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Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Effect of Chronic Apical Periodontitis in Primary Molars on Succedaneous Permanent Teeth: An Observational
Nileshrao Patil1, Aruna P Vishwakarma2, Romalpreet Singh3
1Department of Conservative Dentistry and Endodontics, Jawahar Medical Foundation's (JMF) Annasaheb Chudaman Patil Memorial (ACPM) Dental College, Dhule, IND.
Introduction:
Periapical infection of primary molars affects the development of permanent teeth (premolars). Therefore, the present study was conducted to test the null hypothesis in children aged 4-10 years with chronic apical periodontitis (CAP) of the primary molars.
Materials And Methods:
A retrospective, cross-sectional study was conducted on 185 panoramic radiographs of healthy children aged 4-10 years with CAP in the primary molars. A total of 256 infected primary molars (144 teeth in females, 112 teeth in males) were analyzed, radiographically, and compared with 245 healthy primary molars on the contralateral side. Permanent successors were evaluated for follicular damage, maturation, morphology, and deviation in the eruption path. Primary molars were evaluated for root resorption. Sixteen permanent teeth on the affected side and five teeth on the control side were excluded due to abnormal development. Student's t-test and the chi-square test were used to analyze the data.
Results:
The null hypothesis is rejected. There were significant differences in the developmental status of permanent successors on the affected side, compared to the normal side at four to seven years (p<0.05). There were no significant sex differences in the abnormalities of permanent successors on the affected side (p>0.05). As the root resorption of the primary molars increased, the follicular damage observed in the permanent successors also increased (p<0.05), which suggests that, as the infection of primary molars increases, more damage is caused to underlying permanent successors (premolars).
Conclusion:
Apical periodontitis of the primary molars retards the development of permanent successors (premolars), affects their shape, causes follicular damage, and alters the eruption path.
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