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Background and Aims Skeletal age estimation is as a transformative process, where the descriptive skeletal age indicator is translated into a chronological age. One of the limitations of the numerous methods used for examining age status is that as soon as the development sites have completed growth, which is relatively early, accurate age determination becomes challenging and more difficult. A synchondrosis is a joint cartilaginous in nature between two immovable bones that serves to allow growth until the hyaline cartilage is converted into bone before or during early adult life. The age of spheno‐occipital synchondrosis (SOS) ossification is relatively late, compared with other cranial base synchondroses. Hence, knowing the accurate age of SOS closure can have an important impact in the medical, forensic, and anthropological fields. The aim of our study is to evaluate the use of the SOS as a means of skeletal age estimation in Cameroon. Methods We carried out a cross‐sectional analytical study using CT scans. Our study period included patient radiological files from January 2022 to April 2024 at the radiological unit of the Yaoundé University Teaching Hospital (YUTH) and two radiological centers in Yaoundé. We used a five‐stage SOS closure classification going from Stage 1 where the SOS is completely open to Stage 5 where there is complete fusion of SOS and the scar obliterated. Results We retained 312 participants, 171 (54.8%) of which were males and 141 (45.2%) were females with a sex ratio of 1.2. The mean age in our study was 17.4 ± 11.9 years. The first decade was the most represented with 34.6%. The mean age of closure for Stage 1 was 4.8 ± 3.3 years and for Stage 5 was 28.6 ± 7.8 years and the differences were statistically significant. Comparing the SOS closure with sex, we observed no clear difference between males and females, with their mean ages also being similar. In Stage 1 the mean age for males was 5.1 years and the mean age for females was 4.1 years. Conclusion SOS closure in our study was as from the mean age of 23.5 years. SOS closure is linked to age in our study with a progressive increase in closure stage with age. SOS Stage 1 mean age of closure was at 4.8 years followed by 12.9 years then 19.9 years, 23.5 and finally 28.6 years at Stage 5, respectively. With respect to sex, there was no difference in SOS closure between males and females in all stages but Stage 1 in our study.

Development of the craniofacial skeleton requires interactions between progenitor cells and the collagen-rich extracellular matrix (ECM). The mediators of these interactions are not well-defined. Mutations in the discoidin domain receptor 2 gene ( DDR2 ), which encodes a non-integrin collagen receptor, are associated with human craniofacial abnormalities, such as midface hypoplasia and open fontanels. However, the exact role of this gene in craniofacial morphogenesis is not known. As will be shown, Ddr2 -deficient mice exhibit defects in craniofacial bones including impaired calvarial growth and frontal suture formation, cranial base hypoplasia due to aberrant chondrogenesis and delayed ossification at growth plate synchondroses. These defects were associated with abnormal collagen fibril organization, chondrocyte proliferation and polarization. As established by localization and lineage-tracing studies, Ddr2 is expressed in progenitor cell-enriched craniofacial regions including sutures and synchondrosis resting zone cartilage, overlapping with GLI1 + cells, and contributing to chondrogenic and osteogenic lineages during skull growth. Tissue-specific knockouts further established the requirement for Ddr2 in GLI +skeletal progenitors and chondrocytes. These studies establish a cellular basis for regulation of craniofacial morphogenesis by this understudied collagen receptor and suggest that DDR2 is necessary for proper collagen organization, chondrocyte proliferation, and orientation. We each have unique facial features that are key to our identities. These features are inherited, but the mechanisms are poorly understood. People with the genetic disease spondylo-meta-epiphyseal dysplasia, or SMED, have characteristic facial and skull abnormalities including a flattened face and shortened skull. SMED is associated with mutations that inactivate the gene encoding a protein called discoidin domain receptor 2 (DDR2), which is a receptor for collagen. Collagen is the major structural protein in the human body, supporting the structure of cells and tissues. It also controls cell behaviors including growth, migration and differentiation, and it helps form tissues such as cartilage or bone. At least some of the effects of collagen on cells depend on its interaction with DDR2. Since the facial and skull abnormalities in mice with mutations that stop DDR2 from working correctly resemble those of SMED patients, these mice can be used to understand the cellular basis for this disease, as well as the role of DDR2 in the embryonic development of the face and skull. Therefore, Mohamed et al. set out to understand how loss of DDR2 causes the characteristic facial and skull defects associated with SMED. Mohamed et al. used mice that had been genetically modified so that DDR2 could be inactivated in skeletal progenitor cells, cartilage cells and bone cells (osteoblasts). Examining these mice, they found that the shortened skulls and flat face characteristic of mice lacking DDR2 are due to bones at the skull base failing to elongate correctly due to defects in the growth centers that depend on cartilage. Mohamed et al. also discovered that the cells that normally produce DDR2 are the progenitors of cartilage and bone-forming cells, which partly explains why lacking this protein leads to issues in growth of these tissues. In addition to shedding light on the causes of SMED, Mohamed et al.’s results also provide general insights into the mechanisms controlling the formation of facial and skull bones that depend on interactions between cells and collagen. This information may help explain how other abnormalities in the face and skull emerge, and provide a basis for how the shape of the skull has changed during human evolution. In the future, it may be possible to manipulate the activity of DDR2 to correct skull defects.

