chondro.site

Hyaline cartilage TEM. Chondrocytes arranged in chondrons contain extensive rough endoplasmic reticulum (RER); surrounding matrix shows type II collagen fibrils interspersed with proteoglycans. Six-day-old mouse, demineralized bone.

Michael J.F. Blumer · CC BY 4.0

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Articular cartilage ECM zonal architecture. Superficial zone: collagen II fibers aligned parallel to articular surface (resists shear). Deep zone: fibers aligned perpendicular to bone interface (absorbs compression).

Bautista, Park, Mazur, Aaron, Bilgen · CC0

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Human articular chondrocyte TEM (non-loading control arm). Panel A: autophagosomes, lysosomes, and autolysosomes showing normal autophagy activity. From a study of mechanical loading effects on OA chondrocytes; non-loading arm is the baseline control.

Sato, Iwata, Yamamoto et al 2026, Int J Mol Sci · CC BY 4.0

source · fig. Fig 1A

Human growth plate chondrocyte TEM. Resting zone (RZ) and proliferative zone (PZ) chondrocytes showing heterochromatin (asterisks) and lysosomes (arrowheads). Panel b from a study of cellular quiescence in the resting zone.

Avijgan, Lopez-Perez, Galicia et al 2026, Bone Research · CC BY 4.0

source · fig. Fig b (TEM panel)

Hyaline cartilage histological section, H&E stain. Chondrocytes in lacunae visible within the cartilage matrix.

Nbnidhi · CC BY 4.0

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Safranin-O/Fast Green staining of knee articular cartilage. Red areas indicate preserved cartilage proteoglycans; green areas show depletion. From a DMM-induced OA model study of FGF9 intra-articular delivery.

Lo, Chen, Huang et al 2026, Bone and Joint Research · CC BY 4.0

source · fig. Safranin-O panel

Tibial plateau articular cartilage, spontaneous OA. Safranin O and IHC for CollagenX, MMP-13, Aggrecan, Caspase-3 across age groups. Scale bar 100 um.

Wang, Wei, Xue et al 2021, BMC Musculoskeletal Disorders · CC BY 4.0

source · fig. multi-stain composite panel

Human osteochondral explant H&E. Preserved (normal), lesioned (OA), and treated cartilage regions in the same section. Subchondral bone visible beneath cartilage.

Sayedipour, Mazzini, Tuerlings et al 2026, Osteoarthritis and Cartilage Open · CC BY 4.0

source · fig. H&E comparison panel

Ferroptosis is activated in osteoarthritic chondrocytes and contributes to cartilage degeneration (A) Heatmap of whole-transcriptome sequencing comparing normal chondrocytes and OA chondrocytes. (B) Volcano plot showing differentially expressed ferroptosis-related genes. (C) GO enrichment analysis indicating dysregulation of iron homeostasis and glutathione metabolism in OA. (D) Immunohistochemical (IHC) staining of human OA cartilage and mouse cartilage tissues showing ACSL4 and GPX4 expression. Scale bars, 200 μm.

Mai, Zhu, Liu et al 2026, iScience · CC BY 4.0

PMID 42565176 · fig. Figure 1

chondrocyte-proliferation-cc4.png

Chondrocyte proliferation and differentiation in 3D bioprinted scaffold. Human chondrocytes cultured in nanofibrillated cellulose-alginate scaffold stained for collagen type II (red) and cell nuclei (blue). From a study of scaffold-supported cartilage tissue engineering.

Apelgren P, Amoroso M, Lindahl A, Brantsing C, Rotter N, Gatenholm P, et al. · CC BY 4.0

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Hypertrophic zone of the epiphyseal growth plate, light microscopy. Large hypertrophic chondrocytes in lacunae with calcified matrix visible. Demonstrates the transition from proliferative to hypertrophic zone preceding ossification.

Robert M. Hunt · Public domain

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Hyaline cartilage section, polarised light microscopy. Collagen II fibers appear birefringent. Parallel superficial zone fibers and perpendicular deep zone fibers are visible as distinct birefringence patterns reflecting zonal architecture.

Emmanuelm at en.wikipedia · CC BY 3.0

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Hyaline cartilage histological section, H&E stain. Chondrocytes are visible as dark-staining nuclei within clear lacunae in the pale cartilage matrix. Basophilic (blue-purple) matrix reflects proteoglycan and collagen content.

