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. 2026 Jul 10;26:1918. doi: 10.1186/s12903-026-09187-5

A histopathological case-control study of severe turner teeth and normal teeth: structural and compositional alterations in pulp and periodontal tissues

Tiankai Di 1,2,#, Yuhan Liu 1,#, Jinlong Xu 2, Xiaodong Zhang 3, Jun Li 3, Lulu Wang 1,✉, Yujiang Chen 1,4,✉
PMCID: PMC13637313  PMID: 42426693

Abstract

Objective

Turner teeth are developmental defects of permanent teeth commonly associated with disturbances affecting the corresponding primary predecessors, particularly infection or trauma. Although their clinical features have been described in previous reports, detailed histopathological characterization of severe Turner teeth, especially with respect to pulp tissue alterations, remains limited. This case-control study compared severe Turner teeth with normal teeth, focusing primarily on structural and molecular alterations in pulp tissue and descriptively on periodontal tissue morphology. Enamel structure and composition were not directly investigated.

Materials and methods

Ten extracted severe Turner teeth and ten extracted normal teeth from orthodontic patients were included. Hematoxylin and eosin staining and Masson trichrome staining were used to evaluate pulp, apical, and periodontal tissue morphology. Immunofluorescence staining was performed in pulp tissue sections to assess markers related to stemness (CD105), vascularization (CD31), innervation (βIII-tubulin), dentinogenesis (DSPP and RUNX2), extracellular matrix organization (Vimentin and FN1), inflammation (IL-1β and TNF-α), and Wnt/β-catenin signaling (β-catenin, AXIN1, and AXIN2).

Results

Compared with controls, severe Turner teeth showed a thinner odontoblast layer, a less continuous dentin-pulp interface, disorganized apical pulp fibers, reduced vascular distribution, irregular periodontal fiber arrangement, and a thinner cementum layer. In pulp tissue, CD105, CD31, βIII-tubulin, DSPP, RUNX2, Vimentin, FN1, and β-catenin expression levels were lower in Turner teeth, whereas IL-1β, TNF-α, AXIN1, and AXIN2 expression levels were higher (all P < 0.05).

Conclusion

Severe Turner teeth were associated with coordinated histopathological alterations in pulp tissue architecture, marker expression, and periodontal morphology. These findings provide tissue-level evidence that severe Turner teeth are accompanied by an altered pulp microenvironment and provide a histopathological basis for future mechanistic and clinical studies.

Keywords: Turner teeth, enamel hypoplasia, dental developmental anomaly, inflammatory microenvironment, Wnt/β-catenin signaling pathway

Background

Turner teeth refer to a dental developmental anomaly characterized by the hypoplasia of enamel [1]. This condition results in discolored, malformed, or undersized teeth, primarily affecting the permanent dentition [2]. Turner teeth can adversely affect oral health, leading to esthetic concerns, increased susceptibility to caries, and potential functional impairment. The clinical manifestations of Turner teeth can vary widely among affected individuals, necessitating a thorough understanding of their histopathological characteristics. A better understanding of these features may improve the biological basis for diagnosis and management of affected teeth.

Turner teeth are generally considered to result from localized disturbances affecting the developing permanent tooth germ, most commonly infection or trauma involving the corresponding primary predecessor, including early childhood caries, dental abscesses, or traumatic injury [1, 2]. The prognosis for individuals with Turner teeth varies, depending largely on the severity of enamel defects and the health of the surrounding periodontal structures [3]. While some patients may mainly present with esthetic concerns, others may also experience functional impairment and therefore require more extensive clinical management. Current management of Turner teeth is largely based on visible crown defects and restorative needs [3]. However, the biological status of the underlying pulp tissue may also be clinically relevant, because alterations in pulp organization, vascularization, innervation, inflammation, and extracellular matrix composition could influence tooth vitality, reparative capacity, and treatment planning.

Despite increasing clinical recognition of Turner teeth, current management is still mainly guided by visible crown defects rather than by tissue-level biological characterization [3]. In particular, the status of the underlying pulp tissue remains insufficiently defined. Because pulp organization, vascularization, innervation, inflammatory status, and extracellular matrix composition may influence tooth vitality and reparative capacity, characterizing these features in severe Turner teeth may provide biologically relevant information for future clinical assessment.

