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العنوان
Prevalence Of Molar Incisor Hypomineralization Among Children Treated With Asthmatic Drugs During Their First Three Years Of Life:
المؤلف
Girgis, Marina Girgis Azmy.
هيئة الاعداد
باحث / مارينا جرجس عزمى جرجس
مشرف / سعاد عبد المنعم عبد المنعم
مشرف / عزه كمال عبد المجيد
مشرف / مروة على فؤاد
الموضوع
Molar Incisor Hypomineralization, MIH, Asthma, Asthmatic children, Asthmatic drugs, Etiology.
تاريخ النشر
2022.
عدد الصفحات
xvii, 122, [1] P. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
Periodontics
تاريخ الإجازة
1/1/2022
مكان الإجازة
جامعة القاهرة - الفم والأسنان - Pedodontics
الفهرس
Only 14 pages are availabe for public view

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Abstract

Aim: This study aimed to assess the prevalence of MIH among children treated with asthmatic drugs during their first three years of life.
Methodology: The study included 160 asthmatic patients(8-12 years) attending the Outpatients’ pediatric pulmonary unit of both; Agouza police hospital, Giza, & Abu Rish Japanese Pediatric Hospital, Cairo, Egypt. Data about medical history, onset, duration, and, types of asthmatic drugs were obtained from the parents and the hospitals’ medical records. Clinical examination was performed to diagnose the presence or absence of Molar Incisor Hypomineralization and its severity. The collected data were statistically analyzed.
Results: Among the whole study population, 23.1 % had MIH, where 15% had mild MIH, 4.4% were moderate, and only 3.8 % of them had severe MIH. All of the MIH cases were taking corticosteroids in combination with beta-2-agonist, and/or antihistamines. The prevalence of MIH was higher in males 25.2 % than in females 19.3 %, however, all the severe MIH cases were only found among females.
Conclusion: Children treated with asthmatic drugs during their first three years of life showed an increased risk for Molar Incisor Hypomineralization with a higher prevalence among males than females. Corticosteroid inhalers can be considered to be one of the postnatal etiological factors of MIH, either when prescribed alone, or in combination with a beta-2 agoni.