The synchondroses formed via endochondral ossification in the cranial base are an important growth center for the neurocranium. Abnormalities in the synchondroses affect cranial base elongation and the development of adjacent regions, including the craniofacial bones. In the central region of the cranial base, there are two synchondroses present—the intersphenoid synchondrosis and the spheno-occipital synchondrosis. These synchondroses consist of mirror image bipolar growth plates. The cross-talk of several signaling pathways, including the parathyroid hormone-like hormone (PTHLH)/parathyroid hormone-related protein (PTHrP), Indian hedgehog (Ihh), Wnt/β-catenin, and fibroblast growth factor (FGF) pathways, as well as regulation by cilium assembly and the transcription factors encoded by the RUNX2 , SIX1 , SIX2 , SIX4 , and TBX1 genes, play critical roles in synchondrosis development. Deletions or activation of these gene products in mice causes the abnormal ossification of cranial synchondrosis and skeletal elements. Gene disruption leads to both similar and markedly different abnormalities in the development of intersphenoid synchondrosis and spheno-occipital synchondrosis, as well as in the phenotypes of synchondroses and skeletal bones. This paper reviews the development of cranial synchondroses, along with its regulation by the signaling pathways and transcription factors, highlighting the differences between intersphenoid synchondrosis and spheno-occipital synchondrosis.

The cranial base is formed by endochondral ossification and functions as a driver of anteroposterior cranial elongation and overall craniofacial growth. The cranial base contains the synchondroses that are composed of opposite-facing layers of resting, proliferating and hypertrophic chondrocytes with unique developmental origins, both in the neural crest and mesoderm. In humans, premature ossification of the synchondroses causes midfacial hypoplasia, which commonly presents in patients with syndromic craniosynostoses and skeletal Class III malocclusion. Major signaling pathways and transcription factors that regulate the long bone growth plate—PTHrP–Ihh, FGF, Wnt, BMP signaling and Runx2—are also involved in the cranial base synchondrosis. Here, we provide an updated overview of the cranial base synchondrosis and the cell population within, as well as its molecular regulation, and further discuss future research opportunities to understand the unique function of this craniofacial skeletal structure.

Objective To investigate the anatomical indexes and anatomical positional indexes of the atlantoaxial synchondroses in normal Chinese Han children aged 1–6 years, and to analyze the changing law of the atlantoaxial cartilage union with the growth and development of age and its influence on the atlantoaxial ossification in children. Methods A retrospective collection of CT imaging of 160 cases of normal cervical spine in children aged 1 to 6 years old was conducted. The cases were divided into six age groups, with each group representing a one-year age range. Measure the morphological anatomical indicators and anatomical positional indicators of the atlantoaxial synchondroses. Record and statistically analyze the measurements of each indicator. Results Measurements were taken on various parameters of the atlantoaxial synchondroses. TD, SD, height, area, and perimeter all gradually decreased among the groups. Distance between bilateral atlantal anterolateral synchondroses increased gradually from Group A to Group F, while the angle formed along the long axis in the cross-section showed a decreasing trend. Distance between the axoid dentolateral synchondroses and between the neurocentral synchondroses increased gradually from Group A to Group F, with the angle value in the cross-section showing a gradual decrease, and distance from the odontoid apex increasing from Group A to Group F. Conclusions The atlantoaxial synchondroses gradually decrease in size with age, and ossification levels increase with age, with faster ossification occurring during a 1–2 years-old period. The anterolateral synchondroses, dentolateral synchondroses, and neurocentral synchondroses all gradually ossify towards the lateral direction with increasing age.

