Connective Tissue III Flashcards
What are the two steps of long bone formation?
Long bones form at the diaphysis at the primary ossification center. A second ossification center eventually arises in one or both of the epiphyses, thus there is an invasion of osteoclasts in the epiphyses.
How do bones continue to grow in length after ossification?
The epiphyseal growth plate is cartilage that persists through childhood. Chondrocytes proliferate in lines that are parallel to the length of the bone, and the epiphyseal plate grows by interstitial growth. The length of the bone is driven by proliferation of chondrocytes. The process of chondrocyte proliferation must be carefully controlled to ensure both the rate and orientation of cell division is correct.
What is the consequence of a fracture that separates the epiphyseal growth plate from the rest of the bone?
The epiphyseal growth plate will die and bone growth will cease. These fractures must be surgically repaired quickly.
How do long bones grow in width after ossification?
Appositional growth may continue at the surface through proliferation of osteoprogenitors at the surface. These give rise to osteoblasts which create more bone material at the perichondrial surface.
What are the basic principles governing the relationship of osteoblasts and osteoclasts?
Osteoblasts and osteoclasts both stimulate and inhibit each other. This is controlled in both time and space, so at different times or locations, one activity may be encouraged and the other inhibited, and vis versa. Controlled by environmental conditions, stress conditions, hormone levels, etc.
What is an osteon and how are they formed?
An osteon is a unit of compact bone with a central channel containing blood vessels and a series of concentric rings of compact bone formed around it. They are formed through bone remodeling by osteoclasts and careful timing of osteoprogenitors to lay down new bone. They are generally found in the outermost regions of the bone.
What are the two different surfaces of bone?
The periosteum outside the bone and the endosteum inside the bone. They have the same cell makeup, but different relative acitivities of the osteoblasts and osteoclasts determined the structure of these types of bone. High osteoblast/clast activity forms the endosteum and low osteoblast/clast activity forms the periosteum.
Why does the majority of Ca2+ come from the endosteum?
The woven (or trabecular) structure of the endosteum provides greatly increased surface area for the exchange of Ca2+.
What are short range signals in bone remodeling?
Short range signaling - polypeptide growth factor/morphogens that directly control the activity of bone and cartilage cells. Wnt & TGF-beta. TGF-beta include bone morphogenetic proteins (BMPs), which are protein ligands that bind to cell surface receptors and trigger protein kinase cascades, altering gene expression.
What does the disease FOP result from and cause?
A tranlocation of BMP4 to a lymphocyte resulting in over expression. FOP leads to bony formations in loose connective tissues. Likely due to ectopic expression of BMP4 in connective tissues leading to MSC/osteoprogenitor initiation of osteoblast lineage.
What are the hormones that cause long range signaling of bone remodeling?
Long range signaling - blood borne hormones that control bone metabolism, including calcitonin (increases calcium deposition), parathyroid hormone (increases calcium mobilization, but can also promote calcium deposition) and steroid hormones. Secreted into the blood by endocrine glands
Two non-chemical methods of signaling bone remodeling.
Nerve activity - parasympathetic innervation of bones can manipulate bone remodeling, but the mechanism are not well known.
Mechanical stress - use of bones and muscle tension on bones alters bone metabolism. Even gravity has an affect on bone metabolism. There must be stretch receptors present to trigger short range morphogenetic signaling pathways.
What is a major disease that affects the coupled remodeling sequence of osteoblasts and osteoclasts?
Osteoporosis causes bones to become increasingly fragile and thinner. Bone deposition is decreasing, thus either osteoclast activity must be increased or osteoblast activity must be inhibited. Osteopetrosus is a disease that leads to excessive bone thickening and also causes fragility of bone structures. Osteomalacia, a disease that results from a failure to properly mineralize bone, likely due to problems in the vesicles that deliver calcium phosphatases
