Stereophotogrammetric surface anatomy of the anterior cruciate ligament's tibial footprint: Precise osseous structure and distances to arthroscopically-relevant landmarks.

BACKGROUND: While femoral tunnel malposition is widely recognized as the main technical error of failed anterior cruciate ligament (ACL) surgery, tibial tunnel malposition is likely underrecognized and underappreciated. PURPOSE: To describe more precisely the qualitative and quantitative anatomy of the ACL's tibial attachment in vitro using widely available technology for stereophotogrammetric surface reconstruction, and to test its applicability in vivo. METHODS: Stereophotogrammetric surface reconstruction was obtained from fourteen proximal tibias of cadaver donors. Measurements of areas and distances from the center of the ACL footprint and the footprint of the obtained bundles to selected arthroscopically-relevant anatomic landmarks were carried out using a three-dimensional design software program, and means and 95% confidence intervals were calculated for these measurements. Reference landmarks were tested in three-dimensional models obtained with arthroscopic videos. MAIN FINDINGS: The osseous footprint of the ACL was described in detail, including its precise elevated limits, size, and shape, with its elevation pattern described as a quarter-turn-staircase-like ridge. Its internal indentations were related to inter-spaces identified as bundle divisions. Distances from the footprint center to arthroscopically relevant landmarks were obtained and compared to its internal structure, yielding a useful X-like landmark pointing to the most accurate placeholder for the ACL footprint's "anatomic" center. Certain structures and reference landmarks described were readily recognized in three-dimensional models from arthroscopic videos. CONCLUSIONS: Stereophotogrammetric surface reconstruction is an accessible technique for the investigation of anatomic structures in vitro, offering a detailed three-dimensional depiction of the ACL's osseous footprint.

Activin/TGFbeta and BMP crosstalk determines digit chondrogenesis.

The progress zone (PZ) is a specialized area at the distal margin of the developing limb where mesodermal cells are kept in proliferation and undifferentiated, allowing limb outgrowth. At stages of digit morphogenesis the PZ cells can undergo two possible fates, either aggregate initiating chondrogenic differentiation to configure the digit blastemas, or to die by apoptosis if they are incorporated in the interdigital mesenchyme. While both processes are controlled by bone morphogenetic proteins (BMPs) the molecular basis for such contrasting differential behavior of the autopodial mesoderm remains unknown. Here we show that a well-defined crescent domain of high BMP activity located at the tip of the forming digits, which we termed the digit crescent (DC), directs incorporation and differentiation of the PZ mesenchymal cells into the digit aggregates. The presence of this domain does not correlate with an exclusive expression domain of BMP receptors and its abrogation by surgical approaches or by local application of BMP antagonists is followed by digit truncation and cell death. We further show that establishment of the DC is directed by Activin/TGFbeta signaling, which inhibits Smad 6 and Bambi, two specific BMP antagonists expressed in the interdigits and progress zone mesoderm. The interaction between Activin/TGFbeta and BMP pathways at the level of DC promotes the expression of the chondrogenic factor SOX9 accompanied by a local decrease in cell proliferation. Characteristically, the DC domain is asymmetric, it being extended towards the posterior interdigit. The presence of the DC is transitorily dependent of the adjacent posterior interdigit and its maintenance requires also the integrity of the AER.

Tendon-muscle crosstalk controls muscle bellies morphogenesis, which is mediated by cell death and retinoic acid signaling.

Vertebrate muscle morphogenesis is a complex developmental process, which remains quite yet unexplored at cellular and molecular level. In this work, we have found that sculpturing programmed cell death is a key morphogenetic process responsible for the formation of individual foot muscles in the developing avian limb. Muscle fibers are produced in excess in the precursor dorsal and ventral muscle masses of the limb bud and myofibers lacking junctions with digital tendons are eliminated via apoptosis. Microsurgical experiments to isolate the developing muscles from their specific tendons are consistent with a role for tendons in regulating survival of myogenic cells. Analysis of the expression of Raldh2 and local treatments with retinoic acid indicate that this signaling pathway mediates apoptosis in myogenic cells, appearing also involved in tendon maturation. Retinoic acid inhibition experiments led to defects in muscle belly segmentation and myotendinous junction formation. It is proposed that heterogeneous local distribution of retinoids controlled through Raldh2 and Cyp26A1 is responsible for matching the fleshy and the tendinous components of each muscle belly.