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Assessment of Inflammatory Cytokines in Molar Incisor Hypomineralization-affected First Permanent Molars: A Clinical
Seray Sahin1, Nihal Sehkar Oktay2, Sukriye Calişkan3
1Department of Pediatric Dentistry, Faculty of Dentistry, Marmara University, Istanbul, Türkiye.
Introduction:
Molar incisor hypomineralization is a developmental enamel defect that weakens tooth structure, increasing susceptibility to caries, hypersensitivity, and treatment challenges. This study aimed to evaluate pro- and anti-inflammatory cytokine levels in the pulp of molar incisor hypomineralization-affected and nonmolar incisor hypomineralization (MIH) first permanent molars.
Methods:
This study analyzed pulpal inflammatory mediator levels in blood samples collected from 85 first permanent molars (38 (44.7%) with MIH and 47 (55.3%) without) requiring pulp treatment in systemically healthy children aged 8-13 years. During routine treatment, sterile cotton pellets were placed on the pulp exposure site for approximately 1 minute to obtain samples. Based on clinical findings and bleeding time, teeth were classified as reversible pulpitis, symptomatic or asymptomatic irreversible pulpitis. Clinical assessment included the Schiff cold air sensitivity score, periapical index and cold test. The collected samples were stored in lithium heparin-coated tubes at -70 °C, and the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-4, IL-6, IL-8, IL-10, IL-13, matrix metalloproteinase (MMP)-3, MMP-8, and MMP-9 were analyzed using the enzyme-linked immunosorbent assay method.
Results:
In the molar incisor hypomineralization group, 18 (47.4%) teeth had reversible pulpitis, 8 (21%) symptomatic, and 12 (31.6%) asymptomatic irreversible pulpitis; corresponding numbers in the non-MIH group were 20 (42.6%), 11 (23.4%), and 16 (34%), respectively. Molar incisor hypomineralization-affected molars showed higher TNF-α, IL-4, IL-13, MMP-3, and MMP-8 levels than non-MIHs (P < .05). Subgroup analyses demonstrated that inflammatory marker levels were higher, particularly in MIH-related pulpitis subgroups (P < .05). These differences were mainly observed in biomarkers such as IL-4, IL-13, and MMP-8. Tooth maturity showed no overall differences, though IL-4 was higher in immature MIH teeth (P < .05).
Conclusion:
Elevated cytokine levels in molar incisor hypomineralization-affected teeth suggest severe pulp inflammation (TNF-α), a strong anti-inflammatory response (IL-4, IL-13), and inflammation-related tissue destruction (MMP-3, MMP-8), potentially leading to subclinical inflammation and increased pulpal damage.