Ganímedes · CC BY-SA 3.0

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Histological cartilage evaluation in femoral condyles. Representative hematoxylin-eosin-stained sections of osteaoarthritic (OA) femoral condyles and their contralateral healthy (HT) from (A,D) SHAM: sham surgery, treated with placebo; (B,E) CONT: control, operated knees treated with placebo; (C,F) ASU: operated knees treated with avocado/soybean unsaponifiables. (G) The bar graph shows semiquantitative histological scores for cartilage structure (CART), chondrocyte abnormalities (CHOND), tidemark integrity (TIDEMARK), and total score (TOTAL) in the previously mentioned groups. Asterisks (*) indicate significant differences with the contralateral HT joint and the hash (#) indicates significant differences with the SHAM-OA group. Four-point stars denote chondrocyte clusters, black arrows denote empty lacunae, and dashed arrows denote surface undulations and irregularities.

Sabucedo-Suarez, Munoz, Permuy et al 2026, Frontiers in Veterinary Science · CC BY 4.0

PMID 42290786 · fig. Figure 7

Transmission Electron Microscopy (TEM) analysis. ( A ): In chondrocytes of the non-loading group, a large number of autophagosomes and lysosomes showing the autophagy process, as well as autolysosomes after digestion of organelles, were observed. ( B ): In chondrocytes of the 1 h loading group, although fewer in number than in the no-load group, autophagosomes, lysosomes, and autolysosomes were seen indicating that the autophagy process was observed. ( C ): In chondrocytes of the 3 h loading group, the number of autophagosomes and autolysosomes was lower compared to the no-load and 1 h loading groups. On the other hand, there were numerous degenerated organelles that had not undergone autophagy within the chondrocytes. This suggests the accumulation of defective mitochondria and abnormal cellular proteins within the cells. ( D ): The numbers of autophagosomes, lysosomes, and autolysosomes per cell were significantly lower in mechanical loading groups than in non-loading group (* p < 0.01).

Sato, Iwata, Yamamoto et al 2026, International Journal of Molecular Sciences · CC BY 4.0

PMID 42653480 · fig. Figure 4

Transmission Electron Microscopy (TEM) analysis. (A): In chondrocytes of the non-loading group, a large number of autophagosomes and lysosomes showing the autophagy process, as well as autolysosomes after digestion of organelles, were observed. (B): In chondrocytes of the 1 h loading group, although fewer in number than in the no-load group, autophagosomes, lysosomes, and autolysosomes were seen indicating that the autophagy process was observed. (C): In chondrocytes of the 3 h loading group, the number of autophagosomes and autolysosomes was lower compared to the no-load and 1 h loading groups. On the other hand, there were numerous degenerated organelles that had not undergone autophagy within the chondrocytes. This suggests the accumulation of defective mitochondria and abnormal cellular proteins within the cells. (D): The numbers of autophagosomes, lysosomes, and autolysosomes per cell were significantly lower in mechanical loading groups than in non-loading group (* p < 0.01).

Sato, Iwata, Yamamoto et al 2026, International Journal of Molecular Sciences · CC BY 4.0

PMID 42653480 · fig. Figure 4

Transmission Electron Microscopy (TEM) analysis. (A): In chondrocytes of the non-loading group, a large number of autophagosomes and lysosomes showing the autophagy process, as well as autolysosomes after digestion of organelles, were observed. (B): In chondrocytes of the 1 h loading group, although fewer in number than in the no-load group, autophagosomes, lysosomes, and autolysosomes were seen indicating that the autophagy process was observed. (C): In chondrocytes of the 3 h loading group, the number of autophagosomes and autolysosomes was lower compared to the no-load and 1 h loading groups. On the other hand, there were numerous degenerated organelles that had not undergone autophagy within the chondrocytes. This suggests the accumulation of defective mitochondria and abnormal cellular proteins within the cells. (D): The numbers of autophagosomes, lysosomes, and autolysosomes per cell were significantly lower in mechanical loading groups than in non-loading group (* p < 0.01).