Therefore, this study aimed to compare severe Turner teeth with normal teeth, focusing primarily on histopathological and molecular alterations in pulp tissue and secondarily on morphological changes in periodontal tissue. Hematoxylin and eosin staining and Masson trichrome staining were used to evaluate tissue architecture, and immunofluorescence staining was used to assess markers related to stemness, vascularization, innervation, dentinogenesis, extracellular matrix organization, inflammation, and Wnt/β-catenin signaling. The null hypothesis was that severe Turner teeth would not differ from normal teeth in histomorphology or in the expression levels of the evaluated pulp markers.

Materials and methods

Study design

Sample collection and eligibility criteria.

Inclusion Criteria:

  1. Age: Participants were aged between 8 and 18 years to ensure representation of the developmental stage of teeth.

  2. Diagnosis: Included participants had been clinically diagnosed with severe Turner teeth and had a documented history of infection affecting the corresponding primary predecessor. The diagnosis was based on the following criteria:
    1. Enamel Developmental Defect: The crown surface exhibits localized pits, defects, or groove-like fissures, accompanied by hypomineralization of enamel (manifesting as chalky white or yellowish-brown discoloration). Concurrently, reduced crown size and irregular morphology (e.g., incisal edge defects or abnormal occlusal surface structure) may be present.
    2. History of Primary Tooth Infection: The anatomically corresponding primary tooth must have a documented history of chronic periapical periodontitis (e.g., caries-related/traumatic infection, recurrent abscesses, or radiographically confirmed periapical radiolucency).
    3. Exclusion of Systemic Disorders: Systemic diseases such as hereditary enamel hypoplasia, dental fluorosis, or other similar conditions must be excluded.

  3. Sample Type: Only extracted permanent teeth were eligible, with the extraction directly related to the developmental anomalies of the teeth.

  4. Informed Consent: Participants or their guardians were provided written informed consent, permitting the use of samples for research purposes.

Exclusion Criteria:

  1. Comorbidities: Individuals with systemic diseases or other hereditary conditions that affect tooth development, such as dental developmental syndromes, were excluded.

  2. Caries and Trauma: Teeth that have been compromised due to trauma, severe caries, or other pathological conditions leading to structural loss or deformation would not be included.

  3. Ongoing Treatment: Individuals currently undergoing orthodontic treatment, endodontic therapy, or any other medical interventions that could influence tooth structure were excluded from the study.

  4. Sample Integrity: Samples that are contaminated or improperly handled during collection were excluded from analysis.

  5. Retainable Teeth: Teeth diagnosed as Turner teeth but determined by a clinician to be retainable through therapeutic intervention would be excluded.

In the control group, permanent premolars from children aged 8 to 18 years were extracted for orthodontic reasons. Children with a history of drug allergy, systemic disease, or familial genetic disorders affecting tooth development were excluded. After tooth extraction, the teeth were categorized into their groups. Finally, the number of teeth at each stage of the study was analyzed histologically as follows: Turner tooth Group: 10, Control Group: 10. All samples were obtained from the School of Stomatology, Fourth Military Medical University, Xi’an, China. This study was approved by the Ethics Committee of the Stomatological Hospital of the Fourth Military Medical University of the Chinese People’s Liberation Army (IRB-REV-2018016; approved on March 6, 2018). Furthermore, the guardian of each participant signed an informed consent form. This study was not preregistered. Because this was an exploratory histopathological analysis of clinically collected extracted teeth rather than an interventional clinical trial, no prospective registry entry was completed.

Because extracted severe Turner teeth are uncommon in clinical practice, the sample size was determined by case availability during the study period; therefore, the present study should be interpreted as exploratory/pilot in nature. To further support interpretation of the quantitative findings, effect sizes and post hoc power values were calculated for the principal immunofluorescence comparisons.

