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The representative stages of early tooth development in the mouse embryo. ( A , C , E , G ) molar tooth germ stages; ( B , D , F , H ) incisor tooth germ stages. ( A and B ) Dental lamina stage (E11.5): the oral epithelium thickens locally to form the molar and incisor tooth germs. ( C and D ) Early bud stage (E12.5): the epithelial thickening invaginates into the subjacent mesenchyme which condenses around the epithelial bud. ( E and F ) Late bud stage (E13.5): increased proliferation of the dental epithelium causes it to invaginate further into the dental mesenchyme; ( G and H ) Cap stage (E14.5): differential proliferation within the dental epithelium causes a population of the dental mesenchyme, the dental papilla, to be surrounded by the convoluting dental epithelium. Abbreviations: DE, dental epithelium; DM, dental mesenchyme; DP, dental papilla; EK, enamel knot.
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Vertebrate Msx genes are unlinked, homeobox-containing genes that bear homology to the Drosophila muscle segment homeobox gene. These genes are expressed at multiple sites of tissue-tissue interactions during vertebrate embryonic development. Inductive interactions mediated by the Msx genes are essential for normal craniofacial, limb and ectodermal...
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... craniofacial organs form from multiple embryonic tissues including the cranial neural crest derived cells, prechordal mesoderm, and the embryonic craniofacial ectoderm. Normal craniofacial morphology develops as a consequence of complex interactions between these embryonic tissues, and requires precise regulation of cell movement, growth, patterning, and differentiation of craniofacial tissues. Genetic studies have revealed the involvement of numerous genes in these processes, including genes encoding a variety of transcription factors, growth factors and receptors[1]. Mutations in genes that influence any of these processes would cause craniofacial abnormalities, such as facial clefting and craniosynostosis, which are among the most frequent congenital birth defects in humans[2]. Among the critical factors involved in craniofacial development are members of the Msx homeobox gene family. The vertebrate Msx genes were initially cloned from mice and identified as homologous to the Drosophila muscle segment homeobox gene ( msh )[3, 4]. Subsequently, Msx genes have been isolated from a variety of orga- nisms, including ascidians[5, 6], sea urchin[7], zebrafish [5, 8], frogs[9], birds[10-12], and humans[13]. The mammalian Msx gene family consists of 3 physically unlinked members, named Msx1 , Msx2 , and Msx3 [14, 15]. Msx3 is only expressed in the dorsal neural tube, in a pattern resembling that of the prototypical Drosophila msh gene[16, 17]. However, in developing vertebrate embryos, Msx1 and Msx2 are widely expressed in many organs; particularly at the sites where epithelial- mesenchymal interactions take place[15]. Most notably, Msx1 and Msx2 are strongly expressed in the developing craniofacial regions in an overlapping manner to some extent, indicating a role for Msx genes in craniofacial development[18-21]. During embryonic development, the face and neck are derived from swellings or buds of embryonic tissue, the branchial arches that originate bilaterally on the head. The neural crest cells generate most of the skeletal and connective tissue structures of the craniofacial region, while the mesoderm forms the musculature and endothelial lining of arteries of the future face and neck. The establishment of pattern in the craniofacial region is partly determined by the axial origin of the neural crest Msx genes and craniofacial develpoment cells within each arch and partly by regional epithelial- mesenchymal interactions[22, 23]. In the mouse embryo, cranial neural crest cells originate from the posterior midbrain-hindbrain regions and migrate ventrolaterally into the branchial arches[24-28]. Within the branchial arches, the different populations of crest cells do not intermingle, but instead maintain the positional cues acquired by their rostral-caudal origins in the brain. This segregation of crest cell populations is established early in organogenesis by the apoptotic elimination of crest cells from specific levels of the hindbrain, giving rise to three distinct streams of migratory crest cells. Although this patterning of crest cells depends upon their rostral- caudal origin, this pattern does show some level of plasticity[29-31]. For example, the knockout of Hoxa-2 in mice caused the second arch to produce skeletal elements normally found in the first arch. This result suggests that the Hox genes can specify pattern in arches caudal to the first arch, which does not express this class of genes[32]. Further patterning of the crest cells within the arches involves a reciprocal series of epithelial- mesenchymal interactions mediated by several growth factor signaling pathways[33-38]. The mammalian face develops from