Assessment of Inflammatory Biomarkers in Molar-Incisor Hypomineralization-Affected First Permanent Molars

Molar-Incisor Hypomineralization (MIH) is a qualitative developmental enamel defect that predominantly affects the permanent first molars and frequently involves incisors. Characterized by demarcated opacities and structurally compromised enamel, MIH increases the susceptibility of teeth to post-eruptive breakdown, rapid caries progression, and functional and aesthetic impairments. Globally, MIH prevalence ranges from 2.9% to 44%, and in Turkey, it has been reported between 7.7% and 24%, indicating significant public health relevance. The etiology of MIH is considered multifactorial, involving complex interactions among genetic, systemic, and environmental factors across prenatal, perinatal, and postnatal periods. Environmental toxins, such as bisphenol A (BPA), and systemic conditions like low birth weight, preterm birth, and early childhood illnesses, have been implicated. Microscopic studies demonstrate decreased mineral content, altered hydroxyapatite crystal structure, and reduced microhardness in MIH-affected enamel. These properties compromise enamel integrity, facilitate bacterial penetration, and increase the risk of pulpal involvement. MIH-affected dentin typically exhibits widened dentinal tubules, increasing dentin permeability and promoting rapid stimulus transmission to the pulp. Clinically, this is associated with hypersensitivity, difficulty in achieving anesthesia, and pulpal inflammation. However, the specific inflammatory profiles of pulps in MIH-affected teeth have not been thoroughly studied. This controlled clinical study aims to investigate and compare the levels of proinflammatory (TNF-α, IL-6, IL-8) and anti-inflammatory (IL-4, IL-10, IL-13) cytokines, as well as tissue degradation markers (MMP-3, MMP-8, MMP-9), in the pulpal blood of MIH-affected versus non-affected first permanent molars. A total of 85 first permanent molars requiring pulp therapy were selected from systemically healthy children aged 8 to 13 years. Based on MIH status, the teeth were categorized into MIH and control groups. Clinical evaluation included assessment using the MIH Treatment Need Index (MIH-TNI), Schiff Cold Air Sensitivity Scale, Periapical Index (PAI), cold test responses, and other clinical signs of pulpitis. Pulpal blood samples were collected under sterile conditions using cotton pellets, transferred into lithium heparin-coated tubes, and stored at -70°C. Enzyme-linked immunosorbent assay (ELISA) was used to quantify the levels of TNF-α, IL-4, IL-6, IL-8, IL-10, IL-13, MMP-3, MMP-8, and MMP-9. This study is expected to provide novel insights into the pathophysiology of MIH-related pulp inflammation and contribute to the development of improved diagnostic and treatment strategies in pediatric dentistry.