Microfracture therapy is commonly used in the clinical treatment of small cartilage defects in the knee, based on the theory that the cartilage defect can be repaired by creating a fracture gap to release the multifunctional osteoblasts of the subchondral bone. A recent review of the history and current trends in microfracture treatment of small cartilage defects of the knee by Adam B. Yanke et al. in the journal Orthopedics is presented below.
A highly promising start.
It is well known that the complex intra-articular environment means that once cartilage damage occurs in the joint, it lacks the ability to repair itself. The subarticular cartilage surface has pluripotent mesenchymal stem cells that can regenerate cartilage by entering the cartilage surface through gaps in the broken cartilage surface, and their regenerative capacity is far more useful than chondrocyte crawling repair.
Based on these foundations, Steadman et al. first introduced microfracture therapy in 1997, which quickly became the mainstay of clinical treatment for articular cartilage injuries, and Steadman reported encouraging clinical outcomes after microfracture surgery even at 17-year postoperative follow-up. But it is puzzling why so many clinicians are still going back and forth in search of more effective treatments than microfracture for symptomatic cartilage defects.
Moving forward in embarrassment.
As microfracture techniques have become widely available in the clinic, several late studies on microfracture for symptomatic cartilage defects have not supported the efficacy of microfracture. One study completed by Goyal et al. highlighted that in patients treated with microfracture, transient clinical functional improvement could be obtained early on, while at 2-5 years of follow-up, the clinical outcome deteriorated sharply even when the patient had a very mild cartilage defect.
A closer look at microfracture treatment techniques suggests that the poor outcomes may also be due to the “technical simplicity” of the specimen. Microfracture treatment of most traumas, although requiring special techniques, can be accomplished without additional ancillary equipment, using only arthroscopic techniques, without detailed preoperative planning, and without special preoperative education.
These “easy conditions” for performing microfracture techniques have led to an unrestricted expansion of the indications for the use of this technique in clinical practice. The “simplicity” of the technique has led clinicians to pay less attention to conditions that may affect the outcome of microfracture treatment, such as poor knee axis, meniscus damage or loss, or ligament instability.
One of the main clinical principles for determining whether a treatment technique is the treatment of choice is that a good outcome is achieved with that treatment option, without burying the possibility of further management if the outcome deteriorates later. conducted functional follow-up and found that the clinical functional prognosis of this population was poor.
In addition, in some of the authors’ study centers, patients with only minor cartilage defects treated with microfracture therapy developed clinical symptoms. Based on the above facts, the previous claim that microfracture therapy has no impact on long-term treatment options and clinical prognosis needs to be further examined.
The use of microfracture therapy in clinical practice requires special techniques and postoperative rehabilitation strategies, including removal of the calcified cartilage layer (CCL), use of a continuous CPM machine, and strictly protected weight-bearing exercises, in addition to the selection of the appropriate population for the indication.
A study by the Canadian Association of Orthopaedic Surgeons found that these dispositions varied greatly among physicians, with approximately 45% of physicians not removing the calcified cartilage layer during microfracture treatment, 59% not restricting patient weight bearing postoperatively, and 98% not using a CPM machine for postoperative rehabilitation exercises.
The conditions that allow a better microfracture treatment outcome as summarized by the current study data are.
Patients less than 40 years of age, cartilage defect less than 4 cm2, body mass index less than 30 kg/m2, Tegner score greater than 4, no previous history of joint surgery, removal of calcified cartilage layer, stable cartilage structure at the wound margin after debridement, very short duration of articular cartilage wear symptoms before treatment, cartilage defect at the femoral condyles, more than 66% of the cartilage defect site with postoperative repair The postoperative cartilage defects were filled with more than 66% of the repair tissue, and strict postoperative rehabilitative exercise measures and weight-bearing restrictions were in place.
A meta-analysis completed by Negrin et al. found that microfracture treatment resulted in a relatively satisfactory functional prognosis after strict selection of indications and standardized techniques.
Zigzagging into the cold.
Although clinical reports of microfracture treatment for cartilage defects are currently mixed, it remains the standard by which other new techniques are evaluated. Many scientists have embarked on stem cell research to address the issue of cartilage cell storage. However, the aforementioned research encountered an obstacle in the practical process. In 1997, the US FDA formed the TRG (Tissue Research Group) to guide the research process for human cells, tissues and cellular and tissue-based products.
These guidelines suggest that cells or tissues undergoing research without receiving any instrumentation or drugs may not be considered clinical trials, and that tissue specimens may not be altered in their basic structure while undergoing research, both of which may be excluded from FDA regulation. However, in many cases, studies often do not meet the above requirements and are rejected by the FDA.
For example, in 2011, a study that examined demineralized bone matrix as a storage structure for chondrocytes was rejected by the FDA because the bone matrix studied had changed its structure and was not the original tissue structure.
For example, in 2013, a study of bone marrow-derived MSCs was stopped by the FDA for not meeting TRG standards, because the expansion of MSCs into a biologic product was included in the FDA’s complex regulatory and approval pathway for clinical trials. The FDA’s stringent regulations were originally intended to improve the safety of clinical trials, but in some ways did undermine the incentive for many biotech innovation companies to move forward.
The sun rises on the horizon.
Due to the large number of patients with osteochondral defects and the heavy financial burden they pose, microfracture therapy is becoming the basis for a variety of new treatment options until there is an effective treatment option. As a result, reports of improved outcomes of microfracture therapy have begun to increase in the clinical literature, with some of the more groundbreaking advances including easier access to the bone marrow in the lateral compared to the medial space.
Chiseling through subchondral bone 6 mm is better than chiseling through 2 mm to obtain cartilage filling; cartilage formation is better at the femoral talus site than at the femoral condyle; and the area of tissue necrosis caused by the heat generated by the electric drill bit is less than that caused by the gristle pin. Continued improvements in microfracture treatment techniques will increase the number of chondrocytes and the integrity of the repair tissue, and preserve the subchondral bone even after microfracture treatment.
Since the core components of tissue engineering include tissue scaffold, growth factors, and cellular components, the current focus of clinical research in microfracture treatment is to enhance the production of these core components in the treated individual, with the goal of this phase being to improve the body’s ability to preserve the clot (tissue scaffold for chondrocyte growth) or to improve the environment for cell exposure (tissue growth factors and cellular components).