Sato, Iwata, Yamamoto et al 2026, International Journal of Molecular Sciences · CC BY 4.0

PMID 42653480 · fig. Figure 4

Ch@P maintains mitochondrial homeostasis by regulating mitophagy. (A) TEM images of mitochondria in chondrocytes after different treatments. (B-F) Immunofluorescent staining and quantitative analyses of cytosolic ROS level, mitochondrial ROS level, JC-1 monomers (green) and JC-1 aggregates (red) in different groups. (G-K) The protein expression of mitophagy-related markers (Pink1, Parkin, LC3B and Pgc1alpha) in different groups. (L) Co-localisation of LC3B and Tom20 in different groups. (M) The diagram shows that Ch@P maintains mitochondrial homeostasis by activating mitophagy. Data are presented as means +/- SD derived from three or four replicates. * p < 0.05, ** p < 0.01 and *** p < 0.001.

Chang, Kong, Jin et al 2026, Exploration · CC BY 4.0

PMID 42494574 · fig. FIGURE 5

Ch@P maintains mitochondrial homeostasis by regulating mitophagy. (A) TEM images of mitochondria in chondrocytes after different treatments. (B-F) Immunofluorescent staining and quantitative analyses of cytosolic ROS level, mitochondrial ROS level, JC-1 monomers (green) and JC-1 aggregates (red) in different groups. (G-K) The protein expression of mitophagy-related markers (Pink1, Parkin, LC3B and Pgc1alpha) in different groups. (L) Co-localisation of LC3B and Tom20 in different groups. Data are presented as means +/- SD derived from three or four replicates.

Chang, Kong, Jin et al 2026, Exploration · CC BY 4.0

PMID 42494574 · fig. FIGURE 5

Ultrastructural changes in collagen fibril organization in the MM region of cartilage in intact (Ctrl) and W1 postsurgery cartilage. (A) Representative immunofluorescence staining for type II collagen (Col II) in cartilage sections at different stages of OA progression (intact to W6 postsurgery). (B) Magnified Col II and DAPI images, showing detailed Col II changes in the cartilage matrix during OA progression (scale bar, 200 um). (C and D) Representative overview images of collagen in medial cartilage obtained by summing SHG signal across all polarization angles. (E and F) Pixel-based heat maps showing the principal orientation of collagen fibrils in MM regions, with representative examples from the Ctrl and W1 groups (n = 3). Colors closer to purple indicate fibrils more parallel to the cartilage surface, whereas colors closer to red indicate fibrils more perpendicular to the cartilage surface. (G and H) Heatmaps depicting the degree of alignment of collagen fibrils in MM regions, corresponding to those in (E) and (F). Brighter colors indicate higher fibril alignment (scale bars, 50 um). (I and J) Depth-dependent line plots of (E) and (F), showing the mean principal orientation of collagen fibrils (blue lines) within each row and their heterogeneity (light blue shading) across cartilage depth, normalized from articular surface to cement line. (K and L) Corresponding depth-dependent line plots for (G) and (H), showing the row mean values of collagen fibril alignment (red lines) and the heterogeneity within each row (light red shading), normalized from cartilage surface to cement line. D3, 3 days; W1, 1 week; W3, 3 weeks; W6, 6 weeks.

Zhou, Hu, Yada et al 2026, Science Advances · CC BY 4.0

PMID 42685225 · fig. Fig. 3.

Transmission Electron Microscopy (TEM) analysis. (A): In chondrocytes of the non-loading group, a large number of autophagosomes and lysosomes showing the autophagy process, as well as autolysosomes after digestion of organelles, were observed. (B): In chondrocytes of the 1 h loading group, although fewer in number than in the no-load group, autophagosomes, lysosomes, and autolysosomes were seen indicating that the autophagy process was observed. (C): In chondrocytes of the 3 h loading group, the number of autophagosomes and autolysosomes was lower compared to the no-load and 1 h loading groups. On the other hand, there were numerous degenerated organelles that had not undergone autophagy within the chondrocytes. This suggests the accumulation of defective mitochondria and abnormal cellular proteins within the cells. (D): The numbers of autophagosomes, lysosomes, and autolysosomes per cell were significantly lower in mechanical loading groups than in non-loading group (* p < 0.01).