Histological examination

HE and Masson staining was performed using the detection protocol of the staining kit (Solarbio, G1120 and G1340, China). Immunofluorescence staining was performed on the sections to quantify and compare each protein expression in tooth pulp samples. Primary antibodies (anti-CD31 antibody (Abcam, ab28364, UK), anti-βIII tublin antibody (Abcam, ab18207, UK), anti-CD105 (Abcam, ab252345, UK), anti-DSPP (Abcam, ab216892, UK), anti-RUNX2 (Abcam, ab192256, UK), anti-Vimentin (Abcam, ab8978, UK), anti-FN1 antibody (Abcam, ab2413, UK), anti-IL-1β antibody (Abcam, ab283818, UK), anti-TNFα antibody (Abcam, ab1793, UK), anti-β-catenin antibody (Abcam, ab6302, UK), anti-AXIN1 antibody (Abcam, ab133221, UK) and anti-AXIN2 antibody (Abcam, ab192230, UK)) was incubated at 1:200 for 2 h, followed by a secondary antibody (Goat Anti-Rabbit IgG H&L, Alexa Fluor 555, (Abcam, UK, at 1/200 dilution)) for 1 h at room temperature. The slides were sealed in a mounting medium containing 4’,6-diamidino-2-phenylindole (DAPI, Vector Laboratories, H1200, USA, dilution to 10 µg/ml) for further image acquisition. Images were captured using a microscope (Leica, M205FA, Wetzlar, Germany), and mean optical densities of contrast tissue sections were quantified using ImageJ.

Statistical analysis

All statistical analyses were performed using SPSS Statistics version 22.0 (IBM, Armonk, NY, USA). Quantitative data are presented as mean ± standard deviation (SD). Before between-group comparisons, data distribution was assessed using the Shapiro–Wilk test, and homogeneity of variance was evaluated using Levene’s test. For variables that satisfied the assumptions of normality and homogeneity of variance, differences between the severe Turner tooth group and the control group were analyzed using two-tailed independent-samples Student’s t tests. When homogeneity of variance was not met, Welch’s t test was used. Exact P values are reported to four decimal places, with P < 0.05 considered statistically significant.

Because this was an exploratory case-control histopathological study involving a relatively uncommon clinical sample, effect sizes and post hoc statistical power were additionally calculated for the main quantitative immunofluorescence outcomes. Effect sizes were expressed as Cohen’s d. Post hoc power analysis was performed using G*Power version 3.1 (Heinrich Heine University Düsseldorf, Düsseldorf, Germany), based on the observed effect size for each principal between-group comparison, assuming a two-tailed α level of 0.05. These additional analyses were included to provide a more comprehensive interpretation of the quantitative findings and to address the limitation of the relatively small sample size.

Results

Representative clinical presentation of a severe turner tooth

General data: the child, male, was 8 years old

Chief complaints and present medical history: He presented to the Department of Pediatric Stomatology with delayed eruption of permanent anterior teeth. The 61 tooth had a history of apical periodontitis before tooth loss. Past, personal and family history were unremarkable. Examination: (1) intraoral and maxillofacial examination revealed bilaterally symmetrical faces with normal opening, 21 tooth erupting buccally, red and swollen gingiva, and no abnormal secretions (Fig. 1A). (2) imaging examination: CBCT showed 21 dental dysplasia, root curvature and too short (Fig. 1B).

Fig. 1.

Fig. 1

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Clinical case of Turner tooth extraction. A: Frontal view of oral examination and maxillary and mandibular coincidence view of the patient. B: CBCT showed dysplasia and dilaceration of 21 tooth

Diagnosis: 21 Turner tooth.

Treatment options: extraction of 21 tooth.

Before treatment, the imaging data were repeatedly read, fully communicated with the patient ‘s guardian, informed the patient’ s guardian of the possible risks during tooth extraction, the patient ‘s guardian understood all risks and requested tooth extraction and received all treatment risks, and signed the parental informed consent form.