the coordinated growth and differentiation of five facial primordia, the single medial frontonasal prominence, the paired maxillary prominences, and paired mandibular prominences, which are located around the primitive mouth or stomodeum, as illustrated in Fig 1a and 1b. As development proceeds in the frontonasal prominence, localized thickenings of the surface ectoderm called nasal placodes develop. These placodes invaginate, while their margins thicken, to form the nasal pits and the lateral and medial nasal prominences. The maxillary prominences of the first branchial arch grow toward the future midline of the face. They fuse with the lateral nasal prominence on each side, then fuse with the medial nasal prominences, and finally with the intermaxillary segment of the frontonasal process to form the upper jaw and lip. In a similar way, the paired mandibular primordia fuse along their medial edge to form the lower jaw and lip. The frontonasal prominence forms the forehead and nose. Fusion of these approaching primordia results in the formation of a bilateral epithelial seam, which is later replaced by connective tissue[39-41] giving rise to a confluent lip. Clefts of the upper lip occur as a result of the failure of the maxillary prominence to merge with the medial nasal prominences on one side (producing a unilateral cleft) or on both sides (producing bilateral clefts). Failure of fusion of the paired mandibular prominences occurs far less frequently and results in clefts of the lower lip and jaw[42]. Cell research, 13(6), Dec, 2003 Craniofacial morphogenesis continues with the outgrowth and fusion of tissues that form the palate or the roof of the mouth. The palate forms from two primordia, the primary palate and the secondary palate. A single, median, wedge-shaped mass of mesenchyme extending internally from the frontonasal prominence forms the primary palate. The secondary palate develops bilaterally as two vertical projections, the palatal shelves, from the internal surfaces of the maxillary prominences (Fig 2). As morphogenesis proceeds, the shelves become oriented horizontally allowing them to approach each other and fuse medially. Failure of the palatal shelves to fuse leads to a cleft palate. A number of human congenital syndromes such as Treacher Collins Syndrome and Pierre Robin Syndrome have accompanying craniofacial abnormalities, which include a cleft palate[43]. Misre- gulation of the timing, rate, or extent of outgrowth of the palatal shelves results in clefts of the palate[44, 45]. Failure of fusion of the palatal shelves often, though not always, occurs in conjunction with cleft lip[46]. Another important morphogenetic event in the facial tissues is odontogenesis and this phase of craniofacial morphogenesis has been extensively studied. Tooth formation is regulated by inductive tissue interactions between the oral epithelium and the subjacent mesenchyme of the first arch. The four histologically distinct stages of tooth development are: 1) the dental lamina, 2) the bud, 3) the cap, and 4) the bell stage (Fig 3)[47]. In the mouse, tooth initiation becomes morphologically distinguishable at E11.5 by the thickening of the dental epithelium to form the dental lamina at the prospective sites of tooth formation. The cells of the dental lamina proliferate and on E12.5, start to invaginate into the underlying mesenchyme. At the bud stage, the mesenchyme proliferates and condenses around the invaginating epithelial bud. As a result of differential proliferation, the dental epithelium next convolutes around the condensed mesenchyme (now referred to as the dental papilla) in the cap (E14.5) and bell stages (E16.5). E14. 5 marks the onset of the definitive stages of tooth morphogenesis. In the cap and bell stages, transient signaling centers called primary and secondary enamel knots develop in the epithelium. They serve as organizing centers of tooth morphogenesis and cusp formation. In the final steps of odontogenesis, enamel-secreting ameloblasts and dentin-secreting odontoblasts differentiate from the dental epithelium and mesenchyme, respectively. Thus, an intricate set of epithelialmesenchy- Sylvia ALAPPAT et al mal interactions generates the species-specific pattern of odontogenesis. Another craniofacial structure pertinent to our discussion on Msx genes is the skull. The skull (Fig 4) is a composite of multiple bones that are organized primarily into the neurocranium which includes the cranial vault and the viscerocranium that comprise the facial bones as well as the palatal, pharyngeal, temporal and auditory bones. The neurocranium whose function is to protect the brain and the sense organs derives from mesenchyme of both neural crest and mesodermal origin. The ...
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... The copyright holder for this preprint this version posted March 13, 2024. ; https://doi.org/10.1101/2024.03.08.584153 doi: bioRxiv preprint the cells of the dental lamina proliferate at E12.5, leading to a dramatic increase in WNT signaling activity [95]. ...