Sato, Iwata, Yamamoto et al 2026, International Journal of Molecular Sciences · CC BY 4.0

PMID 42653480 · fig. Figure 4

Endocytosis of cartilage matrix is impaired by dynasore. A-B Super-resolution microscopy images showing F-actin staining at the plasma membrane of pre-hypertrophic chondrocytes (white arrows) and quantification of the F-actin thickness in all zones. C Transmission electron microscopy (TEM) images of examples of shallow, U-shaped and Omega-shaped endocytic pits (white arrows) observed in the metatarsals. D Coated pits in pre-hypertrophic chondrocytes. Note the abundance of extracellular matrix (ECM) and fiber-like structures (black arrow heads) in the dynasore-treated group. E Quantification of shallow, U-shaped and Omega-shaped pits in the epiphysial cartilage. F TEM images reveal cartilage endocytosis in hypertrophic chondrocytes. Chondrocytes uptake collagen fibril-like electron-dense extracellular structures (black arrowheads) in endocytic-like pits/vesicles (white arrowheads). By contrast, dynasore-treated bones contained chondrocytes with over-accumulation of ECM in the extracellular space. RZ: resting zone; PZ: proliferative zone; HZ: hypertrophic zone. Metatarsals were cultured for 6 days.

Marchan-Alvarez, Koikkara, Zhou et al 2026, BMC Biology · CC BY 4.0

PMID 42464284 · fig. Fig. 6

Endocytosis of cartilage matrix is impaired by dynasore. A-B Super-resolution microscopy images showing F-actin staining at the plasma membrane of pre-hypertrophic chondrocytes (white arrows) and quantification of the F-actin thickness in all zones. C Transmission electron microscopy (TEM) images of examples of shallow, U-shaped and Omega-shaped endocytic pits (white arrows) observed in the metatarsals. D Coated pits in pre-hypertrophic chondrocytes. Please, note the abundance of extracellular matrix (ECM) and fiber-like structures (black arrow heads) in the dynasore-treated group. E Quantification of shallow, U-shaped and Omega-shaped pits in the epiphysial cartilage. F TEM images reveal cartilage endocytosis in hypertrophic chondrocytes. Chondrocytes uptake collagen fibril-like electron-dense extracellular structures (black arrowheads) in endocytic-like pits/vesicles (white arrowheads). By contrast, dynasore-treated bones contained chondrocytes with over-accumulation of ECM in the extracellular space. RZ: resting zone; PZ: proliferative zone; HZ: hypertrophic zone.

Marchan-Alvarez, Koikkara, Zhou et al 2026, BMC Biology · CC BY 4.0

PMID 42464284 · fig. Fig. 6

ECM production by chondrocytes and chondrosarcoma cells cultured as single cells under static and compressive conditions. (A) Schematic summary of the experimental design. Chondrocytes expressing ACAN (red) and COL1A1 (green) (B) or COL1A1, 2, and 6 (green) (C) in static conditions (top) and exposed to cyclic compression (bottom). Chondrosarcoma expressing ACAN (red) and COL1A1 (green) (D) or COL1A1, 2, 6 (green) (E) in static culture (top) and exposed to compression (bottom). White arrows indicate protein deposition in the surrounding of the cells which we consider as protein protrusions. Percentage of cells presenting protein protrusions out of the 40 considered cells for chondrocytes (F) and chondrosarcoma cells (G). Scale bars: 20 um

Paggi, Porsul, Le Gac et al 2026, Cartilage · CC BY 4.0

PMID 42464887 · fig. Figure 4.

Therapeutic effect of piezoelectric hydrogel in human osteoarthritis cartilage samples. (A) Experimental design schematic. After culturing human osteoarthritis cartilage samples in vitro for one week, the hydrogel was replaced weekly, and cartilage samples were collected after 3 weeks. (B) SO/FG staining of different groups of cartilage samples. Scale bar, 200 um. (C, D, E) Immunohistochemical staining results of P16, COL2A1, and MMP13. Scale bar, 100 um. Statistical analysis was performed using one-way analysis of variance (ANOVA) combined with Tukey's post hoc test. n = 5, * p < 0.05, *** p < 0.001. ns, no significant difference.

Zheng, Yan, Liu et al 2026, Advanced Science · CC BY 4.0

PMID 42301238 · fig. FIGURE 8

ECM production by chondrocytes and chondrosarcoma cells cultured as single cells under static and compressive conditions. (A) Schematic summary of the experimental design. Chondrocytes expressing ACAN (red) and COL1A1 (green) (B) or COL1A1, 2, and 6 (green) (C) in static conditions (top) and exposed to cyclic compression (bottom). Chondrosarcoma expressing ACAN (red) and COL1A1 (green) (D) or COL1A1, 2, 6 (green) (E) in static culture (top) and exposed to compression (bottom). White arrows indicate protein deposition in the surrounding of the cells which we consider as protein protrusions. Percentage of cells presenting protein protrusions out of the 40 considered cells for chondrocytes (F) and chondrosarcoma cells (G). Scale bars: 20 um.

