Orthopedic soft tissues

• The ACL consists of two bundles: the Posterior-lateral (PL) bundle, located on the posterior lateral aspect of the tibia plateau, and the Anterior-medial (AM) bundle, located on the anterior lateral aspect of the tibia plateau.
• With cessation growth, formation of apophyseal ring via mineralization of CEP over outer annulus fibrosus.
• In extension, the AM and PL bundles are parallel and fairly under high tension, both contributing to limiting hyperextension.
• In flexion, the AM and PL bundles are twisted, X-shaped, and the femoral insertions are horizontally aligned, providing anterior stability.
• The ACL prevents hyperextension, internal rotation of tibia relative to femur and provides anterior stability, so translating the tibia relative to the femur in the anterior direction.
• In terms of hyperextension, both bundles contribute, with the AM and PL bundle both contributing in parallel and fairly under high tension.
• In anterior stability, the AM bundle provides a lot of stability in flexion and also a lot of stability in extension, although a bit less than in flexion.
• The PL bundle hardly provides stability in flexion as in flexion this bundle is almost running vertically.
• In extension, the PL bundle provides stability.
• The ACL prevents internal rotation of tibia relative to femur and provides rotational stability, with the AM and PL bundle both contributing.
• The AM and PL bundle are tensed when providing a lot of stability and not tensed when providing no stability.
• The ACL contains fibroblast type of cells and is embedded with synovial fluid of the knee, which contains synovial fibroblasts.
• Mesenchymal type of cell can be found in the ACL that upon micro damage or rupture can proliferate and contribute to the healing of this tissue.
• The ACL contains at least one cell type, which is the ACL fibroblastic cell type, aligning with the collagen matrix.
• A collagen fiber has a wavy crimped morphology, and the ACL cells are stacked end to end, matching the wavy collagen morphology.
• The cells are star like shaped, with long cell extensions which fills the void in between the matrix surrounding them and can be used to either have contact with other cells but are mainly used to fetch nutrients in an almost avascular tissue.
• There are different communication pathways in the ACL: focal adhesion mediated, where cells connect to environment and focal adhesion complexes provide signalling to cells what is happening, soluble factors from the surroundings can signal to the cells, and ECM ligands is related to the focal adhesion mediated signalling.
• On the cell membrane are stretch activated ion channels; Ca2+ mediated signalling, where when applying stretch to tissue you also apply stretch to cells so the stretch activated ion channels are stimulated whereby calcium signalling is mediated.
• When stretching tissue you stretch cells and then also the nucleus, nuclear deformation is a very strong cue for signalling.
• Cartilage will be maintained where you have low hydrostatic stress and low principal strain, bone is formed where you have high hydrostatic stress and low principal strain.
• The growth of the bone takes place in the epiphyseal growth plate and then a certain part of that plate turns into bone.
• Formation of a joint cavity occurs on day 17.5 of embryonic development.
• Both strain and formation of a joint line inhibit GDF-5, causing preservation of the chondrocyte phenotype and prevention of joint cavity formation if a joint is immobilized.
• Strain rate affects the behavior of tissue, causing it to behave stiffer as the rate increases.
• Mesenchyme condensation turns into cartilage at the center of cartilage, where hypertrophic chondrocytes form and induce angiogenesis, bringing in osteoblasts to make bone, the primary center of ossification.
• Interfiber sliding is important for viscoelasticity, as the amount of strain in a fiber is lower than the total strain in the tissue due to interfiber sliding.
• Collagen fibers are viscoelastic contributors, it takes time for them to elongate and for the gap regions to increase.
• Mesenchymal condensation leads to the formation of chondrocytes or fibroblast, which can form cartilage and connective tissue.
• HA synthesis in the cavity causes swelling, which separates cells if they are not connected.
• After initial primary center of ossification, bone grows towards both ends, forming secondary centers of ossification.
• Different structures, such as fibula tibia and femur, become visible on day 15 of embryonic development.
• Bone grows through the epiphyseal plate when born, we have two cartilage parts: Articular cartilage and Remains.
• The epiphyseal growth plate, a plate of cartilage, forms between primary and secondary ossification and is responsible for growth of bone.
• Joint formation occurs during embryonal development and it continues to grow as we grow into adults.
• Secondary ossification starts at the center of cartilage due to loading.
• The meniscus becomes visible on day 16.5 of embryonic development.
• Apoptosis of a few cells in the cavity causes a connection between cells to be lost.
• Wnt’s in the joint region stimulate Sox9 and inhibit Noggin, leading to interzone formation and new joint formation at a distance where active Noggin protein concentration recovers from the inhibitory signals from the previously formed interzone.
• Sliding, a reduction of the stress concentration, is a time-dependent effect that needs more time the faster you elongate the tissue.
• If strain rate is very low, only the elastic response of material is observed.