After conception, specialized cells develop into embryonic bones.   At sixteen pre-natal weeks, embryos have completely formed skeletons composed only of connective tissue and cartilage.   During vaginal childbirth and toddler falls, this pliable connective tissue and cartilage bones readily resist physiological breakdowns (injuries).   However, skeletal pliability decreases the effectiveness of muscle contractions.   Therefore, from embryo to adult, ossification centers develop that convert these connective tissue and/or cartilage pliable bones to mineralized rigid adult bones.

     Embryonic ossification centers form when fibroblasts and osteoblasts congregate in their genetically determined locations.   Fibroblasts manufacture new collagenous fibers and osteoblasts manufacture bone.   Fibroblasts cover the surfaces of the ossification centers with thick fibrous membranes (perichondrium) and osteoblasts convert this perichondrium to bone tissue.   This new bone tissue cements the collagenous fibers together.

     Osteoblasts also continually produce into new osteoblasts.   When osteoblasts add bone to the free ends of ossification centers, bones lengthen.   When osteoblasts add bone at right angles of ossification centers, bones widen.   In these ways, new bone tissue continuously expands to gradually convert the connective tissue and cartilage of embryonic bones to mineralized adult bones.

     Connective tissue bones are called 'membrane' bones.   The brain vault, facial skeleton and parts of the clavicle and mandible are membrane bones.   During embryonic growth and development, membrane bones develop centralized fibro-cellular proliferations.   From these centralized centers, osteoblasts lay down new bone.

     While membranous bones interstitially grow to adult size, intra-membranous centers increasingly convert connective tissue and cartilage to mineralized bone.   After mineralized bone fills the margins of membranous bones, osteoblasts continue to lay down new bone at their free surfaces (sutures).   Adjoining suture lines continue to enlarge membrane bones to adult size by 'appositional bone growth.' Appositional bone growth occurs wherever two ossifying bone surfaces contact.   When osteoblasts completely ossify across suture lines, skulls cease enlarging.

     Embryonic clavicle and mandible membranous bones contain both connective tissue and cartilage.   Consequently, intra-membranous ossification first converts the connective tissue to new bone, then intra-cartilaginous ossification converts the cartilage to new bone.

     Axial bones, such as the vertebral column and rib bones, and the appendicular bones for the arms and legs are cartilage bones.   In cartilage bone, osteoclasts resorb the cartilage while the osteoblasts lay down new bone.

     Fibroblasts and osteoblasts congregate in middles of embryonic cartilage bones to form the ‘diaphysial’ ossification centers.   At diaphysial ossification centers, osteoclasts resorb the cartilage and the osteoblasts lay down new bone starting at mid-shaft and extending toward both ends of the length of the bones.

     Fibroblasts and osteoblasts also congregate at the ends of long bones and at specialized muscle attachment locations.   These ossification centers are ‘epiphysial’ centers.   With two femur and one tibia exceptions, epiphysial centers develop after childbirth and some do not appear until puberty.

     The surface of the epiphysial centers that face the ends of the bones are the ‘articular’ surfaces.   Cells that manufacture articular cartilage are the ‘chondrocytes’.   Chondrocytes produce hyaline cartilage.   Hyaline cartilage never mineralizes.   When mineralized bone development approaches hyaline cartilage, the growth of the bone’s length stops.

     The surface of the epiphysial centers that face the encroaching diaphysial centers from the center of long bones are the ‘metaphysial’ surfaces.   Growth cartilage separates diaphysial centers from epiphysial centers.   Long bone growth occurs at these metaphysial plates.   The proximal metaphysial plates contribute more to long bone growth than the distal metaphysial plates.

     During the early adolescence rapid bone growth spurt, metaphysial plates thicken considerably.   During the decreasing rate of bone growth in later adolescence, osteoblasts gradually encase the fibroblasts until their supply of perichondrium which they convert to mineralized bone exhausts.   After the metaphysial plates completely convert all cartilage to mineralized bone, the epiphysial trabeculae become contiguous with the diaphysial trabeculae.   At this point, the completely mineralized bones have achieved their adult length.

     Traction, compression and leverage stresses stimulate osteoblastic activity to lay down new bone tissue.

     Traction stress occurs when muscle contractions powerfully pull on their attachments to the two bones.   When muscles attach to broad bone areas, the traction stress spreads evenly across the attachment.   When tendons attach to small bone areas, the traction stress focuses on the small areas.   To strengthen muscle attachments against more powerful actions, osteoblasts lay down more new bone.

     Metaphysial growth also occurs where tendons attach to bones.   Because muscles exert their greatest mechanical stress at angles to bone's longitudinal axes, new bone grows laterally from central shafts.   The directions and severities of mechanical stresses determine the directions and amounts of lateral bone growth.   Traction epiphyses are epiphysial centers to which muscles attach.

     Traction stress causes a common adolescent ailment, ‘Osgood Schlatter's disease’.   Osgood Schlatters occurs where the tendon of the four muscles that comprise the 'quadriceps' muscle attaches to the tibial tuberosity epiphysis on the proximal, anterior surface of the tibia.   During early adolescent rapid skeletal growth and development, running and jumping activities can overly stress this tibial tuberosity epiphysis.   Because physicians fear that future strong muscle contractions might pull the tibial tuberosity epiphysis away from the tibia, they prescribe inactivity until additional osteoblastic bone growth strengthens the tuberosity.

     In baseball pitching, traction stress occurs when the five muscles that attach to the medial epicondyle ossification center operate during the forearm acceleration phase of baseball pitching.   Far too frequently, young men pitching competitively pull their medial epicondyle ossification center away from the shaft of their humerus.   This injury irreparably damages the pitching elbow.   This injury alters the groove through which the ulnar nerve travels behind the medial epicondyle.   Chapter 8 contains an example of an unfortunate young pitcher who permanently destroyed his medial epicondyle for baseball pitching.

