Американский Научный Журнал RISK FACTORS FOR CONGENITAL MALFORMATIONS OF THE MAXILLOFACIAL REGION

Annotation. The article provides a review of the literature on the study of the causes of congenital malformations and dentofacial anomalies, the identification of which is a prerequisite for substantiating and conducting an integrated system for the prevention of this pathology in children and adolescents Скачать в формате PDF
American Scientific Journal № ( 31) / 2019 11

11. Чуйкин С.В., Давлетшин Н.А., Викторова
Т.В., Шайхутдинова. Д.И. Этиология, патогене з,
клиника и профилактика врожденной расщелины
верхней губы и неба. Уфа, 2007 .
12. Галеева Р.Р., Чуйкин С.В. Клинические
результаты стоматологического обследования
дете й с детским церебральным параличом
//Уральский ме дицинский журнал, 2014. - № 3
(117). - С. 36 -38.
13. Чуйкин С.В., Штанько М.И. Некоторые
физико -химические и биохимические показатели
ротовой жидкости у лиц пожилого и старческого
возраста//Институт стоматологи и. 2013. № 2 (59).
С. 72 -73.
14. Акатьева Г.Г., Чуйк ин С.В., Снеткова Т. В.,
Гаянова А.З., Байбурина Э.К. Оценка
гигиенических знаний школьников по уходу за
полостью рта // в сборнике: «Материалы
одиннадцатого сибирского конгресса "
Стоматология и челюстно - лицевая хирургия» с
международным участием Всеросс ийского
симпозиума" Новые технологии в стоматолог ии "
2016. С. 10 -12.
15. Чуйкин С.В., Джумартов Н.Н., Чуйкин
О.С., Кучук К.Н., Гринь Э.А., Чуйкин Г.Л.,
Муратов А.М., Гильманов М.В. Клинико -
анатомические формы врожденной расщелины
губы и неба в регионе с экот оксикантами. //
Проблемы стоматологии. 2019. Т. 1 5. № 3. С. 127 -
132.
16. Чуйкин С.В., Давлетшин Н.А., Чуйкин
О.С., Кучук К.Н., Джумартов Н.Н., Гринь Э.А.,
Гильманов М.В., Муратов А.М. Алгоритм
реабилитации дете й с врожденной расщелиной
губы и неба в регионе с экотоксикантами //
Проблемы стоматологии. 2019. Т. 15. № 2. С. 89 -96.
17. Чуйкин С.В., Викторов С.В., Чуйкин О.С.
Применение генетических маркеров в
прогнозировании стоматологических заболеваний.
Монография. -LambertSaarbruchen, 2013. -361с.
18. Чуйкин С.В., Топ ольницкий О.З., П ерсин
Л.С. Врожденная расщелина верхней губы и нёба.
Монография. -LambertSaarbruchen, 2012. -593с.
19. Состояние слизистой оболочки полости
рта при заболеваниях внутренних органов/Чуйкин
С.В., Ма кушева Н.В., Акатьева Г.Г., Акмалова
Г.М., Афлаха нова Г.Р., Егорова Е.Г., Снеткова Т.В.,
Чуйкин О. С., Чуйкин О.С. и др.; под ред. Чуйкин
С.В. 1 -е изд. Уфа: ООО "Печатный домъ", 2016.

RISK FACTORS FOR CONG ENITAL MALFORMATIONS OF THE MAXILLOFACIA L REGION

Chuikin Oleg Sergeyevich
Viktorovna Viktorova Tat yana
Gilmanov Marsel Venerevich
Muratov Azamat Maratovich
Galiakberov Ildar Shafkatovich
Department of Pediatric Dentistry and Orthodontics,
Bashkir State Medical University , Ufa

Annotation . The article provides a review of the literature on the study of the causes of congenital
malformations and dentofacial anomalies, the identification of which is a prerequisite for substantiating and
conducting an integrated system for the prevention of this pa thology in children and adolescents.
Key words : congenital malformations; neural tube defects; crevices of the upper lip and palate, dentition.

