Level D· Scientific groundwork from lab and animal studiesNarrative ReviewPubMed

Articular Cartilage Tissue Engineering: Cells, Bioinstructive Scaffolds, Immunological Microenvironment, and Emerging Technologies.

Mosaid S., Jihad Y., Jihad M., Marudanayagam A., Lee P.

Narrative Review on Cartilage Damage, published in Bioengineering (Basel) (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Bioengineering (Basel) (2026)
Country
Switzerland
Reported sample size
—
Source database
PubMed
PMID
42510461
DOI
10.3390/bioengineering13070795

Abstract (original English)

Focal articular cartilage defects retain limited intrinsic repair capacity owing to the avascular, alymphatic and aneural nature of hyaline cartilage. Marrow-stimulation procedures often generate mechanically inferior fibrocartilage with declining benefit within 2-5 years in larger or high-demand lesions, while matrix-induced autologous chondrocyte implantation (MACI) achieves durable 10-year benefit but remains constrained by two-stage logistics, in vitro dedifferentiation and cost. This review integrates the cellular, biomaterial, biochemical and immunological dimensions of articular cartilage tissue engineering with quantitative benchmarks and a critical reading of failure modes, scalability and regulatory standing. We benchmark MACI against single-stage chondron- and progenitor-based therapies; examine mesenchymal stromal cells (MSCs) from bone marrow, adipose, synovium and the infrapatellar fat pad with a mechanistic dissection of the Wnt/β-catenin, IHH-PTHrP, RUNX2/MEF2C and HIF-1α inputs driving hypertrophic drift; reframe scaffolds as bioinstructive environments delivering mechanical, biochemical and tribological cues, including stimuli-responsive and 4D-printed systems and low-intensity pulsed ultrasound (LIPUS) as a non-invasive adjunct; develop the immunological dialogue between altered native cartilage, the infrapatellar fat pad-synovium unit and engineered construc

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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