Nearby cells within tissues communicate through ligand-receptor signaling interactions. Emerging spatial transcriptomic technologies provide a tremendous opportunity to systematically detect ligand-receptor signaling, but no method operates at cellular resolution in the spatial context. We developed CytoSignal to infer the locations and dynamics of cell-cell communication at cellular resolution from spatial transcriptomic data. CytoSignal is based on the simple insight that signaling is a protein-protein interaction that occurs at a specific tissue location when ligand and receptor are expressed in close spatial proximity. Our cellular-resolution, spatially-resolved signaling scores allow several novel types of analyses: we identify spatial gradients in signaling strength; separately quantify the locations of contact-dependent and diffusible interactions; and detect signaling-associated differentially expressed genes. Additionally, we can predict the temporal dynamics of a signaling interaction at each spatial location. CytoSignal is compatible with nearly every kind of spatial transcriptomic technology including FISH-based protocols and spot-based protocols without deconvolution. We experimentally validate our results in situ by proximity ligation assay, confirming that CytoSignal scores closely match the tissue locations of ligand-receptor protein-protein interactions. Our work addresses the field's current need for a robust and scalable tool to detect cell-cell signaling interactions and their dynamics at cellular resolution from spatial transcriptomic data.
... Since the bone morphology was severely affected, we investigated whether the mutant DVL1 viruses initiates crosstalk with the BMP pathway. We specifically measured the effects on gBMP2 which promotes chondrogenesis in the micromass culture system (Fischer et al., 2002) and gMSX1, a homeobox gene expressed abundantly during craniofacial development (Alappat et al., 2003). Interestingly, only hDVL1 1519* upregulated gBMP2 and gMSX1 compared to wt hDVL1 ( ...
Robinow Syndrome (RS) is a rare disease characterized by craniofacial malformations and limb shortening linked with mutations in seven WNT pathway genes. Our objective was to investigate the functional effects of frameshift mutations the intracellular adaptor protein, Dishevelled ( DVL1 ; c.1519 Δ T , p.Trp507Glyfs*142) on chicken craniofacial development. Misexpression of wt (wt) or mutant h DVL1 variants in vivo caused upper beak shortening (wt DVL1 n=8/14; DVL1 ¹⁵¹⁹ Δ T 12/13). At early stages of development, the DVL1 ¹⁵¹⁹ Δ T inhibited frontonasal mass narrowing, chondrogenesis, and proliferation. To test whether the phenotypes were caused due to the abnormal C-terminal peptide in DVL1 ¹⁵¹⁹ Δ T , we designed two additional constructs. The DVL1 1519* (DVL1 507* ) retains first 30 amino acids of the C-terminus while DVL1 1431* (DVL1 477* ) removes the entire C-terminus. DVL1 1519* injected embryos had normal beaks while DVL1 1431* caused high mortality and the phenotypes were like the DVL1 ¹⁵¹⁹ Δ T . In frontonasal micromass cultures, both DVL1 ¹⁵¹⁹ Δ T and DVL1 1431* inhibited skeletogenesis while the DVL1 1519* resembled wt DVL1 and GFP cultures. In luciferase assays DVL1 ¹⁵¹⁹ Δ T , DVL1 1519* and DVL1 1431* weakly activated the WNT canonical and non-canonical JNK-PCP pathways compared to wt DVL1 . Furthermore, we observed that variant DVL1 507*fs is stalled in the nucleus similar to hDVL1 477* , possibly due to the abnormal C-terminus interfering with the nuclear export sequence. wtDVL1 and DVL1 507* were distributed in nucleus and the cytoplasm. Our RS- DVL1 1519ΔT avian model recapitulates the broad face and jaw hypoplasia and demonstrates defects in both branches of WNT signaling. This is the first study to clarify the role of abnormal C-terminus in ADRS and to recognize the importance of an uncharacterized C-terminal sequence.
Summary Statement
Functional and biochemical studies on chicken embryos with the Robinow syndrome (RS) DVL1 variant demonstrate defects in skeletogenesis and both branches of WNT signaling. This is the first study to establish a link between the RS facial defects and the mutated C-terminal sequence. We identified first 30 amino acids of the DVL1 C-terminus are sufficient for normal development.
... A total of 453 and 238 genes were upor downregulated in 1540C compared to wild-type mice [|Fc| ≥ 1.5, false discovery rate (FDR) < 0.05, Supplementary Table S4]. We found that DEGs included Msx1, Dlx1 and Dlx2, which were known to be essential for skeletal morphology (Alappat et al., 2003;Levi et al., 2022). Notably, several histone H4 cluster genes, such as H4c2, H4c6 and H4c14 were upregulated in 1540C mice, suggesting that the arginine to cysteine substitution of Gli3 commonly affects ...
