September 11th, 2009 by admin
Relatively little interceptive orthodontic treatment is carried out
in the primary dentition, before the eruption of any permanent
teeth. The dental arches are generally well aligned. There may be
an increased incisor overjet, or a Class III incisor relationship, but
these occlusal features are seldom so pronounced that they give
rise to comment. Crowding of the primary dentition is usually
expressed as an absence of spacing—the primary teeth are well
aligned and unspaced—crowding will become evident when the
permanent teeth erupt.
Early loss of a primary first molar may allow mesial drift of the
second molar. This is difficult to prevent when the child is so
young. The techniques employed are the same as those suggested Read the rest of this entry »
September 7th, 2009 by admin
The value of non-sugar sweeteners in caries prevention is
addressed in Chapter 10. Xylitol was introduced as a non-sugar
sweetener on the basis of the fact that it is not metabolized by
bacteria such as S. mutans. This on its own is clearly advantageous,
but an added bonus is that xylitol has an antibacterial effect. This
is because the xylitol molecule, a sugar alcohol, is structurally Read the rest of this entry »
July 22nd, 2009 by admin
This is a localised disorder of development affecting a group of
teeth in which there are severe abnormalities of enamel, dentine
and pulp.
The disorder is not hereditary and the aetiology is unknown.
A few cases have been associated with facial vascular naevi or
abnormalities such as hydrocephalus. There is no sex or racial Read the rest of this entry »
July 22nd, 2009 by admin
Enamel matrix is formed in normal quantity but poorly calcified.
When newly erupted, the enamel is normal in thickness
and form, but weak and opaque or chalky in appearance.
The teeth tend to become stained and relatively rapidly worn
Fig. 2.9 Close-up of X-linked hypoplastic type amelogenesis
imperfecta. These teeth from an affected female show the typical vertical
ridged pattern of normal and abnormal enamel as a result of Lyonisation.
Fig. 2.10 Amelogenesis imperfecta X-linked hypoplastic form in a
male. This premolar has a cap of enamel so thin that the shape of the
tooth is virtually that of the dentine core.
away. The upper incisors may acquire a shouldered form due to
the chipping away of the thin, soft enamel of the incisal edge
(Fig. 2.13). There are dominant and recessive patterns of
inheritance.
July 22nd, 2009 by admin
The enamel is normal in form on eruption but opaque, white to
brownish-yellow. The teeth appear similar to mottled fluoride
effects (Figs 2.14 and 2.15). However, they are soft and vulnerable
to attrition, though not as severely as the hypocalcified
type.
There are several variants of hypomaturation defects such as
a more severe, autosomal dominant (type 4) of hypomaturation
combined with hypoplasia.
July 22nd, 2009 by admin
Hypoplastic amelogenesis imperfecta
The main defect is in formation of the matrix. The enamel is
randomly pitted, grooved or very thin, but hard and translucent
(Fig. 2.8). The defects tend to become stained, but the teeth are
not especially susceptible to caries unless the enamel is scanty
and easily damaged.
The main patterns of inheritance are autosomal dominant and
recessive, X-linked, and (a genetic rarity) an X-linked dominant
type. In the last there is almost complete failure of enamel
formation in affected males, while in females the enamel is
ridged (Figs 2.9-2.11). Occasionally cases are difficult to
classify (Fig. 2.12).
July 14th, 2009 by admin
The main causes of mouth ulcers in children are:
• Local causes (e.g. trauma)
• Recurrent aphthae
• Associated with systemic disease (e.g. coeliac
disease)
• Drugs (e.g. cytotoxics)
• Irradiation of the mucosa.
Recurrent aphthous stomatitis (RAS)
20% of children may have a haematinic deficiency.
1-3% may have coeliac disease. A smaller number Read the rest of this entry »
July 14th, 2009 by admin
Any disorder that upsets the normal: local
reactions of the blood vessels; platelet activities;
i nteraction of specific coagulation factors that
circulate in the blood (Fig. 180).
Coagulation defects Read the rest of this entry »
July 14th, 2009 by admin
Multifactorial inheritance. Chromosomal
abnormalities represent fewer than 5% of the total.
Ventricular septa[ defect 28%; atrial septal defect
10%; pulmonary stenosis 10%; patent ductus
arteriosus 10%; tetralogy of Fallot 10%; aortic
stenosis 7%; coarctation of the aorta 5%; Read the rest of this entry »
July 14th, 2009 by admin
1 in 600 children under the age of 15 in the UK.
Leukaemias. Abnormal proliferation of white blood
cells (48% of all childhood cancers).
Solid tumours. Affecting tissues: central nervous
system 16%; lymphoma 8%; neuroblastoma 7%; Read the rest of this entry »
