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Background: Symptomatic, full-thickness chondral defects often are associated with meniscal deficiencies. These are difficult problems to manage in the young, high-demand patient population. A number of differing techniques have been published with no consensus. While more recent techniques have favored minimally invasive approaches, an open approach with tubercle osteotomy to maximize visualization of all knee compartments can still provide favorable outcomes when using a careful technique and postoperative protocol. Indications: Young, high-demand patients with long-standing meniscal deficiency and resultant chondral defects are indicated for cartilage restoration and preservation procedures. A meniscal allograft transplantation is indicated in symptomatic patients with prior total or subtotal meniscectomy. It is important to address other concomitant pathology such as instability, alignment, and chondral defects. Concomitant procedures are often performed with meniscal transplants, including osteochondral allograft transplantation for larger defects. Technique Description: This surgical technique video demonstrates a tibial tubercle osteotomy approach to gain access to both the medial and lateral tibiofemoral compartments. An arthroscopic-assisted bone slot technique was performed for meniscal allograft transplantation. Appropriately sized osteochondral allograft bone plugs were then transplanted onto the medial and femoral condyles with a press fit technique. Results: At 1-year follow-up, the presented patient has regained full motion and are back to full activities. Discussion/Conclusion: Full-thickness chondral defects associated with meniscal deficiency in a young, high-demand patient is a difficult problem to manage. Recent results using minimally invasive approaches have demonstrated favorable mid- and long-term outcomes. In patients with pathology that may preclude a minimally invasive approach, an open technique with osteotomy can still have a promising outcome. Patient Consent Disclosure Statement: The author(s) attests that consent has been obtained from any patient(s) appearing in this publication. If the individual may be identifiable, the author(s) has included a statement of release or other written form of approval from the patient(s) with this submission for publication.

A broadly known method to stimulate the growth potential of axons is to elevate intracellular levels of cAMP, however the cellular pathway(s) that mediate this are not known. Here we identify the Dual Leucine-zipper Kinase (DLK, Wnd in Drosophila) as a critical target and effector of cAMP in injured axons. DLK/Wnd is thought to function as an injury ‘sensor’, as it becomes activated after axonal damage. Our findings in both Drosophila and mammalian neurons indicate that the cAMP effector kinase PKA is a conserved and direct upstream activator of Wnd/DLK. PKA is required for the induction of Wnd signaling in injured axons, and DLK is essential for the regenerative effects of cAMP in mammalian DRG neurons. These findings link two important mediators of responses to axonal injury, DLK/Wnd and cAMP/PKA, into a unified and evolutionarily conserved molecular pathway for stimulating the regenerative potential of injured axons.