Changes in genomic structures underlie phenotypic diversification in organisms. Amino acid-changing mutations affect pleiotropic functions of proteins, although little is known about how mutated proteins are adapted in existing developmental programs. Here we investigate the biological effects of a variant of the GLI3 transcription factor (GLI3R1537C) carried in Neanderthals and Denisovans, which are extinct hominins close to modern humans. R1537C does not compromise protein stability or GLI3 activator-dependent transcriptional activities. In contrast, R1537C affects the regulation of downstream target genes associated with developmental processes. Furthermore, genome-edited mice carrying the Neanderthal/Denisovan GLI3 mutation exhibited various alterations in skeletal morphology. Our data suggest that an extinct hominin-type GLI3 contributes to species-specific anatomical variations, which were tolerated by relaxed constraint in developmental programs during human evolution.
... Dental mesenchymal cells and dental epithelial cells are essential cell population for tooth development (Lumsden 1988). Early tooth morphogenesis undergoes sequential histological changes defined as bud, cap, and bell stages (Alappat et al., 2003). At E12.5, the dental epithelium rapidly invaginates into the underlying mesenchyme to form the epithelial tooth bud. ...
Histone lactylation on its lysine (K) residues has been reported to have indispensable roles in lung fibrosis, embryogenesis, neural development, inflammation, and tumors. However, little is known about the lactylation activity towards histone lysine residue during tooth development. We investigated the dynamic patterns of lactate-derived histone lysine lactylation (Kla) using a pan-Kla antibody during murine tooth development, including lower first molar and lower incisor. The results showed that pan-Kla exhibited temporo-spatial patterns in both dental epithelium and mesenchyme cells during development. Notably, pan-Kla was identified in primary enamel knot (PEK), stratum intermedium (SI), stellate reticulum (SR), dental follicle cells, odontoblasts, ameloblasts, proliferating cells in dental mesenchyme, as well as osteoblasts around the tooth germ. More importantly, pan-Kla was also identified to be co-localized with neurofilament during tooth development, suggesting histone lysine lactylation may be involved in neural invasion during tooth development. These findings suggest that histone lysine lactylation may play important roles in regulating tooth development.
... For instance, the jaw extension displays strong expression of msx1, msx2 and msx3, which are involved in dentary development in other fish. Specifically, msx1 leads to mesenchymal stem cell proliferation, while msx2 appears to impair chondrogenic differentiation in favour of osteogenesis (Alappat et al., 2003;Figures 4, 6). ...
Evolutionary novelties—derived traits without clear homology found in the ancestors of a lineage—may promote ecological specialization and facilitate adaptive radiations. Examples for such novelties include the wings of bats, pharyngeal jaws of cichlids and flowers of angiosperms. Belonoid fishes (flying fishes, halfbeaks and needlefishes) feature an astonishing diversity of extremely elongated jaw phenotypes with undetermined evolutionary origins. We investigate the development of elongated jaws in a halfbeak ( Dermogenys pusilla ) and a needlefish ( Xenentodon cancila ) using morphometrics, transcriptomics and in situ hybridization. We confirm that these fishes' elongated jaws are composed of distinct base and novel ‘extension’ portions. These extensions are morphologically unique to belonoids, and we describe the growth dynamics of both bases and extensions throughout early development in both studied species. From transcriptomic profiling, we deduce that jaw extension outgrowth is guided by populations of multipotent cells originating from the anterior tip of the dentary. These cells are shielded from differentiation, but proliferate and migrate anteriorly during the extension's allometric growth phase. Cells left behind at the tip leave the shielded zone and undergo differentiation into osteoblast‐like cells, which deposit extracellular matrix with both bone and cartilage characteristics that mineralizes and thereby provides rigidity. Such bone has characteristics akin to histological observations on the elongated ‘kype’ process on lower jaws of male salmon, which may hint at common conserved regulatory underpinnings. Future studies will evaluate the molecular pathways that govern the anterior migration and proliferation of these multipotent cells underlying the belonoids' evolutionary novel jaw extensions.
... Además, pueden asociarse anomalías como fusión vertebral, cervical y torácica, tetralogía de Fallot, comunicación interventricular, fístula traqueo-esofágica, atresia esofágica y malformaciones pulmonares de grado variable (desde la segmentación anormal hasta hipoplasia o aplasia unilateral) (6). Otras posibles hipótesis causales incluyen la teoría de la interrupción vascular y formación de hematomas de Poswillo, neurocristopatía de Opitz y expresión deficiente de los genes homeobox Msx, que en modelos animales produce alteraciones de los tejidos derivados del primer arco branquial (7,8). y micrognatia, ambas ausentes en el SG, mientras que la microftalmia está ausente en este síndrome (14). ...