Paggi, Porsul, Le Gac et al 2026, Cartilage · CC BY 4.0

PMID 42464887 · fig. Figure 4

miR/PBNP@Gel restored mitochondrial function in OA chondrocytes. (A) JC-1 staining of mitochondrial membrane potential in chondrocytes under H2O2 (200 uM, 24 h) and different treatments. Red indicates JC-1 aggregates and green indicates JC-1 monomers (scale bar: 10 um). (B) SIM images mitochondrial cristae morphology in chondrocytes treated with H2O2 (200 uM, 24 h) with different materials (scale bar: 5 um), and zoom images highlight cristae structure (scale bar: 1 um). (C) Seahorse analysis of oxygen consumption rate over time in chondrocytes under H2O2 (200 uM, 24 h) and different treatments. (D-E) Quantitative analysis of basal respiration and maximal respiration (n = 6). (F) MitoTracker Green staining of mitochondrial morphology in chondrocytes treated with H2O2 (200 uM, 24 h) with different materials (scale bar: 5 um). (G) TEM imaging of chondrocyte mitochondrial ultrastructure following H2O2 (200 uM, 24 h) with different materials (scale bar: 500 nm), and zoom images highlight key structural details (scale bar: 200 nm). (H) Quantification of intracellular ATP content in chondrocytes treated with H2O2 (200 uM, 24 h) with different materials (n = 3). Data are presented as mean +/- SEM. *P < 0.05, ***P < 0.001, ***P < 0.0001.

Cai, Lv, Zhang et al 2026, Advanced Science · CC BY 4.0

PMID 42400930 · fig. FIGURE 6

Changes in microtubule bundles in mitotic chondrocytes in response to substrates with different stiffnesses. a Representative CLSM images showing changes in microtubule bundles in chondrocytes in response to soft/stiff substrates. The cyan arrows indicate microtubule connections between the two cells. b Top-view CLSM images showing morphological changes in the microtubules of individual chondrocytes in response to soft/stiff substrates. c Quantitative analysis of the total number of microtubules in the cytoplasmic region showed that more microtubule bundles were formed on the stiff substrate than on the soft substrate. The results are based on 30 cells from five independent experiments. d Representative CLSM images showing the distribution of microtubules in mitotic chondrocytes in response to soft or stiff substrates (n = 5). Boxed areas (right) indicate changes in microtubule bundles at the center of the two nuclei. White arrows indicate different morphologies and distributions of microtubule bundles in the center of the two immature nuclei at anaphase. e Quantitative analysis of the number of microtubule bundles at the center of the two nuclei in mitotic chondrocytes. The results are based on 15 cells from five independent experiments.

Duan, Zhou, Su et al 2026, Bone Research · CC BY 4.0

PMID 41617674 · fig. Fig. 3

In vitro chondrogenesis of hBMSC microtissues differentiated with or without BMP2 in chondrogenic or hypertrophic conditions. Sections of cartilaginous microtissues from different culture conditions (+/-BMP2) (chondrogenic/hypertrophic medium) were stained for GAGs (Safranin O and Toluidine blue staining), collagen type I, collagen type II, collagen type X, VEGF and ALP after day 28 of culture.

Staubli, Sobrevals Alcaraz, van Es et al 2026, Regenerative Biomaterials · CC BY 4.0

PMID 42179884 · fig. Figure 2

miR/PBNP@Gel attenuated chondrocyte senescence and improved cartilage matrix metabolism. (A) Hematoxylin and eosin staining of cartilage tissue morphology in different treatment groups. Up: overview (scale bar: 500 um); Down: zoomed view (scale bar: 100 um). (B) Safranin O/fast green staining of cartilage glycosaminoglycan content. Up: overview (scale bar: 500 um); Down: zoomed view (scale bar: 100 um). (C) SA-beta-Gal staining of senescent chondrocytes in cartilage tissues (scale bar: 100 um). (D) Immunohistochemical staining of Col2a1, Mmp13, Aggrecan and P21 in cartilage tissues (scale bar: 100 um). (E-G) Western blot analysis and grayscale quantification of P16 and P21 protein expression in cartilage tissues ( n = 4). Data are presented as mean +/- SEM. One-way ANOVA with Tukey's post hoc test was used for multiple comparisons. ** p < 0.01, **** p < 0.0001.

