Lower dental pulp oxygen saturation in children with molar incisor hypomineralization: a cross-sectional study

Abstract

This study evaluated the oxygen saturation of pulp tissue (SaO₂) in first primary molars (FPM) with and without molar incisor hypomineralization (MIH) and explored the correlations between MIH severity and pulp SaO₂ levels. The cross-sectional design involved 29 children (16 girls and 13 boys, aged 7–11 years), yielding 116 FPM. The FPM were categorized into groups based on the presence or absence of MIH: Group 1 (G1) included teeth without MIH (n = 48); Group 2 (G2), mild MIH cases (n = 30); and Group 3 (G3), severe MIH cases (n = 38). Pulse oximetry was used to assess SaO₂, with measurements conducted twice for each tooth, each lasting 30 seconds. Significant variations in the SaO₂ levels were observed relative to the severity of MIH. The median SaO₂ in G1 was 94% (IQR 90–98%), while MIH cases showed lower levels: 79% (IQR 71.5–83.5%) for mild MIH (G2) and 68% (IQR 55–75%) for severe MIH (G3) (p < 0.001). The FPM affected by MIH (G2 and G3) demonstrated lower SaO₂ levels than those in G1, with severe cases exhibiting even lower levels than mild cases. This study provides important insights into the relationship between MIH severity and pulp SaO₂ and suggests significant implications for clinical management strategies.

Descriptors:
Molar Hypomineralization; Oximetry; Dental Pulp; Pediatric Dentistry

Introduction

Molar incisor hypomineralization (MIH) is a qualitative defect in tooth development characterized by opacities that range from creamy white to brownish yellow in the first primary molars (FPM) and may include other tooth groups, such as incisors or second molars.¹-⁵ These hypomineralized lesions result in porous enamel, which is susceptible to post-eruptive fractures due to masticatory forces.⁶,⁷ Additionally, MIH predisposes individuals to dental caries and increased dental hypersensitivity, potentially affecting their quality of life.⁸-¹⁰ MIH is diagnosed in children, and the estimated global prevalence of MIH is approximately 13.5%,¹⁰ with moderate-to-severe cases accounting for 36.3% of the total incidence.¹⁰,¹¹

MIH can be classified into mild and severe categories, with the latter often presenting with significant dental hypersensitivity.¹¹ It has been hypothesized that the porosity of the enamel facilitates bacterial infiltration into the dentinal tubules, potentially leading to chronic pulp inflammation,¹²,¹³ thereby suggesting a correlation between MIH and altered pulp physiology, which is associated with dental hypersensitivity.

Depending on the severity of the defect, pulpal inflammation in teeth with MIH may progress to necrosis.¹³ Early diagnosis and treatment are essential for favorable prognoses in these patients.³,⁵ Conventional pulpal diagnostics, such as cold and heat sensitivity tests, are often poorly tolerated by children, and to overcome these limitations, pulse oximetry, a noninvasive true vitality test, has been developed for measuring oxygen saturation levels (SaO₂) in blood flow.¹⁴-¹⁹

Numerous studies have established its efficacy in assessing SaO₂in teeth across various conditions, such as permanent teeth with periodontal attachment loss,¹⁵ recently traumatized teeth with impaired nerve response,¹⁶ and vital and non-vital states including open apices,¹⁷-¹⁹,²⁰ a condition that MIH patients may present. ²² Pulse oximetry offers significant advantages as a rapid and effective tool for true vitality testing compared to conventional methods and is generally well accepted in pediatric populations.¹⁷,²¹

Despite its potential, the use of pulse oximetry in children with MIH remains unexplored. This method offers a promising alternative for diagnosing pulpal conditions in pediatric patients, providing measurements independent of pain perception. Furthermore, this study aimed to assess SaO₂ in FPM with and without MIH using pulse oximetry and to investigate potential correlations between the severity of MIH and SaO₂ levels.

Methods

Setting

This cross-sectional observational study was conducted between May and September 2023 at the Pediatric Dentistry Clinic of School of Dentistry of Ribeirão Preto, located in Ribeirão Preto, SP, Brasil. This study aimed to evaluate SaO₂ in the FPM of children aged 7–11 years.

