EPI 390 Lecture 9Outline of Last Lecture I. Metadata analysis and Retrospective studiesII. Osteoporosis vs. OsteoarthritisIII. Ethics of PharmacologyIV. Osseointegration Outline of Current Lecture I. Epiphyseal Plate and bone growtha. Hydroxyapatite bone tissueb. RicketsII. Osteoporosis model a. Effect of puberty on bone healthb. Effect of Menopause on bone healthc. Growth curvesd. Common sites for fragility fracturesIII. Comparing bone cellsIV. Osteoporosis preventionV. Pott’s diseaseCurrent LectureLecture 9 (February 13, 2014)I. Epiphyseal Plate and bone growtha. The epiphyseal plate is one of 3 main growth plates in the bones that are used to incorporate new bone mass into growing bones. b. Main role is bone elongation, particularly in long bones (i.e. the tibia).c. Typically works in small children and growing adolescents; by adulthood, once growth has slowed or stopped, it has transformed into the epiphyseal line.d. Longitudinal bone growth is the primary determinant for the amount of bone minerals available in the reservoire. Hydroxyapatite bone tissuei. Hydroxyapatite is a form of calcium apatite that makes up 70% of bones. Some individuals/groups (based on ethnicity, age, gender, etc.) are more prone to depleting the reservoirs of this mineralf. RicketsThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.i. A disease in small, growing children predominantly, that is characterized by poorly mineralized bone, so they are highly prone to fragility fracture.ii. The weight bearing bones (i.e. femurs) are particularly prone to fragility fracture.iii. Lifestyle factors (i.e. insufficient dietary calcium and lack of physical activity) can influence incidence of Ricketsiv. Increased urbanization led to an increase in Rickets; this was due to the increased pollution and decrease in exposure to vitamin D (from tall buildings as well as the smog)1. There was also less room to move around, and poverty conditions prevented sufficient dietary fulfillment.II. Osteoporosis model a. Peak Bone growth – The amount of bone tissue present at the end of skeletal maturation and growth.i. This definition is slightly controversial due to the fact that men and women measure different peak bone mass, which leads to the misconception that women have less BMD. 1. This is not necessarily true because men tend to have a higher peak bone mass due to the fact that they are larger. Proportional to size, though, men and women typically have a similar reservoir of bone tissue available. b. Effect of puberty on bone healthi. Adolescence represents another spurt in skeletal growth, and is essentially the end of the growth period in which bone minerals can still be added to the reservoir.c. Effect of Menopause on bone healthi. Menopausal and postmenopausal women are more prone to loss of BMD due to the change in hormones. Skeletal growth has already ceased, so there is no means of replenishing the reservoir of bone minerals.d. Growth curvesi. The Classic Osteoporosis Model for men and women1. Bone mass increases through adolescence until the epiphyseal plates close, around age 20, and the peak bone mass are reached, around age 30. From there, bone mass gradually decreases as the individual ages (the older an individual is, the faster the decrease in BMD occurs)2. As BMD decreases, the bones become more porous and thin out. The fragility leads to more susceptibility to fractures, particularly in weight bearing bones and key fracture sites.3. The corticular and trabecular portions of the bone undergo thinning in aged men and women (in women this occurs around menopause. It is slightly delayed in men).ii. In common growth curves, you can see that bone mass increases from birth to approximately age 30, where BMD begins to decrease in an arc.iii. A negative growth velocity is experienced post-natal (the fastest growth period) until approximately 5 years of age. A mid growth is then experienced during the toddler stage before the decline in velocity beginsagain. At approximately 13 years of age, the onset of puberty, a sharp spike in growth velocity is experienced – the adolescent growth spurt. Growth velocity then continues until epiphyseal plate closure at 20 years of age, when the velocity levels out and ceases.e. Common sites for fragility fracturesi. Regions of interest – sites typically surveyed for signs of osteoporosis and fragility fracture – are the neck of the femur (near the ball and socket joint of the hip), the cortical bone, and other locations of the epiphyseal plate (i.e. knees, ankles, the shoulder joint)ii. These tend to be weight-bearing areas and so are more susceptible to fracture with BMD loss. They are also points of growth that, if insufficient bone minerals were incorporated, could be weakened.III. Comparing bone cellsa. Osteocytes – are considered to be “true” bone cells. They reside in mature bonesand are typically inerti. May on occasion be involved in synthesis and modification.b. Osteoblasts – Involved in bone growth and repair. Differentiate from osteocytes.i. It is expected that osteoblasts will be more active in individuals who have yet to reach epiphyseal plate closure and are still undergoing skeletal growth.c. Osteoclasts – involved in bone demineralization; contain lysosomes.i. Osteoclasts are more likely to be active in individuals with fragility fractures, and in adults 20 years and older.IV. Osteoporosis preventiona. Optimization of Peak Bone Massi. Exercise to maintain bone strength, particularly during adolescenceii. Incorporation of dietary calcium; ensuring proper dietary nutrition during adolescence to allow the reservoir to be filled.b. Reduce rate of bone lossi. Hormone replacement therapy (not always an ideal or pleasant treatmentfor post-menopausal women who have already suffered through hormone fluxes; i.e. with hot flashes)ii. Moderate alcohol intakeiii. Stop smokingiv. Potential benefits from limiting intake of caffeine, sodas, and the effects of depression (through monitoring hypercorticoidism and the adrenal gland pathway).V. Pott’s diseasea. Pott’s disease is spinal tuberculosis that results in spinal cord compression and deformity. The common location is the thoracic region of the spine.i. The disease manifests itself in spinal compression, pain, leg weakness, and a palpable mass. Paraplegia is also a risk if left untreated.b. Risk