CAJ | 학술논문

目的探讨Ⅰ型胶原α2(COL1A2)和骨钙素(OC)基因多态性以及血清钙调节相关激素与氟斑牙关系.方法选取河南省开封市开封、通许2个县高氟病区及非病区8～12岁儿童作为观察对象,并根据氟斑牙患病情况分为氟斑牙患者,病区对照及非病区对照组.利用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)法检测COL1A2、OC基因多态性;放射免疫分析法测定血清钙、降钙素(CT)及OC.结果 COL1A2 PvuⅡ基因型分布频率为:氟斑牙患者pp占49.3%(37/75)、Pp占32.0%(24/75)、PP占18.7%(14/75);病区对照pp占43.5%(30/69)、Pp占52.2%(36/69)、PP占4.3%(3/69);非病区对照pp占43.8%(42/96)、Pp占40.6%(39/96)、PP占15.6%(15/96).高氟病区携带COL1A2 PP基因型的儿童患氟斑牙的危险性高于病区携带pp基因型的儿童(OR=4.85,95%CI:1.22～19.32).COL1A2 Rsa Ⅰ基因型分布频率:氟斑牙患者rr占50.7%(38/75)、Rr占36.0%(27/75)、RR占13.3%(10/75);病区对照rr占46.4%(32/69)、Rr占46.4%(32/69)、RR占7.2%(5/69);非病区对照rr占45.8%(44/96)、Rr占45.8%(44/96)、RR占8.3%(8/96),3组基因型分布比较差异无统计学意义(P>0.05).OC HindⅢ基因型分布频率:氟斑牙患者hh占48.0%(36/75)、Hb占34.7%(26/75)、HH占17.3%(13/75);病区对照hh占43.5%(30/69)、Hh占43.5%(30/69)、HH占13.0%(9/69);非病区对照hh占47.9%(46/96)、Hh占40.6%(39/96)、HH占11.5%(11/96),3组基因型分布比较差异无统计学意义(P>0.05).氟斑牙患者尿氟及血清OC水平明显高于非病区对照(P<0.05),而氟斑牙患者与病区对照间两指标差异无统计学意义(P>0.05).结论高氟病区儿童COL1A2 PvuⅡ多态性与儿童氟斑牙发生有一定关系;OC HindⅢ基因多态件与儿童氟斑牙发生未见明显有关.
목적 탐토Ⅰ형효원α2(COL1A2)화골개소(OC)기인다태성이급혈청개조절상관격소여불반아관계.방법 선취하남성개봉시개봉、통허2개현고불병구급비병구8～12세인동작위관찰대상,병근거불반아환병정황분위불반아환자,병구대조급비병구대조조.이용취합매련반응-한제성편단장도다태성(PCR-RFLP)법검측COL1A2、OC기인다태성;방사면역분석법측정혈청개、강개소(CT)급OC.결과 COL1A2 PvuⅡ기인형분포빈솔위:불반아환자pp점49.3%(37/75)、Pp점32.0%(24/75)、PP점18.7%(14/75);병구대조pp점43.5%(30/69)、Pp점52.2%(36/69)、PP점4.3%(3/69);비병구대조pp점43.8%(42/96)、Pp점40.6%(39/96)、PP점15.6%(15/96).고불병구휴대COL1A2 PP기인형적인동환불반아적위험성고우병구휴대pp기인형적인동(OR=4.85,95%CI:1.22～19.32).COL1A2 Rsa Ⅰ기인형분포빈솔:불반아환자rr점50.7%(38/75)、Rr점36.0%(27/75)、RR점13.3%(10/75);병구대조rr점46.4%(32/69)、Rr점46.4%(32/69)、RR점7.2%(5/69);비병구대조rr점45.8%(44/96)、Rr점45.8%(44/96)、RR점8.3%(8/96),3조기인형분포비교차이무통계학의의(P>0.05).OC HindⅢ기인형분포빈솔:불반아환자hh점48.0%(36/75)、Hb점34.7%(26/75)、HH점17.3%(13/75);병구대조hh점43.5%(30/69)、Hh점43.5%(30/69)、HH점13.0%(9/69);비병구대조hh점47.9%(46/96)、Hh점40.6%(39/96)、HH점11.5%(11/96),3조기인형분포비교차이무통계학의의(P>0.05).불반아환자뇨불급혈청OC수평명현고우비병구대조(P<0.05),이불반아환자여병구대조간량지표차이무통계학의의(P>0.05).결론 고불병구인동COL1A2 PvuⅡ다태성여인동불반아발생유일정관계;OC HindⅢ기인다태건여인동불반아발생미견명현유관.
Objectives To investigate the relationship between fluorosis polymorphisms in collagen type Ⅰ alpha 2 (COL1A2) and osteocalcin (OC) gene, and serum calciotropic hormone levels. Methods The children between 8 and 12 years of age in Kaifeng and Tongxu cities of Henan Province were chosen to be the object of observation. Accoding to situation of dental fluorosis, they were divided into three groups: dental fluorosis group, non-dental fluorosis group from high fluoride areas, and control group form the control areas. The Pvu Ⅱ and Rsa Ⅰ markers of COL1A2 gene as well as HindⅢ marker of OC gene were genotyped by PCR-RFLP procedure. Calcitonin and osteocalcin levels in serum were measured using radioimmunassays. Results The frequency distribution of COL1A2 PvuⅡ genotype was pp 49.3%(37/75), Pp 32.0%(24/75), PP 18.7%(14/75) in children with fluorosis; pp 43.5% (30/69), Pp 52.2% (36/69), PP 4.3%(3/69) in children without fluorosis from high fluoride areas; and pp 43.8% (42/96), Pp 40.6% (39/96), PP 15.6% (15/96) in the children without fluorosis from control areas respectively. Childrens with the homozygous genotype PP of COL1A2 Pvu Ⅱ had a significantly increased risk of dental fluorosis(OR=4.85, 95%CI: 1.22-19.32) compared to children with the homozygous genotype pp in anendemic fluorosis area. The frequency distribution of COLIA2 Rsa Ⅰ genotype was rr 50.7% (38/75), Rr 36.0% (27/75), RR 13.3%(10/75) in children with fluorosis; rr 46.4%(32/69), Rr 46.4%(32/69), RR 7.2%(5/69) in children without fluorosis from high fluoride areas, and rr 45.8% (44/96), Rr 45.8% (44/96), RR 8.3% (8/96) in the children without fluorosis from control areas respectively. There were no significant differences in the three groups (P>0.05). The frequency distribution of OC Hind Ⅲ genotype was hh 48.0% (36/75), Hh 34.7% (26/75), HH 17.3% (13/75) in children with fluorosis; hh 43.5% (30/69), Hh 43.5% (30/69), HH 13.0% (9/69) in children without fluorosis from high fluoride areas, and hh 47.9%(46/96), Hh 40.6%(39/96), HH 11.5%(11/96) in children without fluorosis from control areas respectively. There were no significant differences in the three groups (P>0.05). Additionally, fluoride levels in urine and OC levels inserum were found to be significantly lower in controls from non-endemic areas compared to cases(P<0.05). However, the differences in urine fluoride and serum OC levels were not observed when cases were compared to controls from high fluoride areas(P>0.05). Conehlsions This study provides the evidence of an association between polymorphisms in the COL1A2 gene with dental fluorosis in populations exposed to high fluoride. There were no correlation between OC Hind Ⅲ genotype and the dental fluorosis.