The study was approved by the Research Ethics Committee of the Research Ethics Committee of the University of São Paulo School of Dentistry of Ribeirão Preto (FORP-USP) (Process Number: CAAE 12161019.2.0000.5419 and was conducted in accordance with the Declaration of Helsinki. The guardians agreed and signed an Informed Consent Form. The research followed the STrengthening the Reporting of OBservational studies in Epidemiology (STROBE) guidelines.²²

Participants and variables

This study investigated the differences in SaO₂ among the groups and the correlation between MIH severity and SaO₂. The participants were categorized into three groups based on the presence and severity of MIH or control: children with FPM without MIH (control group, G1), children with FPM with mild MIH (Group 2 [G2]), and children with FPM with severe MIH (Group 3 [G3]). The MIH classification used in this study was based on the criteria proposed by Ghanim et al.,²³ which consider both the type of enamel defect and the extent of the affected tooth surface. Clinically, mild MIH is characterized by demarcated opacities that are white or creamy in color (code 21) and involve less than one-third of the tooth surface (extent I). In contrast, severe MIH includes yellow or brown opacities (code 22), post-eruptive enamel breakdown (code 3), atypical restorations (code 4), and atypical caries (code 5), particularly when affecting a larger portion of the tooth (extent II or III).

The inclusion criteria were healthy children aged 7–11 years who received dental care during the study period, with at least one fully erupted FPM that was free from carious lesions or previous endodontic treatment. To ensure the reliability of SaO₂ measurements, children were excluded if they had any systemic condition potentially affecting SaO₂ (e.g., diabetes, cardiovascular disease, leukemia, epilepsy, or chronic asthma) or were taking medications such as analgesics, anti-inflammatory drugs, anticonvulsants, anxiolytics, or antihypertensives. For children in the severe MIH group (G3), only FPMs showing no signs of deep caries, periapical radiolucency, fistulas, painful symptoms suggestive of pulpitis, or dentoalveolar abscesses were selected. All eligible patients attending the clinic and whose caregivers provided informed consent were considered for inclusion to minimize selection bias.

The primary outcome of this study was SaO₂, measured using pulse oximetry adapted for dental applications. The main explanatory variable was the severity of MIH. Additional variables included the patient’s age and sex as well as SaO₂ measured in the index finger, which served as a systemic oxygenation reference.

Study size

Sample calculations were performed using an online tool available at http://estatistica.bauru.usp.br/calculoamostral/ta_diferenca_media_independente.php. This calculation incorporated data from Lambert et al. ²⁴, who reported a minimum of 77.52% SaO₂ for pulp vitality, as well as data from a pilot study that compared the pulp oximetry values of 11 healthy first molars and 9 first molars with severe MIH. The estimated standard deviation (SD) was 0.30 (between the control and severe MIH groups), and, based on a minimum difference to be detected of 0.23, with a test power of 80% and a significance level of 95%, the sample required was at least 29 teeth per group.

Data measurements and bias

MIH diagnosis cases and the severity ⁵were conducted by an experienced and calibrated dental surgeon (Kappa > 0.8). To reduce selection bias, all eligible children attending the school during the study period and whose caregivers provided consent were considered for inclusion. The pulse oximetry vitality test was conducted by a calibrated examiner following the methodology outlined by Estrela et al.²⁵(Figure 1A). Another researcher assisted in performing the procedures and was responsible for recording the data. SaO₂ levels were determined using a BCI 3301 portable pediatric pulse oximetry monitoring system (Smiths Medical PM Inc., Waukesha, USA) equipped with 3025 sensors (for teeth) and 3026 sensors (for fingers). To ensure accuracy, the teeth were isolated with cotton rollers, and a saliva sucker was used to control humidity.

Figure 1
Pulse oximeter to SaO2 measurement. A: Device used to activate and display the values of the pulse oximeter. B: The positioning of the pulse oximeter sensors, which were stabilized with a specially designed clamp in element 46.

The pulse oximetry probe was specifically designed to test permanent molars, facilitating the placement of two diodes in parallel to accurately measure SaO₂ levels in the dental pulp (patent registered under Brazil’s Copyright Law No. 9.610/1998, February 28, 2024). A stainless steel adapter was custom-made for this study (Figure 1B). SaO₂ levels were recorded twice for 30 s to ensure correct readability.¹⁷ The average of the two measurements was used as the final value. Additionally, a third measurement was taken with a pulse oximetry probe on the patient’s index finger to determine the blood saturation level.