Congenital malformations (CHD) occupy a
leading position in the structure of childhood
morbidity, disability an d mortality and represent an
important medical and social problem. [1 -10]
The causes of congenital malformations can be
varied: the effects of teratogens, maternal diseases,
chromosomal aberrations, mutations of certain genes,
and others. However, in a sig nificant part of cases, the
nature of VLD remains unknown. It seems most likely
that the etiology of congenital malformations is
multifactorial; in other words, both the genotype of the
mother and the fetus, as well as the influence of
environmental factor s, affect the risk of congenital
malformations. In the 60s of the last century, the first
evidence appeared in the world literature that impaired
folate metabolism and folic acid deficiency in pregnant
women can affect the risk of spontaneous abortion and
neural tube defects in the fetus. [5 -15] This discovery
aroused keen interest: in numerous studies of the 80 -
90s it was shown that the consumption of multivitamins
with a high content of folic acid or folate -rich foods
before conception and in early pregna ncy reduces the
frequency of neural tube defects - as in m others who
already have a baby with such a pathology, and in
women without a history of fetal neural tube defects.
Many of these works were performed on small samples,
and it remained unclear whethe r folate itself or other
multivitamin components had a pro tective effect.
To date, several dozen studies have been carried
out to study the association of polymorphic variants of
folate metabolism genes with the risk of congenital
malformations. Most of th e work was performed on
samples of 200 -300 people in the e xperimental and
control groups and focused on several of the most
studied single nucleotide polymorphisms (SNPs), such
as MTHFR C677T (rs1801133), RFC1 A80G
(rs1051266), MTR A2756G (rs1805087 ), MTH FD1
G1958A (rs2236225).
In recent years, large works have begun to appear
that analyze the associations of certain nucleotide
substitutions with different types of CDF. However,
associations with specific SNPs identified in some
studies are not always repr oduced in other studies. With
confidence, only the associa tion of the MTHFR 677TT

12 American Scientific Journal № ( 31) / 20 19
genotype with a neural tube defect can be stated, and
only in populations of non -Latin European origin
(Germans, Poles, English, etc.). This association was
also confirmed in the Russian sample [5].
As a result of a number of studie s, it was found
that in pregnant women with a fetal neural tube defect,
an increase in the blood level of homocysteine amino
acid is observed, associated with impaired function of
the enzyme 5,10 -methylenetetrahydrofolate reductase
(MTHFR). With a decrea se in MTHFR function,
delivery and metabolism of folic acid consumed by the
body are disrupted. The lack of folic acid, the
metabolites of which act as coenzymes in the
biosynthesis of amino acids, DNA and RNA, leads to
the development of hyperhomocysteine mia and
disruption of the mitotic activity of cells in critical
stages of embryogenesis, which possibly contributes to
the development of various congenital malformations
of the fetus. [16 -19]
Accor ding to the literature, the MTHFR gene
polymorphism caused by the replacement of C677T
reduces the activity of the enzyme
methylenetetrahydrofolate reductase, which leads to
the accumulation of homocysteine and a decrease in the
level of DNA methylation. This suggests that the
accumulation of homocysteine or the violation of
methylation plays a role in the etiology of a neural tube
defect [9].
Among other genetic loci, associations of which
were reproduced in at least two studies, RFC1 A80G
(rs1051266), for which the association of the GG
genotype with the ris k of neural tube defect was shown,
MTHFD1 G1958A (rs2236225), is the association of
the A allele with the risk of neural defect tubes, MTRR
A66G (rs1801394) - association of the GG genotype
with the risk of neural tube defect, MTHFR C677T
(rs1801133), - association of the T allele with the risk
of cleft lip and palate, and congenital malformations of
the circulatory system, BHMT G742A (rs3733890 -
risk of neural labor defect ki. It should be noted th at
mainly such a type of congenital malformations as a
neu ral tube defect was investigated, while the study of
other types of congenital anomalies is very small [11].
The most common congenital malformations are
congenital clefts of the upper lip and palat e. The birth
rate of children with this defect is up to 38 % of all
malformations in children [2, 3].
In the study of CDF, it is worth paying attention to
subgroups within the same group. For example, when
examining the congenital malformations of the
maxillofacial region, cleft palate and cleft upper lip, as
well as various types of adentia, should be exa mined
separately. The variety of samples according to the
degree of representation of defects of various etiologies
in them can lead to a significant difference in the
results.
The causes and risks of dentition ar e varied. All
risk factors are divided into three groups of
manageability: “managed”, “hard to manage”,
“unmanaged”. Most risk factors are manageable, i.e.
timely elimination or weakening of their action
prevents the formation of dentofacial anomalies. The
“controlled” risk factors for the formatio n of
dentoalveolar anomalies include: low fluorine content
in drinking water; a decrease in the immunological
reactivity of the body (frequent colds, rickets, etc.);
early artificial feeding; improper posture duri ng sleep
and wakefulness; the prevalence of soft foods in the
diet; impaired breathing, swallowing, chewing;
irrational use of nipples (dummies); bad habits (sucking
fingers, objects, tongue, lips, etc.). “Hard -to-manage”
risk factors include chronic and a cute illness of the
mother during pregnancy ; toxicosis of pregnant
women, the threat of termination of pregnancy, anemia,
premature and postponed birth; birth complications;
asphyxia, malnutrition, hemolytic disease, allergic and
infectious diseases of the child, etc. Uncontrollable
factors include factors that we cannot influence, such as
heredity.
In areas of the Republic of Bashkortostan with
developed petrochemicals, the prevalence of
dentoalveolar anomalies was found in 36.0% of
preschool children [Muk hametova E.Sh., 1991] and in
46.6% of schoo lchildren [Averyanov SV, 1999]. In
Beloretsk, the Republic of Bashkortostan, the
prevalence of school -age children was 66.3% [S.
Averyanov. et al., 2003]. In the city of Ufa, which is the
center of the petrochemic al industry of the Republic of
Bashkortosta n, a high level of prevalence of
dentoalveolar anomalies in children is revealed
(71.20%). In the structure of dentoalveolar anomalies
among all examined children, combined anomalies
prevail - 47.72%, anomalies of individual teeth make
up 19.63%, anomalies of the dentition - 16.68%,
anomalies of occlusion - 15.97% [5].
S.A. Gunaeva (2006) when examining 2375
children living in a city with a petrochemical industry,
risk factors were identified at different periods o f the
formation of the dentofacial system. Thus, in children
during a temporary bite, the prevalence of risk factors
and impaired functions of the dentofacial system is
47.37 ± 3.18%, and in the early shift bite, along with an
increase in the number of den tofacial anomalies, the
frequency of risk f actors also increases to 54.24 ± 1.93
% In a late shift and permanent bite, the frequency of
risk factors decreases to 27.10% and 25.93%,
respectively [5].
Congenital cleft of the upper lip and palate
belongs to t he category of the most severe
malformation s of the maxillofacial region. The
frequency of this pathology according to different
authors varies in the range from 12 to 36% of all human
malformations [S.V. Dyakova et al., 2002; V.V.
Roginsky et al., 2002].
In the Republic of Bashkortostan, the birth rate of
children with congenital cleft of the upper lip and palate
is higher than the national average [1, 3, 9].
It has been revealed that over the years in the
Republic of Bashkortostan, congenital cleft of the
upper lip and palate has occupied the firs t place in
frequency among all malformations in children, with an
increase in the dynamics over the past 4 years from
14.2% to 16.4% [2].
Shaikhutdinova D.I. (2005) analyzed the
incidence of congenital malformatio ns in the Republic
of Bashkortostan. Accord ing to the data obtained in

