Concisely describes the regulation of bone remodeling in detail.
Welcome my friends to another path oh video today we continue our discussion on the regulation of bone remodeling using the knowledge obtained about the regulation of the bmu in the last video scientists decided to develop a monoclonal antibody that acts very similarly to opg if it acts like o pg hopefully you understand that it would favor bone retention this
Antibody is called denosumab or prolia and has been approved for treatment of postmenopausal osteoporosis it is given subcutaneously every six months denosumab reduces the risk of both vertebral and non vertebral fractures remember that the interaction of ranked l and ranked results in the production of osteo class let’s show how prolia works prolia blocks the
Rank l rank interaction to prevent the formation of osteo class less osteo class means less bone breakdown during prolia treatment it is important to monitor the patient’s calcium levels since prolia can cause hypocalcemia calcium levels in the blood and extracellular fluid can affect neurons permeability of sodium calcium will bind to sodium channels and keep
Them closed since prolia causes hypocalcemia calcium levels will be lower so more sodium channels will be open more sodium goes from high to low entering the cell to cause depolarization and greater frequency of action potentials if calcium levels are low enough conditions of excitation like prestigious muscle twitching and laryngeal spasms may occur due to the
Rapid turnover rate of the jawbone prolia treatment increases the risk for something called osteonecrosis of the jaw or the jaw bone begins to deteriorate for this reason it is important to assess dental status on a regular interval it is also important to regularly assess for signs of infection because prolia treatment may lead to neutropenia another important drug
That regulates the activities of the b mu is known as teriparatide or for tail this drug is a recombinant pth and is indicated for the treatment of osteoporosis and glucocorticoid induced osteoporosis but wait i thought earlier we mentioned that pth causes breakdown of bone matrix well it was discovered that a pth is given in low intermittent doses like once a day
For tail has the opposite effect or it has an anabolic effect on bone it does this by increasing the numbers of osteoblasts and inhibiting their apoptosis it is unclear why low intermittent levels of pth and high sustained levels of pth have the opposite effect forteo tends to cause hypercalcemia so it’s important to monitor for nausea and vomiting constipation
Lethargy and muscle weakness let’s review why hypercalcemia tends to slow system’s down remember that calcium will bind to sodium channels and keep them closed since forteo causes hypercalcemia calcium levels will be higher in the ecf so more sodium channels will be closed since less sodium can enter the cell the neurons will become more hyperpolarized and send
A lower frequency of action potentials this brings about conditions of less activation like constipation lethargy and muscle weakness the pair of follicular cells of the thyroid gland secrete a hormone called calcitonin which helps helps calcium be retained in the bone drug formulations of this hormone have been developed that are used to treat osteoporosis this
Drug may be administered by nasal spray or it may be injected another drug known as raloxifene or avista used for breast cancer prophylaxis in postmenopausal women with osteoporosis it acts like estrogen in regards to bone and remember estrogen acts to increase osteoblast activity over osteoclast activity favoring bone formation this drug is a selective estrogen
Receptor modifier or cirm this indicates that it has favorable effects on bone but will decrease the risk of uterus and breast cancers however it should be noted that this drug will increase the risk for venous thromboembolism does this concludes our video on bone regulation thanks for watching
Transcribed from video
Bone Regulation Part 2 By PhysioPathoPharmaco