Statistical analysis

The Kolmogorov–Smirnov test was used to evaluate normality, which indicated a significant deviation (p < 0.05). Non-parametric tests were used for group comparisons: the Mann–Whitney test was used to compare the exposed (with MIH) and non-exposed groups, while the Kruskal–Wallis test was used to assess differences among groups (G1, G2, and G3). Significant results from the Kruskal–Wallis test were further analyzed using the Dwass-Steel-Critchlow-Fligner post hoc test for pairwise comparisons. The Spearman’s correlation test was used to evaluate the relationship between MIH severity and pulp oximetry data. A 5% significance level was adopted, and all analyses were performed using Jamovi software, version 2.3 (www.jamovi.org/about.html; Newcastle, Australia).

Results

This study included 29 children (16 girls, 13 boys) with 116 FPM evaluated. In G1, 12 children had 48 FPM with a mean age of 9.29 years. The MIH groups (G2 and G3) included 17 children, with 30 FPM in G2 and 38 FPM in G3. The diagram illustrates the study design and includes participants (Figure 2).

Figure 2
Diagram of the study design. FPM: First primary molars, MIH: Molar incisor hypomineralization, N: Number of teeth evaluated.

Table 1 presents the descriptive data on age and SaO₂ levels stratified by MIH severity and sex. No significant age differences were observed among the three groups (p = 0.582). However, a highly significant difference in SaO₂ levels was found (p < 0.0001). In G1, the mean SaO₂ was 91.19% (SD 7.44) for females and 93.81% (SD 3.66) for males. G2 showed mean SaO₂ levels of 78.38% (SD 8.63) in females and 77.25% (SD 5.25) in males. Finally, G3 exhibited mean SaO₂ levels of 56.45% (SD 19.05) in females and 71.44% (SD 12.67) in males. This indicates that while overall SaO₂ levels were significantly lower in the MIH groups than in the control group, a notable difference in SaO₂ levels between males and females was present within the severe MIH group, warranting further investigation.

Table 1
Descriptive data of sex and SaO2 among MIH severity and sex.

Variables	Severity	Sex	Mean (SD)	Median	Percentiles		p-value
					25th	75th
Age	G1	F	9.50 (0.89)	9.00	9.00	9.50	0.582
		M	9.38 (1.51)	10.00	8.50	10.25
	G2	F	9.31(1.40)	9.00	8.00	11.00
		M	7.00 (0.00)	7.00	7.00	7.00
	G3	F	9.73 (0.63)	10.00	9.00	10.00
		M	9.25 (1.52)	9.50	8.50	10.25
SaO2	G1	F	91.19 (7.44)	93.00	88.00	96.50	< 0.0001*
		M	93.81(3.66)	94.00	90.00	98.00
	G2	F	78.38 (8.63)	79.00	71.50	84.00
		M	77.25 (5.25)	78.50	75.25	80.50
	G3	F	56.45 (19.05)	64.50	46.00	70.00
		M	71.44 (12.67)	73.50	66.75	78.50

• NG1: Control group, G2: Mild MIH, G3: Severe MIH, F: Female, M: Male, SD: Standard deviation, p* statistical difference between groups.

For distributional analyses, MIH severity (G1, G2, and G3) was treated as an ordinal qualitative variable, and SaO₂ values were included in the correlation matrix. Spearman’s correlation test revealed a significant inverse correlation (p < 0.001, r = -0.822), indicating a strong negative relationship between MIH severity and pulpal SaO₂ levels. The Dwass-Steel-Critchlow-Fligner post hoc test for paired comparisons further confirmed significant differences among all groups (p < 0.001) (Figure 3). The distribution of SaO₂ levels followed an increasing order, with G3 showing the lowest levels and G1 showing the highest levels (G3 < G2 < G1).

Figure 3
Correlation between MIH severity (G1 or Control, G2 or Mild MIH; G3 or Severe MIH) and pulp oximetry values. Different symbols (*#&) indicate statistically significant differences between groups.

Table 2 further illustrates this relationship through median SaO₂ values and interquartile ranges. G1 showed a significantly higher median SaO₂ of 94% (IQR: 90-98%) compared with both G2 (79% [IQR: 71.5–83.5%]) and G3 (68% [IQR: 55–75%]) (p < 0.0001). This confirms a strong negative correlation between MIH severity and SaO₂ levels.