RESUMEN El síndrome de Goldenhar, o espectro óculo-aurículo-vertebral, es un síndrome congénito caracterizado por alteraciones en diferentes grados de las estructuras faciales. En ocasiones también existen alteraciones de la columna vertebral y otros defectos óseos, malformaciones cardíacas y anomalías del sistema nervioso central. Un aspecto importante es que, en la mayoría de los casos, estas lesiones son unilaterales. La causa es desconocida. El diagnóstico prenatal solo es posible mediante la identificación de alteraciones morfológicas, ya que no existen marcadores genéticos para el diagnóstico. La enfermedad no es mortal, pero las alteraciones cráneo-faciales graves pueden poner en peligro la vida en el periodo posnatal. El tratamiento consiste en cirugía plástica reconstructiva. Se presenta un caso de diagnóstico prenatal del síndrome de Goldenhar. ABSTRACT: Goldenhar syndrome, or oculo-auriculo-vertebral spectrum, is a congenital syndrome characterized by alterations in different degrees of facial structures. Further, there are alterations of the spine, other bone defects, cardiac malformations, and central nervous system anomalies. An important aspect is that, in most cases, these lesions are unilateral. The cause is unknown. Prenatal diagnosis is only possible by the identification of morphological alterations, as there are no genetic markers for diagnosis. The condition is not fatal, but severe craniofacial alterations can be life-threatening in the postnatal period. Treatment consists of reconstructive plastic surgery. A case of prenatal diagnosis of Goldenhar syndrome is presented.
... 93 It is possible that differing functional requirements at birth for species at different positions on altricial-precocial spectrum (e.g., extended suckling postpartum for the highly altricial marsupials) may act as drivers for the distinct cranial morphologies observed here ( Figure 3B). 10 Alternatively, or additionally, variation in gene expression timing and spatial patterning, such as the homeobox genes (e.g., MSx1, Barx1, and Dlx2), which are known to influence cell development in the cranial region, 94,95 could also be involved in generating the observed morphological variation across the altricial-precocial spectrum. Further study is needed to identify the mechanisms behind this morphological variation, but our analyses clearly demonstrate an underappreciated role for the altricialprecocial spectrum in regulating cranial morphological evolution within placentals, and not just between marsupials and placentals. ...
Within mammals, different reproductive strategies (e.g., egg laying, live birth of extremely underdeveloped young, and live birth of well-developed young) have been linked to divergent evolutionary histories. How and when developmental variation across mammals arose is unclear. While egg laying is unquestionably considered the ancestral state for all mammals, many long-standing biases treat the extreme underdeveloped state of marsupial young as the ancestral state for therian mammals (clade including both marsupials and placentals), with the well-developed young of placentals often considered the derived mode of development. Here, we quantify mammalian cranial morphological development and estimate ancestral patterns of cranial shape development using geometric morphometric analysis of the largest comparative ontogenetic dataset of mammals to date (165 specimens, 22 species). We identify a conserved region of cranial morphospace for fetal specimens, after which cranial morphology diversified through ontogeny in a cone-shaped pattern. This cone-shaped pattern of development distinctively reflected the upper half of the developmental hourglass model. Moreover, cranial morphological variation was found to be significantly associated with the level of development (position on the altricial-precocial spectrum) exhibited at birth. Estimation of ancestral state allometry (size-related shape change) reconstructs marsupials as pedomorphic relative to the ancestral therian mammal. In contrast, the estimated allometries for the ancestral placental and ancestral therian were indistinguishable. Thus, from our results, we hypothesize that placental mammal cranial development most closely reflects that of the ancestral therian mammal, while marsupial cranial development represents a more derived mode of mammalian development, in stark contrast to many interpretations of mammalian evolution.
... MSX2 and MSX1 are homeobox genes involved in craniofacial development [36], that have previously been associated with craniosynostosis. An MSX2 gain of function mutation is associated with Boston-type craniosynostosis, which most commonly affects lambdoid and coronal sutures [37]. ...