Histological features of pulp and periodontal tissues

As shown in Fig. 2, the results indicated that, compared to the control group, the Turner tooth pulp tissue exhibited a thinner layer of odontoblasts with fewer cellular components. Additionally, the dentin-pulp interface in Turner teeth was less smooth and continuous. In the apical pulp tissue, the arrangement of fibers was disorganized, and there was a reduced distribution of blood vessels, along with an increased cellular component. Furthermore, the periodontal tissue displayed a chaotic arrangement of fibers, and the thickness of the cementum layer was notably reduced (Fig. 2AB). The histopathological findings of Turner teeth reveal significant structural abnormalities compared to normal orthodontic teeth. The observed thinning of the odontoblast layer and reduced cellular components in the pulp tissue suggest impaired odontogenesis, which may contribute to the compromised dentin-pulp interface. The disorganized arrangement of fibers in the apical pulp and reduced vascular distribution may indicate disrupted blood supply and nutrient delivery, further affecting the vitality of the pulp tissue. Additionally, the chaotic fiber alignment and reduced cementum thickness in the periodontal tissue may compromise the overall stability and function of the tooth.

Fig. 2.

Fig. 2

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HE and masson staining results of pulp and periodontal tissue. A Hematoxylin and eosin staining. B Masson trichrome staining. Representative images show the mid-root pulp, apical pulp, and periodontal regions. Severe Turner teeth showed a thinner odontoblast layer, a less continuous dentin-pulp interface, disorganized apical fibers, irregular periodontal fiber arrangement, and a thinner cementum layer compared with control teeth. Turner group, n = 10; control group, n = 10

Expression of CD105, CD31, and βIII-tubulin in pulp tissue

As shown in Fig. 3, the results indicated that the expression of the stem cell marker CD105 was significantly lower in the pulp tissue of Turner teeth(P = 0.0021). Additionally, the vascular count, as indicated by CD31 staining, was markedly reduced compared to the control group (P = 0.0009). Furthermore, the expression of the nerve fiber marker βIII-tubulin was also found to be lower in Turner teeth, highlighting the impaired neurovascular development within the pulp tissue(P = 0.0052). The findings from this study highlight significant deficiencies in the pulp tissue of Turner teeth compared to normal teeth. The lower expression of the stem cell marker CD105 suggests a diminished regenerative capacity within the pulp, which may hinder the healing processes and overall vitality of the tooth. The significant reduction in vascular counts indicated by CD31 staining points to compromised blood supply, potentially leading to ischemia and further detriment to pulp health. Additionally, the decreased expression of the nerve fiber marker βIII-tubulin suggests impaired neurogenesis, which may affect the sensory functions of the tooth.

Fig. 3.

Fig. 3

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The expression of CD105, CD31, and βIII-tubulin in the dental pulp tissue. A-C Representative immunofluorescence images of CD105, CD31, and βIII-tubulin in control and Turner tooth pulp tissues. D-F Quantitative analysis of average fluorescence intensity. Data are presented as mean ± SD. Group comparisons were performed using two-tailed independent-samples t tests. Turner group, n = 10; control group, n = 10. Exact P values: CD105, P = 0.002; CD31, P < 0.001; βIII-tubulin, P = 0.005

Expression of DSPP and RUNX2 in pulp tissue

As shown in Fig. 4, the results revealed that the expression levels of both dentinogenesis markers, DSPP (P = 0.0232) and RUNX2 (P = 0.0288), were significantly lower in the pulp tissue of Turner teeth compared to the control group. This finding indicates a compromised odontogenic potential within the pulp of Turner teeth, suggesting impaired dentin formation and development. The significantly reduced expression of DSPP and RUNX2 in the pulp tissue of Turner teeth underscores the compromised odontogenic potential associated with this condition. DSPP is crucial for the regulation of dentin formation and mineralization. The lower levels of these markers suggest that the odontoblasts in Turner teeth may be less functional or fewer in number, which could impede normal dentinogenesis.

Fig. 4.