Cai, Lv, Zhang et al 2026, Advanced Science · CC BY 4.0

PMID 42400930 · fig. FIGURE 8

Cytoskeleton formation and intercellular microstress could be simulated by single- and multiple-cell component organoids. (A,B) IF analysis of F-actin for investigation of cytoskeleton formation in normal and OA chondrocytes in cell cultures, single- and multi-cell-component organoids, and cartilage in vivo. (C,D) IF analysis of stress-sensitive ion channel PIEZO1 in normal and OA chondrocytes in cell cultures, single- and multi-cell-component organoids, and cartilage in vivo. ns, no significant difference; N = 3 in all groups. The statistical graph is plotted based on the relative fluorescence intensity. **p < 0.01; ***p < 0.001.

Wang, Zhu, Li et al 2026, Frontiers in Bioengineering and Biotechnology · CC BY 4.0

PMID 42465663 · fig. FIGURE 3

RSS enhances chondrocyte aggregation and chondrogenesis while suppressing adipogenesis. (A) Phase-contrast images of micromass cultures with and without RSS treatment. Scale bar: 400 um. (B) Representative images of Alcian blue staining indicating glycosaminoglycan deposition in micromass cultures with and without RSS. Scale bar: 200 um. (C) Representative images of Oil Red O staining showing lipid droplet formation in micromass cultures with and without RSS. Scale bar: 50 um. (D) Quantitative analysis of integrated optical density (IOD) for Alcian blue staining. * p < 0.05, n = 3. (E) Quantification of Oil Red O-positive area. **** p < 0.0001, n = 3.

Zhang, Huang, Zhang et al 2026, Journal of Functional Biomaterials · CC BY 4.0

PMID 42188419 · fig. Figure 3

Piezo1 mediates nuclear mechanotransduction in osteoarthritis. (a) Immunofluorescence of Col2a1 and DAPI of WT Sham, WT DMM and cKO DMM groups. Scale bars: 50 and 20 um. (b) Quantification of COL2 fluorescence intensity of WT Sham, WT DMM and cKO DMM groups (n = 6). (c) Chondrocyte nuclear cross-sectional area of OA cartilage samples of COL2 of WT Sham, WT DMM and cKO DMM groups (n = 30 samples from six WT Sham, WT DMM or cKO DMM mice). (d) Immunofluorescence and co-localization analysis of F-Actin and DAPI of si-NC Ctrl, si-NC Tension, si-Piezo1 Tension, si-NC Yoda1 and si-Piezo1 Yoda1 groups. Scale bars: 50 um. (e) Percentage of cells with perinuclear actin cap of si-NC Ctrl, si-NC Tension, si-Piezo1 Tension, si-NC Yoda1 and si-Piezo1 Yoda1 groups (n = 6). (f) Immunofluorescence of LaminA/C and DAPI of si-NC Ctrl, si-NC Tension, si-Piezo1 Tension, si-NC Yoda1 and si-Piezo1 Yoda1 groups. Scale bars: 15 and 10 um. (g) Nuclear area of ATDC5 cells of si-NC Ctrl, si-NC Tension, si-Piezo1 Tension, si-NC Yoda1 and si-Piezo1 Yoda1 groups (n = 35 in si-NC Ctrl group, n = 30 in si-NC Tension group, n = 36 in si-Piezo1 Tension group, n = 29 in si-NC Yoda1 group and n = 35 in si-Piezo1 Yoda1 group). And point curvature of si-NC Ctrl, si-NC Tension, si-Piezo1 Tension, si-NC Yoda1 and si-Piezo1 Yoda1 groups (from 24 cells per group). (h) Heatmaps of nuclear mechanics related genes expression in con-static, con-stress and cko-stress groups (n = 4). (i) GSEA analysis of nuclear mechanics related pathways in con-static, con-stress and cko-stress groups. (j) TEM images of chondrocytes nuclei in WT sham, WT DMM and cKO DMM groups. (k) Quantification of nuclear pore size and the proportion of euchromatin of chondrocytes in WT sham, WT DMM and cKO DMM groups (from 35 cells per group). (l) TEM images of chondrocytes nuclei in si-NC Ctrl, si-NC Tension and si-Piezo1 Tension groups. (m) Quantification of nuclear pore size and euchromatin ratio of chondrocytes in si-NC Ctrl, si-NC Tension and si-Piezo1 Tension groups (from 35 cells per group). The p value is indicated on the statistical graph. Values are means +/- SDs. Multiple comparison was performed by one-way ANOVA with Tukey's post-hoc analysis.