American Scientific Journal № ( 31) / 2019 13

2005, according to the monitoring results, congenital
cleft lip and palate came out on top among other
malformations of strict accounting and amounted to
17.7% [10].
The clinical charac teristics of children with
congenital cleft upper lip and palate showed a high
incidence of severe forms. These include congenital
cleft palate (38.68%) and combined cleft palate,
alveolar ridge, hard and soft palate (35.31%). Their
total frequency was 73. 99%. More often, congenital
cleft of the up per lip and palate occurred in boys -
55.40% [7].
Chuykin S.V. and Averyanov S.V. conducted an
epidemiological dental examination of 1170 children
aged 6 to 16 years living in the city of Sterlitamak.
Examination of children revealed dentoalveolar
anomalies in 677 children (57.86%). Of these,
anomalies of individual teeth were obs erved in 140
children (11.97%), anomalies of the dentition in 114
(9.74%), anomalies of occlusion in 101 (8.63%),
combined anomalies in 3 22 children (27.52%) ) The
prevalence of dentoalveolar anomalies among the
children of Sterlitamak in the temporary bit e was
38.46%. During the period of an early intermittent bite
in children, the prevalence of dentoalveolar anomalies
was 56.26%. In the p eriod of a late intermittent bite, the
frequency of dentoalveolar anomalies was 60.78%, and
in a permanent bite it incr eased to 61.85% [1, 8].
An analysis of the literature indicates that
researchers are paying close attention to various
antenatal and post natal causative factors of dentofacial
anomalies. Despite the wide coverage of the issue of the
influence of general an d local factors on the
development of dentofacial anomaly, studies of their
relationship are not sufficiently informative and very
contro versial. Thus, the identification of the causes of
pathology of the maxillofacial region, including
genetic, is a prere quisite for the justification and
implementation of their effective prevention.

