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1. Spatial Transcriptomics of TMJ Reveals a Remodeling Fibroblast‐Immune Microenvironment Driving Arthritis Pain

   Lin, Ziying; Jariyasakulroj, Supawadee; Shu, Yang; Chen, Jingyi; Chang, Qing; Ko, Pao‐Fen; Qiu, Yuyueyang; Chen, Feixiang; Ahn, David; Zhao, Zhen; Chen, Jian‐Fu. Advanced Science. vol. 13(18), e19816. March 2026.

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   ABSTRACT Temporomandibular joint (TMJ) arthritis remodels the cartilage, subchondral bone, and synovial tissue with diverse cell changes. The functional importance of the anatomical organization of TMJ cell types and cellular microenvironment in painful arthritis remains largely unknown. Here, we applied seqFISH (sequential Fluorescence In Situ Hybridization) spatial transcriptomics to examine the adult mouse TMJ. We uncovered new cell types and comprehensively mapped anatomical locations of diverse cell types with distinct neighborhoods, revealed arthritis‐induced cell number and cell status changes, and discovered microenvironment remodeling of fibroblast‐immune cells, which are confirmed in patient synovial tissues. Functional and mechanistic studies showed that macrophage‐specific knockout of mouse Igf1 promotes its immune activation and upregulates Il33 in adjacent synovial fibroblasts, resulting in inflammatory fibroblast expansion. In turn, fibroblast‐specific deletion of Il33 alleviates inflammatory macrophages and inflammation, leading to pain mitigation. Thus, spatial transcriptomics maps diverse cell types in TMJ and reveals a remodeling of synovial fibroblast‐immune microenvironment via the Igf1‐Il33 axis, which drives arthritis pain with therapeutic potentials.

2. Gene expression dynamics of human and mouse craniofacial development at the single-cell level

   Khouri-Farah, Nagham; Manchel, Alexandra; Wentworth Winchester, Emma; Schilder, Brian M.; Robinson, Kelsey; Curtis, Sarah W.; Skene, Nathan G.; Leslie-Clarkson, Elizabeth J.; Cotney, Justin. Nature Communications. March 2026.

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3. CSF1R+ macrophage and osteoclast depletion impairs neural crest proliferation and craniofacial morphogenesis

   Ma, Felix; Zhou, Rose Ru Jing; Rosin, Matthew; Zhou, Iris; Ownsworth, Sabrina; Memar, Rouzbeh Ostadsharif; Wong, Vincent B.; Rosin, Jessica M.. Development. , dev.205423. March 2026.

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   Despite a wealth of knowledge on the mechanisms underlying craniofacial morphogenesis during gestation, the roles of fetal macrophages and osteoclasts during this process remain less well characterized. Here, we used the pharmacological inhibitor PLX5622 to disrupt colony stimulating factor-1 receptor (CSF1R) signaling, which is essential for macrophage and osteoclast proliferation, differentiation, and survival. Prenatal PLX5622 exposure resulted in ∼50% depletion of CSF1R+ macrophages, with complete loss of osteoclasts. While there were no notable changes in craniofacial nerve or muscle development, prenatal exposure to PLX5622 resulted in skull doming and cranial suture impairments, in addition to disruptions to development of the premaxilla, mandible, ear ossicles, palate, and cranial base. In response to PLX5622 exposure, cytokine and chemokine signaling was altered and neural crest proliferation was impaired. Our data also highlight sex- and strain-specific differences in PLX5622 phenotypes and together demonstrate that CSF1R+ macrophages and osteoclasts are essential for craniofacial morphogenesis.

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