Extended Abstract (for invited Faculty only) Microfracture/Bone Marrow Stimulation

1.1.3 - Cartilage Repair - The Translational Perspective

Presentation Topic
Microfracture/Bone Marrow Stimulation
Lecture Time
12:30 - 12:45
Potsdam 1
Session Type
Special Session
  • H. Madry (Homburg, DE)
  • H. Madry (Homburg, DE)



Cartilage defects represent common, acquired intra-articular pre-osteoarthritic deformities that disturb as the structural integrity of the osteochondral unit.


It is important to distinguish the well-defined focal non-OA defects such as occurring after trauma from the ill-defined large OA defects. Cartilage regeneration is defined as the identical reduplication of the original hyaline articular cartilage structure, while repair results in a disorganized, non-stratified fibrocartilage. Chondral defects are restricted to the articular cartilage. Based on their depth, they are classified as partial- or full-thickness chondral defects. Osteochondral defects extend into the subchondral bone, disrupting its entire functional unit. Spontaneously, chondral defects are only sparsely repopulated by cells from the synovium while mesenchymal stromal cells (MSCs) originating from the bone marrow induce an (insufficient) repair of osteochondral defects, a paradigm exploited in marrow-stimulating techniques. The reason for treating a symptomatic focal cartilage defect is twofold. First, it is to provide for a repair tissue that fills the defect. Second, the repair tissue restores local joint congruity and stabilizes the adjacent cartilage by integrating with it, restoring load distribution and thereby possibly preventing perifocal OA progression. Although the natural history of an untreated cartilage defect is difficult to predict, lesion size may increase, both in symptomatic or asymptomatic patients and induce OA. In general, symptomatic focal articular cartilage defects extending to more than 50% of cartilage depth are treated. A chondral defect may primarily be treated with a chondral repair technique, leaving the underlying subchondral bone untouched. Small chondral defects can be treated with marrow stimulation techniques, small osteochondral defects with a single osteochondral auto- or allograft. Large chondral defects are ideally managed with autologous chondrocyte implantation. Large osteochondral defects can be treated by combining ACI with autologous cancellous bone grafting, using multiple osteochondral autografts or a large single osteochondral allograft. Surgical refixation of a detached (osteo)chondral fragment, if possible, is highly desirable as it regenerates the original joint congruence.

This talk will outline translational aspects of cartilage repair with a focus on the osteochondral unit. Problems of subchondral bone repair, among which upward migration of the subchondral bone plate, formation of intralesional osteophytes, development of subchondral bone cysts and changes of subchondral bone microarchitecture will be covered. Moreover, effects of instrument morphology on osteochondral repair upon marrow stimulation based on investigations in large animal models of cartilage defects will be outlined. Precise topographical investigations on the development of knee osteoarthritis affected by axial alignment caused by meniscal defects will be elaborated on. Finally, biomaterial based gene therapy approaches for cartilage defects will be covered.


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Sanders TL, Pareek A, Obey MR, Johnson NR, Carey JL, Stuart MJ, et al. High Rate of Osteoarthritis After Osteochondritis Dissecans Fragment Excision Compared With Surgical Restoration at a Mean 16-Year Follow-up. Am J Sports Med 2017; 45: 1799-1805.

Madry H, Hunziker EB. 'Actum ne agas'. Osteoarthritis Cartilage 2021; 29: 300-303.

Orth P, Cucchiarini M, Kohn D, Madry H. Alterations of the subchondral bone in osteochondral repair--translational data and clinical evidence. Eur Cell Mater 2013; 25: 299-316; discussion 314-296.