Fig. 4

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The expression of DSPP and RUNX2 in the dental pulp tissue. A, B Representative immunofluorescence images of DSPP and RUNX2 in control and Turner tooth pulp tissues. C, D Quantitative analysis of average fluorescence intensity. Data are presented as mean ± SD. Group comparisons were performed using two-tailed independent-samples t tests. Turner group, n = 10; control group, n = 10. Exact P values: DSPP, P = 0.023; RUNX2, P = 0.029

Expression of vimentin and fn1 in pulp tissue

Vimentin and FN1 positivity in pulp tissue serves as an important indicator of pulp development. As shown in Fig. 5, the results revealed that the expression levels of both Vimentin (P = 0.0007) and FN1 (P<0.0001) were significantly lower in the pulp tissue of Turner teeth compared to the control group. This finding suggests a compromised extracellular matrix composition and impaired vascularization potential in the pulp of Turner teeth, which may further contribute to their developmental anomalies. The significantly reduced expression of Vimentin and FN1 in the pulp tissue of Turner teeth highlights critical deficiencies in both the structural integrity and vascular development of the pulp. The diminished levels of Vimentin suggest that the mesenchymal cells within the pulp may be less effective in contributing to normal pulp development. FN1, as a key component of the extracellular matrix, plays a vital role in promoting cell adhesion, migration, and vascularization. The lower expression of FN1 in Turner teeth may impede the development of blood vessels within the pulp.

Fig. 5.

Fig. 5

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The expression of Vimentin and FN1 in the dental pulp tissue. A, B Representative immunofluorescence images of Vimentin and FN1 in control and Turner tooth pulp tissues. C, D Quantitative analysis of average fluorescence intensity. Data are presented as mean ± SD. Group comparisons were performed using two-tailed independent-samples t tests. Turner group, n = 10; control group, n = 10. Exact P values: Vimentin, P < 0.001; FN1, P < 0.001

Expression of IL-1β and TNF-α in pulp tissue

As shown in Fig. 6, the results revealed that the expression levels of both inflammatory factors, IL-1β (P = 0.0039) and TNF-α (P = 0.0011), were significantly higher in the pulp tissue of Turner teeth compared to the control group. This finding suggests that the pulp tissue of Turner teeth may be under persistent inflammatory stress, which could adversely affect its development and function. The significantly elevated expression of inflammatory factors IL-1β and TNF-α in the pulp tissue of Turner teeth suggests a persistent inflammatory state that may negatively impact pulp development. Chronic inflammation can disrupt normal cellular processes and lead to adverse effects on tissue regeneration and repair. The elevated levels of these inflammatory cytokines may contribute to a compromised microenvironment, which can hinder the differentiation and function of dental pulp cells.

Fig. 6.

Fig. 6

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The expression of IL-1β and TNF-α in the dental pulp tissue. A, B Representative immunofluorescence images of IL-1β and TNF-α in control and Turner tooth pulp tissues. C, D Quantitative analysis of average fluorescence intensity. Data are presented as mean ± SD. Group comparisons were performed using two-tailed independent-samples t tests. Turner group, n = 10; control group, n = 10. Exact P values: IL-1β, P = 0.004; TNF-α, P = 0.001

Expression of β-catenin, AXIN1, and AXIN2 in pulp tissue

Wnt/β-catenin signaling pathway is a key factor mediating pulp development. However, no research has yet addressed whether abnormal expression of this pathway is related to the developmental anomalies observed in Turner teeth. As shown in Fig. 7, the results revealed that the expression level of β-catenin (P = 0.0015) was significantly lower in the pulp tissue of Turner teeth, while the expression levels of AXIN1 (P = 0.0007) and AXIN2 (P = 0.0232) were significantly higher. This finding suggests an alteration in the Wnt/β-catenin signaling pathway in Turner teeth, which may contribute to their developmental abnormalities. The significantly lower expression of β-catenin, coupled with the higher levels of its negative regulators AXIN1 and AXIN2 in Turner teeth, indicates a disruption in the Wnt/β-catenin signaling pathway. The observed imbalance suggests that the signaling mechanism may be impaired in Turner teeth, potentially contributing to the developmental anomalies associated with this condition.

Fig. 7.