Table 2
Descriptive data of median and interquartile range from SaO2 (%) among the groups.

Severity (n)	SaO2 Median (IQ)	p-value
G1 (n= 48)	94% (90% - 98%)	< 0. 0001*
G2 (n= 30)	79% (71.5% - 83.5%)
G3 (n= 38)	68% (55% - 75%)

• n: number of FPM evaluated, G1: Control group, G2: Mild MIH, G3: Severe MIH, IQ: Interquartile range. p* statistical difference between groups.

Discussion

MIH is characterized by reduced enamel mineral density, poor prism organization, and increased protein content.⁵ It is associated with an increased incidence of dental pulp inflammation.²⁶ The MIH enamel structure presents higher porosity, creating more space for the penetration of stimuli, which is a frequent cause of pulp inflammation and dental hypersensitivity.²⁷.In this study, patients with severe MIH presented lower SaO₂ levels than those with mild MIH or sound teeth.

Studies using pulse oximetry as a complementary tool for measuring SaO₂ levels in dental pulp inflammation in permanent teeth have been conducted under different conditions.¹⁵-¹⁷,¹⁹ Setzer et al.¹⁹ assessed SaO₂ in inflamed and necrotic pulps and found average values of 87.4% for reversible pulpitis, 83.1% for irreversible pulpitis, and 74.6% for pulp necrosis. In our study, we obtained SaO₂ levels of 68% in patients with severe MIH.

Studies have determined that SaO₂ values in permanent healthy teeth are above 79–100%.¹⁴,¹⁷,¹⁹,²⁵. Estrela et al.²⁵ assessed the saturation of the upper and lower permanent molars in 112 teeth and obtained mean SaO₂ values of 83.59% and 86.90%, respectively. Gopikrishna et al.,¹⁴ studying the healthy pulp of upper central incisors, determined an SaO₂ value of 79.31%, and the upper lateral teeth scored 79.61%, whereas Setzer et al.¹⁹ obtained an SaO₂ value of 92.2% in a sample of 60 teeth, including the upper and lower premolars and molars. This condition may differ in teeth with MIH.

Our study emphasizes the correlation between severe MIH and reduced SaO₂ levels in pulp tissue. These findings support the hypothesis that teeth with MIH show inflammatory changes in the pulp tissue.¹³,¹⁴ The severity of MIH directly correlates with diminished SaO₂, indicating the need for continuous endodontic monitoring of teeth with MIH due to intensified pulp inflammation in severe cases. Previous studies have reported similar findings in various pulp conditions, attributing decreased SaO₂ to the inflammatory process and reduced vascularity, with SaO₂ levels ranging from 64.3% to 92.03%, depending on the degree of pulp compromise.¹⁵,⁹,²⁸-³⁰

Pulp inflammation may contribute to a decline in SaO₂ levels in MIH ³². Even in the absence of enamel fracture, the dental pulp tissue in MIH cases exhibited inflammation characterized by heightened pulp nerve density and inflammatory cell infiltration.²⁵ Furthermore, despite fractures, bacterial dentin invasion in hypomineralized enamel may serve as an entry point for oral bacteria through the dentinal tubules. This penetration can result in inflammation of the dental pulp and spontaneous pain, which is attributed to the sensitization of nerve fibers and disruption of blood circulation.¹¹,¹³ In addition, considering that pulp tissue inflammation has the potential to induce tertiary dentin formation, it may result in a decrease in pulp chamber volume and a reduction in vascular suppl. ³¹ These structural alterations may influence SaO₂ levels, as demonstrated in the present study.

Patient age significantly influences the assessment of SaO2 levels in dental pulp. ²⁵,³¹,³²Stella et al.,³² evaluating permanent maxillary central incisors with normal pulp in children/adolescents and adults, observed higher SaO₂ levels in the maxillary incisors of children and adolescents aged 7–13 years than in those of adult patients aged 22–36 years. Similarly, Estrela et al.²⁵assessed different age groups and reported that SaO₂ was significantly reduced in the 40–44-year-old group compared with that in younger individuals aged 20–39 years, suggesting that older patients may present with lower SaO₂ levels,³² even in the absence of pulpal tissue damage. Nevertheless, in our study, lower oximetry values were further reduced in patients with severe MIH. However, caution should be exercised when extrapolating our findings to adults with severe MIH, because physiological age-related changes may not be comparable.

