BONE PAIN MARY JO K. VOELPEL, DO, FACOI, FACNM
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1 BONE PAIN MARY JO K. VOELPEL, DO, FACOI, FACNM
2 LEARNING OBJECTIVES REVIEW THE CAUSES OF BONE PAIN REVIEW PATHOPHYSIOLOGY REVIEW MECHANISMS S REVIEW TREATMENT OPTIONS LOOK TO THE FUTURE
3 LEARNING OBJECTIVES REVIEW BRIEFLY THE CAUSES OF BONE PAIN REVIEW PATHOPHSIOLOGY REVIEW MECHANISMS S REVIEW TREATMENTS LOOK TO THE FUTURE
4 CAUSES OF BONE PAIN ARTHRITIC CONDITIONS PAGET S DISEASE SC SICKLE CELL DISEASE S BONE CANCER
5
6 Bone remodeling replaces approximately 20% of bone tissue annually. This remodeling occurs in 5 cycles with each cycle lasting 4 8 months. All of the above conditions impact this process in one or more cycles.
7 PATHOPHSIOLOGY BONE PAIN ORIGINATES FROM THE PERIOSTEUM LINING BONES AS WELL AS FROM THE BONE MARROW THAT RELAY NOCICEPTIVE SIGNALS TO THE BRAIN CREATING THE SENSATION OF PAIN. BONE TISSUE IS INNERVATED BY BOTH MYELINATED AND UNMYELINATED SENSORY NEURONS.
8 MECHANISMS OF PAIN BONE CANCER IS ONE OF THE MOST DREADED SERIOUS FORMS OF PAIN CREATED BY DESTRUCTION OF BONE TISSUE BY MALIGNANT CELLS AS WELL AS MANY CHEMICAL REACTIONS INDUCING INFLAMMATORY RESPONSES AND TRIGGERING SIGNALS VIA THE SPINAL CORD. INFLAMMATORY LIPIDS (PROSTAGLANDINS) ACTIVATENOCICEPTORS WITHINTHEBONE THE BONE.
9 RANK LIGAND THE RANK LIGAND PLAYS A ROLE IN BONE LOSS DUE TO OSTEOPOROSIS AND DESTRUCTIVE CHANGES DUETO CANCER BY AFFECTING THE WAY IN WHICH OSTEOPROTEGERIN (OPG) BALANCES BONE GROWTH AND LOSS
10 ORIGINS OF BONE CANCER PAIN SENSORY AND SYMPATHETIC INNERVATION OF THE BONES WAS PREVIOUSLY NOT WELL DELINEATED DUE TO HARSH PROCESSING TECHNIQUES INVOLVING FORMALDEHYDE. In the 1960s we began using more sphisticated preservative agents such as gluteraldehyde that preserved the delicate neuron structures within the bone and bone marrow enabling us to begin to look at mechanisms of pain.
11 INITIALLY LOOKING AT ANIMAL MODELS IDENTIFIED NEURAL FIBERS TRAVELING WITH BLOOD VESSELS VIA THE HAVERSIAN AND VOLKMANNS CANALS AND LOCATING THE PATTERNS OF INNERVATION IN THE PERIOSTEUM, MINERALIZED BONE AND BONE MAROW CAVITY. Mach, et al, Sensory and sympathetic innervation y y p of the mouse femur, Neuroscience,113, p
12 MOLECULAR MECHANISMS OF PAIN Pain is the first presenting sign of cancer in over 50% of patients. The mechanisms can be due to pathologic fractures, hypercalcemia, and direct invasion with malignant cells. Glial cells in the CNS such as astrocytes can increas e responsiveness of pain transmission to neurons in the spinal cord and increase pain sensation see diagram
13 CANNABOID RECEPTORS Localization of cannaboid receptors within the superficial dorsal horn of the spinal cord has led to evaluations of alleviation of bone cancer pain via the CB1 activation. Pain can be evoked by movement or just spontaneous. Activation of the cannaboid receptors reduced bone caner related related behaviors that included movement related and not. Minimizing the inflammatory response was crucial.
14 NEWER CONCEPT IN PAIN MANAGEMENT We as osteopathic physicians have always been sensitive to musculoskeletal responses to pain and its effect on controlling pain. Microcurrent electrotherapy has been available for over 50 years, but recently studies have identifedif d benefits in pain management that would complement manipulatin and effectively control pain via reduction of inflammatory substances and breaking thespasm cycle
15 References published in 2004 and 2010 by Carolyn Mcmakin, et al. in Journal of Bodyworkand Movement Therapies have brought attention to the decrease in inflammatory cytokines associated with pain and improvement in sensations of pain that merit a second look at how we approach pain safely and effectively as we move into the next generation of pain management
16 QUESTIONS AND SUMMARY
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