Purpose The spheno-occipital synchondrosis (SOS) is an important site of endochondral ossification in the cranial base that closes prematurely in Apert, Crouzon, and Pfeiffer syndromes, which contributes to varying degrees of midface hypoplasia. The facial dysmorphology of Muenke syndrome, in contrast, is less severe with low rates of midface hypoplasia. We thus evaluated the timing of SOS fusion and cephalometric landmarks in patients with Muenke syndrome compared to normal controls. Methods Patients with Muenke syndrome who had at least one fine-cut head computed tomography scan performed from 2000 to 2020 were retrospectively reviewed. A case–control study was performed of patient scans and age- and sex-matched control scans. SOS fusion status was evaluated as open, partially closed, or closed. Results We included 28 patients and compared 77 patient scans with 77 control scans. Kaplan–Meier analysis demonstrated an insignificantly earlier timeline of SOS fusion in Muenke syndrome ( p  = 0.300). Mean sella-orbitale (SO) distance was shorter (44.0 ± 6.6 vs. 47.7 ± 6.7 mm, p  < 0.001) and mean sella-nasion-Frankfort horizontal (SN-FH) angle was greater (12.1° ± 3.8° vs. 10.1° ± 3.2°, p  < 0.001) in the Muenke group, whereas mean sella-nasion-A point (SNA) angle was similar and normal (81.1° ± 5.7° vs. 81.4° ± 4.7°, p  = 0.762). Conclusion Muenke syndrome is characterized by mild and often absent midfacial hypoplasia, with the exception of slight retropositioning of the infraorbital rim. Interestingly, SOS fusion patterns in these patients are not significantly different from age- and sex-matched controls despite an increased odds of fusion. It is possible that differences in timing of SOS fusion may manifest phenotypically at the infraorbital rim rather than at the maxilla.

Background The neurocentral synchondrosis (NCS) may play an essential role in the formation and progression of scoliosis in pediatric populations. Previous experimental studies have primarily focused on modulating NCS growth through epiphysiodesis with unilateral pedicle screw fixation, which is associated with significant trauma. However, no study has explored the effect of minimally invasive intervention on the NCS to date. Methods Fifteen 6-week-old piglets were randomly assigned to three groups, each containing five animals. In the NCS group, the piglets were subjected to microwave ablation (MWA) of the NCS on the left side under CT guidance. In the sham group, the ipsilateral NCS was punctured under CT guidance, but no particular intervention was carried out, and the puncture needles were removed. In the control group, no intervention was performed. CT scans of the spinal alignment were obtained and analyzed every month after the respective interventions. Results No scoliotic curvature developed in the sham and control groups. A structured scoliosis was observed in all five animals of the NCS group at the first month following the intervention, with increasing deformity every month. All curves were located at the operated levels, with the convexity toward the unablated side. The coronal angle was 13.46 ± 1.62°, 15.49 ± 1.51°, and 19.63 ± 3.22° in the NCS group at the first, second, and third months following the operation, respectively. The height of the vertebral body and the pedicle length on the ablated side in the NCS group decreased compared to those of the other two groups and the contralateral side, showing significant differences. In addition, the spinal canal area in the NCS group was significantly smaller than that of the sham and control groups. Mild vertebral rotation was observed in the NCS group. Histological analysis revealed unilateral chondrocyte necrosis and fibrotic remodeling of NCS at the ablated area. Conclusion Unilateral ablation of the NCS under CT guidance is a minimally invasive procedure that can effectively modulate asymmetric growth of the spine in piglets, leading to scoliosis with convexity toward the unablated side. The ablation of the NCS can adversely affect the growth of the vertebral height, pedicle length, and spinal canal in piglets. Key points Growth imbalance contributes to early scoliosis development, and the neurocentral synchondrosis (NCS) is a key posterior growth center that may influence three-dimensional deformity formation. CT-guided microwave ablation of the unilateral NCS reproducibly induces asymmetric posterior spinal growth with segmental scoliosis and mild rotation in immature piglets. This minimally invasive, non-instrumented large-animal model provides a useful platform to investigate NCS-related growth mechanisms and the early pathogenesis of scoliosis.