Kan, Li, Wang et al 2026, Advanced Science · CC BY 4.0

PMID 42284507 · fig. FIGURE 3

SR retards the degradation and inflammation of articular cartilage matrix. (A) Immunohistochemistry results of Aggrecan, Col2, MMP3, MMP13 and ADAMTS5 proteins. Black arrows indicate a strong positive expression in cartilage tissue. (B) The ratios of immunoreactive positive cells of Col2, MMP3, MMP13 and ADAMTS5 in (A). (C) Immunohistochemistry results of iNOS, TNF-alpha and IL-6 proteins. Black arrows indicate a strong positive expression in cartilage tissue. (D) The ratios of immunoreactive positive cells of iNOS, TNF-alpha and IL-6 in (C). Scale bars, 50 um.

Zhang, Xing, Zhou et al 2026, Frontiers in Pharmacology · CC BY 4.0

PMID 42528752 · fig. FIGURE 4

Transmission Electron Microscopy (TEM) analysis. (A): In chondrocytes of the non-loading group, a large number of autophagosomes and lysosomes showing the autophagy process, as well as autolysosomes after digestion of organelles, were observed. (B): In chondrocytes of the 1 h loading group, although fewer in number than in the no-load group, autophagosomes, lysosomes, and autolysosomes were seen indicating that the autophagy process was observed. (C): In chondrocytes of the 3 h loading group, the number of autophagosomes and autolysosomes was lower compared to the no-load and 1 h loading groups. On the other hand, there were numerous degenerated organelles that had not undergone autophagy within the chondrocytes. This suggests the accumulation of defective mitochondria and abnormal cellular proteins within the cells. (D): The numbers of autophagosomes, lysosomes, and autolysosomes per cell were significantly lower in mechanical loading groups than in non-loading group (* p < 0.01).

Sato, Iwata, Yamamoto et al 2026, International Journal of Molecular Sciences · CC BY 4.0

PMID 42653480 · fig. Figure 4

Fabp5 is a vital regulator in TGF-beta2-induced lipid droplet accumulation. A, qPCR showing that transfection with si-Fabp5-3 at 50 nM for 24 h efficiently knocked Fabp5 down in chondrocytes. Hprt served as the endogenous reference gene. Data from five independent experiments (n = 5) were analyzed by one-way ANOVA and are presented as mean +/- SD. B and C, Western blotting (B) and quantification (C) showing that transfection with si-Fabp5-3 at 50 nM significantly decreased Fabp5 protein expression in chondrocytes. D, representative immunofluorescence micrographs showing that Fabp5 knockdown decreased neutral lipids and lipid droplets in chondrocytes in the presence of TGF-beta2 at 5 ng/ml for 48 h. Neutral lipids and lipid droplets are labeled with BODIPY 493/503 (green), Fabp5 is visualized in red (Alexa Fluor 647), F-actin cytoskeleton is visualized with TRITC-phalloidin (gray, Em565), and nuclei are labeled with Dapi (blue). Scale bars: 20 um (first three columns) and 5 um (last two columns, enlarged images). J, Representative immunofluorescence micrographs showing that TGF-beta2 knockdown decreased neutral lipids and lipid droplets in chondrocytes. Neutral lipids and lipid droplets are labeled with BODIPY 493/503 (green), Fabp5 is visualized in red (Alexa Fluor 647), F-actin cytoskeleton is visualized with TRITC-phalloidin (gray, Em565), and nuclei are labeled with Dapi (blue). Scale bars: 20 um (first three columns) and 5 um (last two columns, enlarged images).

Wei, Pi, Qi et al 2026, The Journal of Biological Chemistry · CC BY 4.0

PMID 42409266 · fig. Figure 3

UDFM the cellular status was observed at varying degrees of freshness. In the fresh group, intact cellular structures were clearly visible, closely resembling those seen in histological staining. The diameter of the chondrocyte lacunae was measured to be 25.28 um and 23.23 um. In contrast, cartilage tissue preserved for more than one day rarely exhibited intact cellular structures.