Fig. 7

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The expression of β-catenin, AXIN1 and AXIN2 in the dental pulp tissue. A-C Representative immunofluorescence images of β-catenin, AXIN1, and AXIN2 in control and Turner tooth pulp tissues. D-F Quantitative analysis of average fluorescence intensity. Data are presented as mean ± SD. Group comparisons were performed using two-tailed independent-samples t tests. Turner group, n = 10; control group, n = 10. Exact P values: β-catenin, P = 0.002; AXIN1, P < 0.001; AXIN2, P = 0.023

Discussion

The findings of this study support an association between severe Turner teeth and coordinated alterations in pulp tissue organization, inflammation-related markers, and developmental signaling-related proteins. Turner teeth often arise from chronic periapical inflammation of the associated primary teeth, which can disrupt normal odontogenesis [1]. The elevated levels of inflammatory markers observed in the pulp tissue suggest that prolonged inflammatory stress can adversely impact developmental processes, potentially leading to defects such as enamel hypoplasia and abnormal tooth morphology. This relationship underscores the importance of managing dental infections in primary teeth to mitigate potential long-term effects on the development of permanent successors. Preventive measures and timely interventions in pediatric dentistry could play a crucial role in reducing the incidence of such anomalies. Based on these findings, the null hypothesis was rejected.

Our results highlight the critical role of neurovascular development and stem cells in regulating pulp tissue formation. The lower expression of stem cell markers and neurogenic factors in the pulp of Turner teeth indicates a compromised capacity for regeneration and healing. Vascularization, as indicated by reduced blood vessel counts, is essential for supplying nutrients and oxygen, thereby supporting pulp vitality [1]. The interplay between neurovascular structures and stem cells is crucial for maintaining a healthy microenvironment in the pulp [4–7]. Disruptions in this delicate balance may lead to significant developmental issues, as seen in Turner teeth. Investigating the interactions between vascular and neural elements in the pulp could provide insights into how to promote better outcomes in affected teeth.

The reduced expression of DSPP and RUNX2 further suggests compromised odontogenic potential in Turner tooth pulp tissue. Turner teeth underscores the compromised odontogenic potential associated with this condition. DSPP is crucial for the regulation of dentin formation and mineralization, while RUNX2 plays a vital role in the differentiation of odontoblasts and the overall development of dental tissues [8–10]. The lower levels of these markers suggest that the odontoblasts in Turner teeth may be less functional or fewer in number, which could impede normal dentinogenesis.

Dental pulp stem cells play a pivotal role in modulating the extracellular matrix (ECM) composition and the inflammatory microenvironment during pulp development [11, 12]. Previous studies have indicated that Vimentin positivity in pulp tissue serves as an important indicator of pulp development [13], while extracellular matrix component FN1 plays a crucial role in promoting vascular development within the pulp [14]. The observed lower expression of ECM components like FN1 and markers such as Vimentin suggests that the structural integrity of the pulp is compromised in Turner teeth. Based on the observed reduction in CD31-positive vascular density alongside diminished FN1 expression in Turner teeth, these findings may align with our group’s established research on FN1-mediated vascular regulation. Previous work suggests that FN1 secreted by DPSCs could critically support angiogenesis through integrin signaling, potentially activating PI3K/AKT pathways to facilitate endothelial functions [14]. In Turner teeth, the attenuated FN1 expression might similarly impede vascular development by disrupting this signaling axis, though other contributing factors warrant consideration. The consistency across these observations suggests FN1 deficiency could compromise angiogenic competence in pathological pulp conditions, highlighting the FN1-integrin pathway as a potential therapeutic target for vascular restoration.

Additionally, pulp stem cells can influence the inflammatory response, as indicated by the elevated levels of pro-inflammatory cytokines such as IL-1β and TNF-α [15]. These cytokines can impair stem cell function and tissue regeneration, creating a cycle that perpetuates inflammation and hinders normal developmental processes [16–20]. Understanding the mechanisms by which pulp stem cells interact with the ECM and inflammatory mediators could inform therapeutic strategies aimed at restoring normal development in Turner teeth [21, 22].

The alterations in the Wnt/β-catenin signaling pathway observed in Turner teeth further underscore its importance in dental pulp development [23–30]. The lower expression of β-catenin, alongside higher levels of AXIN1 and AXIN2, indicates a disruption in this signaling cascade, which is crucial for cellular proliferation and differentiation in the pulp. Moreover, inflammatory factors such as IL-1β and TNF-α may negatively influence Wnt/β-catenin signaling, leading to impaired odontogenesis [31–33]. Understanding how inflammation impacts this pathway is essential for identifying therapeutic targets that could enhance pulp development and regeneration in conditions like Turner teeth. By elucidating the complex interactions between inflammatory responses and key signaling pathways, future research can pave the way for innovative treatments that promote dental tissue repair and regeneration, ultimately improving clinical outcomes for patients with developmental dental anomalies.