Spheno-occipital synchondrosis (SOS) is an important growth area in the craniofacial skeleton. It has been explored in research relate to age assessment and forensic medicine due to its closure in the postnatal period. The aim of this study is to evaluate the growth and development period of SOS on cone-beam computed tomography (CBCT) images with pseudo-color imaging depend on fusion stages. In this cross-sectional retrospective study, 280 CBCT sagittal sections’ images (163 women, 117 men) were used to evaluate the SOS fusion stages by dividing them into five categories. ImageJ version 1.3 software was used to analyze. SOS stages and histogram analyzes were evaluated. The significance level was set at p  = 0.05. In the evaluation of synchondrosis stages according to gender and age, the incidence of stages 4 and 5 in individuals aged 15–25 years was statistically significantly higher ( p  < 0.01) compared to stages 1 and 2 in individuals aged 5–14 years. The mean minimum, maximum and open histogram values of synchondroses in the same age group were also statistically significantly higher ( p  < 0.05). In the assessment of synchondrosis maturation using three-way ROC analysis, histogram analyses indicated Stage 1 for data below 68.33, Stage 3 for data above 104.5, and Stage 2 for values in between. ImageJ histogram analysis can numerically reveal radiographic differences between SOS fusion stages and can perform staging on pseudo-colored cross-sectional CBCT images. Different image processing software can reveal differences between phases through false coloring.

The cranial base synchondrosis (CBS) is a critical growth center in the craniofacial region, and its abnormal development can lead to various craniofacial deformities. In a hypoxic microenvironment, hypoxia-inducible factor-1α (HIF-1α) is a crucial regulatory factor for cellular adaptation to low oxygen conditions. However, the role of HIF-1α in the CBS and its mechanisms regulating the function of chondrocytes remain unclear. This study aims to investigate the expression characteristics of HIF-1α in the CBS and its potential mechanisms in regulating mouse spheno-occipital synchondrosis (SOS) chondrocytes (SOSCs). Histological and immunohistochemical staining were utilized to observe the growth pattern of the SOS and the expression characteristics of HIF-1α in the SOS of 1–8 week-old mice. Chemical hypoxia simulation and siRNA technology modulated HIF-1α expression, and potential signaling pathways were detected through transcriptome sequencing. Results indicate that HIF-1α is expressed in all layers of the mouse SOS and is closely associated with cell proliferation and differentiation. In vitro studies demonstrate that enhancing HIF-1α expression enhances cell proliferation and matrix synthesis capacity, improves cell apoptosis, and enhances the expression of chondrogenic markers SOX9 and Collagen II while diminishing osteogenic marker RUNX2 expression. We found that with the upregulation of HIF-1α expression, the PI3K/Akt signaling pathway is activated. In conclusion, our study revealed that HIF-1α regulates the proliferation and differentiation of SOSCs by activating the PI3K/Akt signaling pathway.

Talocalcaneal coalition is a frequent cause of painful rigid flatfoot in adolescents and young adults, resulting from congenital failure of segmentation with fibrous, cartilaginous, or osseous bridging of the subtalar joint. Clinical presentation typically coincides with skeletal maturation and includes hindfoot pain, recurrent ankle sprains, progressive stiffness, and characteristic planovalgus deformity. Although prevalence is likely underestimated, advances in imaging have improved recognition and characterization. Diagnosis relies on the integration of clinical findings with imaging, where computed tomography (CT) remains the reference standard, while magnetic resonance imaging (MRI) enables accurate detection of both osseous and non-osseous coalitions and associated soft-tissue changes. This narrative review aims to provide a comprehensive and updated synthesis of current concepts in talocalcaneal coalition, with specific focus on its clinical implications and contemporary management strategies. We critically analyze diagnostic pathways, including emerging modalities such as weight-bearing CT, and discuss evidence-based indications for conservative treatment, coalition resection, and arthrodesis. Particular attention is devoted to patient selection, prognostic factors, and evolving minimally invasive techniques. Current limitations and areas of controversy are highlighted, emphasizing the need for standardized imaging criteria and optimized treatment algorithms to improve long-term functional outcomes.