do not cover the lower front teeth. Patient breathes
through mouth so the tongue is positioned downwards to make the airways. This causes the
imbalance in the forces and the narrow maxillary arch causing the posterior cross bite

Incidence of caries
In mouth breathers there is the increased incidence of caries as the mouth remains open and
there is dryness. The front upper teeth are affected the most.
In mouth breathers the gingiva is inflamed. This condition is called as the Mouth Breathing
Gingivitis. Most affected is the gingival tissue of upper front teeth. The gums become inflamed
and hyper plastic because the mouth remains open and they are constantly having the affect of
air drying. The salivary flow is also decreased causing the heavy deposit as the self cleansing
effect of the saliva is reduced. The gingiva has the classic rolled up appearance. There is bone
loss and the pocket formation in the inter proximal area if proper oral hygiene is not maintained.






EN white spot lesions
In mouth breathers the gingiva is inflamed. This condition is called as the Mouth Breathing
Gingivitis. Most affected is the gingival tissue of upper front teeth. The gums become inflamed
and hyper plastic because the mouth remains open and they are constantly having the affect of
air drying. The salivary flow is also decreased causing the heavy deposit as the self cleansing
effect of the saliva is reduced. The gingiva has the classic rolled up appearance. There is bone
loss and the pocket formation in the inter proximal area if proper oral hygiene is not maintained.

http://www.dimensionsofdentalhygiene.com/2013/02_February/Features/Dental_Managemen
t_of_Patients_with_Rickets.aspx


SHOWTESXT.pdf
Page 2 sample diagnosis


Public_health
Dental caries
The deciduous teeth erupt from 6 months and are lost by
the early teens. The permanent dentition replaces the
deciduous dentition from the age of 6 years and is
complete by age 21. Teeth are most susceptible to dental
caries soon after they erupt; therefore, the peak ages for
dental caries are 25 years for the deciduous dentition and
early adolescence for the permanent dentition. In
developed countries, there is a trend for older adults
now to retain their teeth for longer, however, if the gums
recede with age the roots of the teeth become exposed,
and, being relatively less mineralised than the tooth
crowns, are susceptible to decay known as root caries7.
Nutritional status affects the teeth during the preeruptive
stage, however, this nutritional influence is much
less important that the post-eruptive local effect of dietary
practices on caries formation. Deficiencies of vitamin D,
vitamin A and protein energy malnutrition (PEM) have
been associated with enamel hypoplasia. PEM and vitamin
A deficiency are also associated with salivary gland
atrophy which subsequently reduces the mouths defence
against infection and its ability to buffer plaque acids.
Navia16 states moderate malnutrition, particularly lack of
protein and deficiencies of certain micronutrients such as
vitamins, zinc and iron, can influence the amount and
composition of saliva limiting the protective effects it has
in the oral cavity.