     Compression epiphyses are the epiphysial centers at ends of bones that withstand mechanical stresses.   When we stand, compression stresses impact the ends of the bones that support body weight.   When we run or jump, we increase compression stresses across joints.   When we hold barbells over our heads, compression stresses traverse across the arm joints.   To withstand increased compression stresses, osteoblasts lay down new bone and osteoclasts create Haversian Canals beneath the articular surfaces.   Haversian Canals strengthen bones against compression stresses.   Compression stresses also influence metaphysial width.   Metaphysial widths determine articular joint widths.

     In baseball pitching, compression stress occurs when the radius bone recoils back against the Capitular surface of the distal end of the humerus at the end of the deceleration phase and start of the recovery phase.   Chapter 8 contains an example of an unfortunate young pitcher who had to have the proximal end of his radius bone removed due to the damage caused by this compression stress.

     When athletes apply force with their long bone ends, they generate leverage stresses in these mid-shafts.   For example, kicking soccer balls leverage stresses the tibial (lower leg) mid-shaft.   To prevent injury, osteoblasts lay down thicker mid-shaft bone matrix.   Because adolescent long bones undergo rapid bone growth spurts, osteoblastic and osteoclastic activities occur at accelerated rates.   Therefore, leverage stresses alter the long bone mid-shafts of adolescents.   For example, adolescent ballet dancers develop curved leg long bone mid-shafts.

     In baseball pitching, leverage stress occurs when pitchers inwardly rotate their humerus bone.   Just recently, a major league pitcher with the Tampa Bay Devil Rays snapped his humerus bone with a pitch during a game. Because adolescent bones have not completely ossified, they are somewhat more pliable than adult bones.   Consequently, adolescent baseball pitchers do not have the same susceptibility to this injury as adult baseball pitchers.

     Adult bones do not lengthen.   Adult bones have fully mineralized.   Adult bones provide solid foundations from which muscles apply force.   Nevertheless, adult bones replenish and respond to mechanical stresses.  

     In long adult bones, spongy bone tissues make up their proximal and distal ends.   Networks of interlacing bone columns (trabeculae) enclose the small multi-sided fatty marrow spaces in spongy bone tissue.   Parallel bone threads occupy these between trabeculae spaces.   Spongy bone tissues fill the marrow space beneath bones’ articular surfaces.   These spongy bone tissues effectively dampen mechanical stress shocks that transfer across articular surfaces.   Strategically located strut-like Haversian Canals also dampen and disperse mechanical stress shocks across joints’ large cross-sectional areas.  

     Compact bone tissues make up long bone shafts.   Compact bone tissues develop from spongy bone tissues.   However, compact bone tissues become much more rigid than spongy bone tissues.   Compact bone tissues surround the marrow canals in long bone shafts.   In bone cortexes, thin bone sheets (lamellae) arrange in cylindrical layers and group around narrow axial marrow canals.   Marrow canals contain blood vessels and some loose connective tissues.  

     Adult bone cortexes have three segments.   The external-most segment (periosteum) has three layers.   From outside to inside, the periosteum contains layers of fibroblast, pre-osteoblast and osteoblast bone cells.   The middle segment constantly regenerates mineralized bone tissues (MBT).   This regenerating layer contains osteoblasts, osteocytes, osteoclasts and Haversian Canals.   The internal-most segment (endosteum) is the bone’s axial canal.   The endosteum contains osteoclasts and pre-osteoclasts.  

     Muscles that arise from bones blend with the periosteum’s fibroblastic layer.   Although fibroblasts have rich blood vessel and nerve supplies, fibroblasts very slowly add new collagenous fibers to bones’ surfaces.   Fibroblasts are protein fibers with the same organic composition as bone, but without the mineral content that hardens protein fibers into mineralized adult bones.   Throughout adulthood, fibroblastic layers remain relatively stable.  

     Immediately beneath fibroblastic layers, pre-osteoblastic layers continually produce mature osteoblasts.   New osteoblasts continually replace old osteoblasts that line entire external (periosteal) mineralized bone tissue surfaces.   All along mineralized bone tissue’s irregular contours, osteoblasts stand shoulder to shoulder one cell deep.   Every day, osteoblasts add their own volume of new bone tissue to periosteal surfaces.   Every three days, new osteoblasts push older osteoblasts into mineralized bone tissues and encase them.   New bone tissues continuously push previously added bone tissues toward marrow canal centers.   Consequently, mineralized bone tissues continually regenerate.  

     Encased osteoblasts cannot add new bone tissue.   However, they can transfer nutrients from the periosteum to the new bone tissue that they added to mineralized bone tissues.   Because encased osteoblasts no longer function as bone tissue manufacturing osteoblasts, researchers call them osteocytes.  

     Osteoclasts locate in mineralized bone tissue and on the cortexes’ endosteal surfaces.   Osteoclasts are many times larger than osteoblasts.   Compression mechanical stresses stimulate mineralized bone tissue osteoclasts to resorb appropriately aligned microscopic cylinders (Haversian canals).   Consequently, without increasing bones’ sizes or mineralizations, Haversian Canals strengthen bones against compression mechanical stresses.  

     Endosteal osteoclasts cover forty percent of mineralized bone tissues’ endosteal surfaces.   Osteoclasts resorb mineralized bone tissues.   Osteoclasts are very mobile.   Every eighteen hours, osteoclasts contact entire endosteal surfaces.   Pre-osteoclasts float freely in bones’ marrow canals and mature into osteoclasts.