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DENTAL MORBIDITY AND BIOCHEMICAL INDICAT ORS OF ORAL FLUID IN CHILDREN
SUFFERING WITH CEREB RAL PARALYSIS

Morozova Natalia Sergeevna
Kashtanova Maria Sergeevna
Moscow State Medical University named after I.M. Sechenov

Annotation . Parents and medical specialists face the fact that for every 1000 children born, there a re from 1
to 2 –3 cases of giving birth to a child with cerebral palsy syndrome. Congenital malformations of th e central
nervous system are characterized by the multiplicity and combination of functional disorders. The maxillofacial
region does not remain i solated from secondary changes in the morphological structure of bones, and damage to
organs and tissues of th e oral cavity becomes an integral part of cerebral palsy syndromes. As a result of damage
to the musculoskeletal system, speech, and mental sphere , children cannot independently carry out rational oral
care, therefore, they need constant care, and they cer tainly need help in taking measures to improve their oral
cavity [1 -4].
Key words : cerebral palsy, dental morbidity, biochemical parameters.

Re levance. Cerebral palsy is one of the most
common diseases worldwide, leading to childhood
disabilities due to impaired motor development. It
occurs due to brain damage during the period of
intrauterine development, childbirth and newborn,
manifested by mo tor disorders (paresis, paralysis,
hyperkinesia, impaired coordination). Given the
development of not only the motor, but also the
intellectual, psycho -speech and emotional spheres, the
following forms of this disease are distinguished:
double hemiplegia, spastic diplegia, hemiparetic form,
hyperkinetic form, atonic -astatic form [5 -13]. The Ural
zone, which include s the Republic of Bashkortostan, is
considered the most unfavorable in terms of child
disability. The reason for the high prevalence of
childhood disability is the high concentration of
industrial enterprises in this territory. In cerebral palsy,
cerebral structures responsible for voluntary
movements are particularly affected. A motor defect is
disabling not only because of the insufficiency or
absence of certain skills, but also because it is a
constant traumatic factor [14 -17]. In addition, most
children with cerebral palsy suffer from mental and
speech changes. Thus, with cerebral pathology, the
most important functions for a person suffer:
move ment, speech, psyche. Congenital malformations
of the central nervous system are characterized by the
multiplic ity and combination of functional disorders.
The maxillofacial region does not remain isolated from
secondary changes in the morphological struct ure of
the bones, and damage to organs and tissues of the oral
cavity becomes an integral part of cerebral pals y
syndromes. As a result of damage to the
musculoskeletal system, speech, and mental sphere,
children cannot independently carry out rational ora l
care and need constant care. Since children are easily
vulnerable to a disease such as cerebral palsy [18 -19] ,
dental measures should be carried out taking into
account the specifics of neuromuscular pathology [1].
Prevention and treatment of dental dise ases of such
children should be of high quality and effective [3].
The aim of our study is to assess the state of the
oral cavity in children with cerebral palsy, studying the
kinematic viscosity and biochemical parameters of the
saliva of children.
Materi als and research methods. We conducted a
clinical examination of children aged 12 -15 years with
a diagnosis of cerebral palsy of various forms (1 group
- 40 people) and healthy children without neurological
pathology (2 control group - 20 people). Children with
cerebral pathology were examined on the basis of the
State Educational Institution “Ufa Special Boarding
School No. 13”. External examination, examination of
the oral cavity, assessment of oral hygiene was carried
out visually and using a standard de ntal tool kit. To
study the hygienic status, we applied the methods of
Fedorov - Volodkina, Schiller - Pisarev tests, PMA and
Green - Vermilion index. The quality of oral hygiene in
patients was evaluated before conducting hygiene
lessons, at the end and a fter a month of controlled
brushing. The oral fluid was collected in the morning
on an empty stomach, and the o ral fluid was collected
in 4.0 ml glass tubes. To determine the kinematic
viscosity of saliva, a VPZh -4 capillary viscometer was
used. Colorimetr ic determination of protein in saliva
was carried out using the BELOK -PGK -NOVO reagent
kit. When the protein in teracts with pyrogallol red and
sodium molybdate, a colored complex forms, the color
intensity of which is proportional to the protein
concentrat ion in the sample. The photometric
determination of calcium in saliva was determined
using a set of reagents CA LCIUM -NOVO. In an acidic