This study has several strengths. First, it analyzed clinically obtained human severe Turner teeth, which are relatively uncommon samples. Second, it combined conventional histology with immunofluorescence-based molecular assessment. Third, it examined multiple biological domains relevant to pulp status, including tissue structure, stemness-related markers, vascular and neural markers, dentinogenesis-related markers, extracellular matrix-associated markers, inflammatory markers, and Wnt/β-catenin-related proteins. From a clinical perspective, the present findings suggest that severe Turner teeth may differ from normal teeth not only at the level of crown morphology but also in the biological condition of the pulp tissue. This may be relevant to clinical decision-making related to pulp preservation, restorative planning, endodontic risk assessment, and long-term follow-up of affected teeth.

Several limitations should be acknowledged. The sample size was small, reflecting the rarity of extracted severe Turner teeth, and this limits statistical precision and generalizability. Although the sample size was limited by the rarity of extracted severe Turner teeth, effect size estimation and post hoc power analysis were performed to provide additional statistical context for the principal quantitative findings. Nevertheless, larger multicenter studies are still required to confirm external generalizability. Therefore, the present study should be regarded as exploratory/pilot in nature. In addition, the molecular analyses were based on immunofluorescence only and were not complemented by functional assays. Periodontal tissue was assessed morphologically but not investigated by molecular staining. Furthermore, the cross-sectional design precludes causal inference.

This study expands the currently limited tissue-level evidence on severe Turner teeth by providing a comparative histopathological analysis of pulp and periodontal alterations. While previous research has predominantly focused on clinical phenotypes and etiological triggers, the present findings indicate coordinated changes in pulp tissue architecture and molecular marker expression in severe Turner teeth. Overall, the study objective was achieved by identifying histopathological and molecular differences between severe Turner teeth and normal teeth, primarily in pulp tissue and descriptively in periodontal tissue.

Conclusion

In this histopathological case-control study, severe Turner teeth showed coordinated alterations in pulp tissue architecture, marker expression, and periodontal morphology when compared with normal teeth. These findings indicate that severe Turner teeth are associated with an altered pulp microenvironment and provide tissue-level evidence that may support future mechanistic investigations and clinical assessment of affected teeth.

Authors’ contributions

Tiankai Di and Yuhan Liu performed the experiment and contributed to the conception of the study, and they are the co-first authors; Jinlong Xu, Xiaodong Zhang and Jun Li contributed significantly to analysis and manuscript preparation. Lulu Wang and Yujiang Chen revised the manuscript and approved the final version to be published, and they are the co-corresponding authors. All authors read and approved the final manuscript.

Funding

This current study was funded by the Natural Science Basic Research Program of Shaanxi Province (Code No.2024JC-YBQN-0966, 2025JC-QYXQ-049); New Technology Project of the Third Affiliated Hospital of Air Force Military Medical University (LX2025-305).

Data availability

The quantitative data supporting the findings of this study, including processed summary data and representative histological images, are included in the article. Additional de-identified data may be made available by the corresponding authors upon reasonable request and in accordance with institutional ethical regulations.

Declarations

Ethics approval and consent to participate

The experimental protocol was approved by the Institutional Review Board (IRB) of FMMU, School of Stomatology (IRB-REV-2018016; approved on March 6, 2018), and an informed consent form agreeing to the contribution of their teeth for research purposes was signed by all donors. Not applicable.

Consent for Publication

Not applicable.

Competing Interests

The authors declare no competing interests.

Footnotes

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Tiankai Di and Yuhan Liu Co-first authors.

Contributor Information

Lulu Wang, Email: wanglulufmmu@hotmail.com.

Yujiang Chen, Email: chenyj@fmmu.edu.cn.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The quantitative data supporting the findings of this study, including processed summary data and representative histological images, are included in the article. Additional de-identified data may be made available by the corresponding authors upon reasonable request and in accordance with institutional ethical regulations.

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