Craniosynostosis is a birth defect where calvarial sutures close prematurely, as part of a genetic syndrome or independently, with unknown cause. This study aimed to identify differences in gene expression in primary calvarial cell lines derived from patients with four phenotypes of single-suture craniosynostosis, compared to controls. Calvarial bone samples (N = 388 cases/85 controls) were collected from clinical sites during reconstructive skull surgery. Primary cell lines were then derived from the tissue and used for RNA sequencing. Linear models were fit to estimate covariate adjusted associations between gene expression and four phenotypes of single-suture craniosynostosis (lambdoid, metopic, sagittal, and coronal), compared to controls. Sex-stratified analysis was also performed for each phenotype. Differentially expressed genes (DEGs) included 72 genes associated with coronal, 90 genes associated with sagittal, 103 genes associated with metopic, and 33 genes associated with lambdoid craniosynostosis. The sex-stratified analysis revealed more DEGs in males (98) than females (4). There were 16 DEGs that were homeobox (HOX) genes. Three TFs (SUZ12, EZH2, AR) significantly regulated expression of DEGs in one or more phenotypes. Pathway analysis identified four KEGG pathways associated with at least one phenotype of craniosynostosis. Together, this work suggests unique molecular mechanisms related to craniosynostosis phenotype and fetal sex.
... The intricate regulation of craniofacial development and differentiation requires a number of transcription factors, such as the MSX family, DLX family, and the SIX family transcription factors, among others (Alappat et al., 2003;Takechi et al., 2013). The SIX family is a group of evolutionarily conserved transcription factors, which are expressed in multiple organs of humans, mice, drosophila, and other organisms, and play an essential role in the development of the craniofacial skeleton, kidney, ear, nose, brain, muscle, and gonads (Serikaku and O'Tousa, 1994). ...
Craniofacial development requires intricate cooperation between multiple transcription factors and signaling pathways. Six1 is a critical transcription factor regulating craniofacial development. However, the exact function of Six1 during craniofacial development remains elusive. In this study, we investigated the role of Six1 in mandible development using a Six1 knockout mouse model (Six1 −/− ) and a cranial neural crest-specific, Six1 conditional knockout mouse model (Six1 f/f ; Wnt1-Cre). The Six1 −/− mice exhibited multiple craniofacial deformities, including severe microsomia, high-arched palate, and uvula deformity. Notably, the Six1 f/f ; Wnt1-Cre mice recapitulate the microsomia phenotype of Six1 −/− mice, thus demonstrating that the expression of Six1 in ectomesenchyme is critical for mandible development. We further showed that the knockout of Six1 led to abnormal expression of osteogenic genes within the mandible. Moreover, the knockdown of Six1 in C3H10 T1/2 cells reduced their osteogenic capacity in vitro. Using RNA-seq, we showed that both the loss of Six1 in the E18.5 mandible and Six1 knockdown in C3H10 T1/2 led to the dysregulation of genes involved in embryonic skeletal development. In particular, we showed that Six1 binds to the promoter of Bmp4, Fat4, Fgf18, and Fgfr2, and promotes their transcription. Collectively, our results suggest that Six1 plays a critical role in regulating mandibular skeleton formation during mouse embryogenesis.
... It could result in racial and ethnic variances in suture patterns. 19 Forensic pathologists, anthropologists, and anatomists all value the morphology of pterion. 20 An impeccable understanding of the architecture of the brain and skull is required for preoperative planning for brain tumour resection. ...
Objective-To assess the anatomical cervical facet joint arthrosis in patients presenting with neck pain and its correlation with age and cervical spinal levels (C3-C7) by CT scan. Material & Methods-The hospital based clinical case control study was conducted for duration of 24 month. Diagnosed OPD cases of neck pain (20-80 years) with suspected facet joint arthrosis in During OPD hours, all clinical history related with neck pain was taken and relevant important information taken through consent. CT scan for the cervical spine region was performed in Radio diagnosis department of MIMS for all the enrolled subject (having neck pain) Journal of Xi'an Shiyou University, Natural Science Edition ISSN : 1673-064X http://xisdxjxsu.asia VOLUME 18 ISSUE 12 December 2022 95-104 Results-Total 83 subjects were enrolled in this with all most equal representation from both sexes i.e males (49.4%) and females (50.6%) with an average age of 57.98 +7.63 years. In our study more severe left cervical facet joint comparison with right cervical facet joint degeneration were observed in 13.3% and 10.5% of study subjects respectively. In almost every subject the neck pain was presenting neurological symptom. Conclusion-The facet joints are a type of synovial joint and the articulation participate in the posterior arch of the vertebrae. They provide important role in important structural stability to the vertebral column. These joints are surrounded with a strong fibrous capsule and connect the superior and interior articular facets of the cervical vertebrae.