Additionally, children aged 7–11 years were included after the complete eruption of the first permanent molar. The age difference was relatively small, and no differences were observed in baseline data between the groups (p = 0.582). However, the timing of root formation completion may vary among children. We believe that this variation does not affect pulpal health status or compromise comparability between groups. However, further studies should focus on children at the same stage of root development to better evaluate potential differences in pulp vitality.

Following the literature,²⁷,³³ the findings of this study revealed an association between Visual Analog Scale and Schiff Cold Air Sensitivity Scale scores and MIH severity. Inflammatory changes within the pulp tissue, as indicated by reduced SaO₂ levels, may contribute to the heightened sensitivity and discomfort experienced by patients with severe MIH. The observed inverse relationship underscores the potential for compromised pulp vitality to manifest as increased pain perception, highlighting the importance of monitoring SaO₂ levels along with hypersensitivity assessments for a comprehensive understanding of the condition in pediatric patients. Future studies should further explore this potential association.

This study provides valuable insights into the relationship between MIH severity and SaO₂. However, it has certain limitations. Although guided by a sample size calculation, the sample size of 29 children may limit the applicability of the findings to a broader pediatric population. In addition, the cross-sectional design restricts the ability to establish causal relationships. Furthermore, the study did not control for potential confounding factors, such as dietary habits or oral hygiene practices, which could have influenced the outcomes. Nevertheless, this study effectively highlights significant differences in SaO₂ levels among the MIH severity groups and establishes a possible correlation between MIH severity and pulp health. These findings contribute to the understanding of MIH and underscore the utility of pulse oximetry as a noninvasive tool for evaluating dental pulp conditions in children, paving the way for future research in this area.

Studying the pulpal condition of teeth with MIH is an important and innovative way of explaining the occurrence of dental pulp inflammation. A proper diagnosis of MIH requires a complementary means to help explain the cause of pulpal inflammation and its possible correlation with the state of subclinical inflammation of the pulpal tissue. Evaluating SaO₂ levels in these patients may be helpful in explaining the painful symptoms observed in this condition.¹⁶,³³ Its accuracy in providing objective data, independence from the patient’s response, and non-invasiveness make it particularly useful in children with MIH.³³ Accurate diagnosis of pulp tissue conditions and, in the case of MIH, pulp inflammation associated with this condition is challenging, as the dental pulp is located inside a cavity and is therefore inaccessible for direct inspection.¹⁶ Thus, the use of pulse oximetry as a complementary tool made it possible to obtain information on SaO₂ levels in teeth with MIH.

Conclusion

This study showed that children with MIH have altered SaO₂ values. These values may be lower in severe cases of MIH. These findings may contribute to the use of auxiliary tools to diagnose pulpal conditions in children with MIH.

Acknowledgment

We express our gratitude to Carlos Estrela for overseeing the patent registration of our work, titled “Dental adaptation device for pulp oximetry levels reading”, Registered under Brazil’s Copyright Law No. 9.610/1998, which involves contributions from Alexandra Mussolino de Queiroz, Jade de Souza Cavalcante, Francisco Wanderley Garcia de Paula-Silva, Fabrício Kitazono de Carvalho, Manoel Damião de Sousa Neto, and Fernando Branco Barletta. This acknowledgment recognizes the significance of the patent in our research and emphasizes that it should not be plagiarized, used, reproduced, or disclosed without the explicit authorization of its respective authors.

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• Data availability:
  The datasets generated and/or analyzed in the current study are available from the corresponding author upon reasonable request.
• Finnacial support:
  Coordenação de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (Capes; Finance Code 001) and the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq; Finance Code 140475/2023-0)

Edited by

• Editor-in-Chief:
  Lucianne Maia

• Associate Editor:
  Mário Tanomaru-Filho

Data availability

The datasets generated and/or analyzed in the current study are available from the corresponding author upon reasonable request.

Publication Dates

• Publication in this collection
  20 Mar 2026
• Date of issue
  2026

History

• Received
  30 Mar 2025
• Accepted
  23 Sept 2025
• Received
  16 Oct 2025