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

Inflamation, Molar-Incisor Hypomineralization (MIH), Pulp Disease, Dental

Molar-Incisor Hypomineralization (MIH), Tooth Hypersensitivity, Pediatric Dentistry, Pulpal Biomarkers

Molar-Incisor Hypomineralization (MIH) is a qualitative developmental defect of enamel primarily affecting the permanent first molars and often incisors. The global prevalence of MIH ranges from 2.9% to 44%. Although the precise etiology of MIH remains unclear, it is considered multifactorial, involving interactions between genetic, environmental, and systemic factors during the prenatal, perinatal, and postnatal periods. Environmental toxins such as Bisphenol A (BPA) have also been implicated in its development. Despite the well-documented impact of MIH on enamel and dentin, little is known about the inflammatory changes in the pulp tissue of these teeth. This controlled clinical study aims to assess the levels of proinflammatory and anti-inflammatory cytokines in the pulp tissues of first permanent molars affected by MIH and compare them with those in non-MIH teeth. The null hypothesis is that there is no statistically significant difference in the levels of these cytokines between MIH-affected and non-affected pulp tissues. The findings are expected to contribute valuable insights into the pathophysiology of MIH-related pulpal involvement and support the development of improved diagnostic and therapeutic strategies. Pulpal blood samples were obtained from 85 first permanent molars of systemically healthy children aged 8 to 13 who underwent pulp therapy. Based on the presence or absence of Molar-Incisor Hypomineralization (MIH), teeth were assigned to either the MIH group or the control group. To evaluate the dental status and detect possible signs of pulpitis, the MIH-TNI index, Schiff sensitivity scale, Periapical Index (PAI), cold test responses, and other clinical parameters were recorded.

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.

No related papers found yet.

Turkey (Türkiye)