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The precise limits of Mysia are difficult to assign. The Phrygian frontier was fluctuating, while in the northwest the Troad was only sometimes included in Mysia. [1] The northern portion was known as "Lesser Phrygia" or (Ancient Greek: μικρὰ Φρυγία, romanized: mikra Phrygia; Latin: Phrygia Minor), while the southern was called "Greater Phrygia" or "Pergamene Phrygia".
In the skeletal muscles connected to tendons that pull on bones, the mysia fuses to the periosteum that coats the bone. Contraction of the muscle will transfer to the mysia, then the tendon and the periosteum before causing the bone to move. The mysia also may bind to an aponeurosis or to fascia. [2]
The periosteum is a membrane that covers the outer surface of all bones, [1] except at the articular surfaces (i.e. the parts within a joint space) of long bones. (At the joints of long bones the bone's outer surface is lined with "articular cartilage", a type of hyaline cartilage .)
The periosteum is formed around the trabeculae by differentiating mesenchymal cells. The primary center of ossification is the area where bone growth occurs between the periosteum and the bone. Osteogenic cells that originate from the periosteum increase appositional growth and a bone collar is formed.
p. Fibrous layer of the periosteum. o. Layer of osteoblasts. im. Subperiosteal bony deposit. There are two types of ossification centers – primary and secondary. A primary ossification center is the first area of a bone to start ossifying. It usually appears during prenatal development in the central part of each developing bone.
Mysians / ˈ m iː ʒ ə n z, ˈ m ɪ ʒ ə n z / (Latin: Mysi; Ancient Greek: Μυσοί, Mysoí) were the inhabitants of Mysia, a region in northwestern Asia Minor. Origins according to ancient authors
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Periostin plays a critical role in the development of cardiac valves and in degenerative valvular heart disease.While periostin usually is localized to the subendothelial layer in healthy heart valves, its levels are highly increased in infiltrated inflammatory cells and myofibroblasts in angiogenic areas in atherosclerotic and rheumatic valvular heart disease in humans.