Zhang, Ma, Wen et al 2026, Journal of Translational Medicine · CC BY 4.0

PMID 41882648 · fig. Fig. 5

/images/chondro/articular-cartilage-zones-1.jpg

Histology of articular cartilage zones showing ECM architecture: superficial zone (parallel collagen fibers, flattened chondrocytes), middle zone (oblique), deep zone (perpendicular, columnar chondrocytes). Safranin O/Fast Green stain. Human knee.

Bautista CA, Park HJ, Mazur CM, Aaron RK, Bilgen B · CC0

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/images/chondro/deep-zone-articular-cartilage-1.jpg

Deep zone of articular cartilage: type II collagen fibers perpendicular to the bone interface, spherical chondrocytes in columnar arrangement. H&E stain. Human knee.

Bautista CA, Park HJ, Mazur CM, Aaron RK, Bilgen B · CC0

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/images/chondro/growth-plate-ultrastructure-1.png

Ultrastructure of growth plate chondrocytes and primary hypertrophic chondrocytes (PHCs) by TEM. Shows organelle-rich cytoplasm and enlarged hypertrophic chondrocyte morphology. Mouse growth plate. CC BY 4.0.

Enishi T, Yukata K, Takahashi M, Sato R, Sairyo K, Yasui N · CC BY 4.0

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/images/chondro/chondrocyte-tem-calcium-1.jpg

Transmission electron micrograph of a chondrocyte, calcium stain. Shows characteristic lacunar structure, nuclear envelope, and organelle-rich cytoplasm. Human articular cartilage.

Robert M. Hunt · CC BY-SA 3.0

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/images/chondro/chondrocyte-tem-calcium-ar-1.jpg

Transmission electron micrograph of a chondrocyte, calcium stain. Shows the lacuna, pericellular matrix, nucleus, and cytoplasmic organelles including rough endoplasmic reticulum. Articular cartilage.

Riad Salih · CC BY-SA 4.0

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/images/chondro/epiphyseal-plate-histology-1.jpg

Histological sections of mouse epiphyseal cartilage (growth plate). Shows the transition from resting/proliferating to hypertrophic zones. H&E stain. Mouse.

Chagin AS, Newton PT · CC BY 4.0

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/images/chondro/hypertrophic-zone-epiphyseal-1.jpg

Hypertrophic zone of the epiphyseal growth plate. Enlarged hypertrophic chondrocytes in columnar stacks above the calcification front. H&E stain. Public domain.

Robert M. Hunt · Public domain

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/images/chondro/cartilage-safranin-o-mouse-1.jpg

Mouse knee joint section, Safranin O and Fast Green stain. Safranin O (red) marks proteoglycan-rich cartilage matrix; Fast Green (blue-green) marks bone and fibrous tissue. Shows articular cartilage layers and subchondral bone.

Kevin Mackenzie, University of Aberdeen · CC BY 4.0

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Representative specimens of human knee joint cartilage (distal femur). (a) macroscopic photograph, (b) H&E staining and Safranin O staining of tissue section. Superficial, middle and deep zones of articular cartilage visible with chondrocytes arranged in characteristic columns in the proliferative and hypertrophic zones. Safranin O staining (red) shows proteoglycan content; reduced staining in degenerated areas indicates matrix loss.

Kiyomatsu H 2026, Journal of biomedical optics · CC BY 4.0

PMID 42812546 · fig. Figure 5

Representative specimens of human shoulder joint cartilage (humeral head). (a) macroscopic photograph, (b) H&E staining and Safranin O staining of tissue section. Safranin O stains proteoglycans red in cartilage matrix; H&E reveals the tissue architecture. Chondrocytes are visible within their lacunae distributed throughout the cartilage zones. Less-degenerated and degenerated areas are indicated.

Kiyomatsu H 2026, Journal of biomedical optics · CC BY 4.0

PMID 42812546 · fig. Figure 4

Histological section of rat knee articular cartilage showing chondrocytes within their lacunae against territorial and interterritorial matrix. Autophagy-related structural changes assessed across OA model groups.

Wang Z 2025, Frontiers in immunology · CC BY 4.0

PMID 41103437

H&E staining of rat knee articular cartilage in a knee osteoarthritis model showing surface fibrillation, chondrocyte cluster formation, and reduced staining of the territorial matrix characteristic of early OA.

Wang Z 2025, Frontiers in immunology · CC BY 4.0

PMID 41103437

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