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Vendor orientation on decal chemistry and endpoint testing; marked thin for compliance purposes, not a primary standard.

Demonstrates that decal agent choice has measurable histological consequences; supports the principle that decal must be validated per specimen type.

Accelerated EDTA method preserves mRNA better than standard EDTA; relevant to labs running molecular assays on bone specimens.

Evaluates fixative-decal combinations for preserving both histology and nucleic acid quality; relevant to pre-analytical SOP design.

Demonstrates that decalcification status affects molecular assay results in bone tumors; validates the CAP pre-analytical reporting requirement in a clinical case series.

Practical review of decal methods organized by agent class; strong acids, organic acids, chelating agents. Useful protocol reference; not a primary standard.

Laboratory-facing guidance on decal optimization; covers endpoint confirmation, solution-to-tissue ratio, and change intervals. Not a primary standard.

Review covers scaffold design, immunological microenvironment, and emerging biotech for focal cartilage defect repair

Migratory progenitor cells emerge from cartilage fragments without enzymatic digestion; retain strong chondrogenic potential

Aging is a primary risk factor for osteoarthritis (OA), yet the mechanisms that preserve extracellular matrix integrity in long-lived connective tissues remain poorly defined

The development of regenerative therapies for osteoarthritis and intervertebral disc degeneration requires non-destructive methods to spatiotemporally monitor extracellular matr...

Cell-based therapy, matrix-associated chondrocyte implantation, engineered scaffolds, and controlled-release biologics reviewed; standardized outcomes emphasized.

ObjectiveMechanical loading is critical for chondrocyte function and cartilage matrix production, yet its effects on clustered chondrocytes in end-stage osteoarthritis and on ch...

ECM identified as central to chondrocyte homeostasis and protection during cartilage development in a human pluripotent stem cell model.

Copper and iron overload converge via cuproptosis, ferroptosis, apoptosis, and autophagy dysregulation to promote chondrocyte death and cartilage destruction.

Background: Hyaluronan (HA) is a critical extracellular matrix component that we have demonstrated to be important for embryonic endochondral bone formation and postnatal synovi...

Biophysical comparison, healthy versus OA chondrocytes, adhesion energy and ECM differ measurably.

Chondrocyte hypertrophy framed as essential to skeletal development and disease, with precise regulation required for homeostasis and repair.

Covers mitophagy and mitochondrial dynamics as levers on chondrocyte survival and OA progression.

Normal autophagy preserves chondrocyte survival and ECM; its decline permits damaged organelle accumulation and drives degradation.

Reviews how inflammatory and immune signaling drives cartilage degeneration in OA, beyond the usual biomechanical story.

Surface property profiling relevant to cartilage tissue engineering, where autologous chondrocytes are the workhorse cell.

Apoptosis, pyroptosis, necroptosis, autophagy, ferroptosis, cuproptosis, and PANoptosis all regulate chondrocyte fate through interlocking molecular networks in OA.

IL-1beta drives caspase-cascade apoptosis and oxidative stress (ROS, iNOS, COX-2, NO) in chondrocytes, the combined process labeled oxiapoptophagy.

2026 review of scaffold and cell-based strategies for physis repair after injury

Reviews senescence as a hallmark linking chondrocyte aging to OA progression.

CAP requires pre-analytical decalcification to be reported where it may affect results; ASCO-CAP guidance requires lab-specific validation of decal-affected IHC, not reliance on published protocols.

Quantitative comparison of DNA and RNA yield after EDTA, formic acid, and nitric acid decalcification; EDTA best for nucleic acid preservation.