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1 7/24/214 Glucocorticoid Induced Osteoporosis: A Journey in Trnsltionl Science I hve nothing to disclose Nncy E. Lne, MD, MACP UC Dvis Professor of Medicine nd Rheumtology Director, Center for Musculoskeletl Helth UC Dvis Scrmento, Cliforni Affilited Fculty UCSF Deprtment of Epidemiology nd Biosttistics, Sn Frncisco Cliforni Frctures Are the Most Common Serious Adverse Event User Nonuser Adverse Events (AEs) (112) (112) Frcture 21 (19%) 8 (7%) Ctrct 17 5 Serious Infection 14 4 GI Bleed or Ulcer 11 4 Dibetic Compliction 8 3 Herpes Zoster 8 1 Myocrdil Infrction 4 4 Stroke 6 1 Glucom 1 1 Deth 2 Sg KG. Am J Med. 1994;96:115. Glucocorticoid-Induced Osteoporosis Most common form of secondry osteoporosis Occurs t ny ge, in both sexes nd cross ethnic groups Approximtely 3-5% of ptients sustin osteoporotic frctures Common long-term uses: Pulmonry nd Rheumtologic disorders Inflmmtory bowel disese Orgn trnsplnttion Neurologicl diseses Skin diseses Adinoff et l. NEJM 1983;39: Michel et l. J Rheumtol 1991;18:84-88 Lems t l. Clin Exp Rheumtol 1995;13:

2 7/24/214 MRI of 4 yr. old Femle with SLE on s nd Lterl Spine Xry of 8 yr. old Femle with PMO Rpid BMD Decline Due to Glucocorticoids in Rheumtoid Arthritis % Chnge Lumbr Trbeculr BMD 4 PBO B Weeks Ln, Ann Int Med 1993;119:996 Prednisone Frcture Incidence is Higher in users thn Nonusers t ny given BMD Nonusers Users Nonusers Users Glucocorticoid-Induced Osteoporosis The gretly compressed bodies of the vertebre were so soft they could be cut with knife Lumbr Spine BMD Femorl Neck BMD Hrvey Cushing, 1932 Vn St et l. A&R 23;48:3224 2

3 7/24/214 Purpose of This Investigtion Women on s hd frctures t higher BMDs thn women with postmenopusl osteoporosis Therefore, we hypothesized tht in ddition to trbeculr bone rchitecturl chnges, there must be bone cell vibility nd other loclized chnges tht lter bone mteril properties in treted subjects compred to estrogen deficient women. 2-2 Trbeculr Bone Volume (% chnges from dy ) Dys Excess In Mice Induces Osteopeni b b = p<,1 from dy b= p<.1 from dy 28 nd 56 Dy Dy 28 Dy 56 Yo et l A & R Excess Induces Rpid Increses in Gene Expression Associted with Osteoclst Activtion nd Bone Resorption Chronic Excess Is Associted With Prolonged Suppression Of Bone Formtion Csf1 C-fms Itgb3 Adm CTX-I (ng/ml) P <.5 vs. 24 Osteoclcin (ng/ml) Dy Dy 7 Dy 28 Dy 56 Trem2 Oscr Cy Nftc1 6 D7 D28 D D7 D28 D56 P <.5 vs. Yo et l A & R 3

4 7/24/214 Excess Increses Expressions Of Wnt Signling Inhibitors Elements of Wnt/{bet}-ctenin Signling Yo et l A & R Krishnn, V. et l. J. Clin. Invest. 26;116: Copyright 26 Americn Society for Clinicl Investigtion Bifunctionl role osteoblst (bone-forming cell) nd osteoclst (bone-resorbing cell) differentition. Summry excess 1. Rpid increses in gene expression for osteoclst ctivtion nd bone resorption 2. Prolonged suppression of bone formtion nd it ppers ssocited with incresed expression of Wnt inhibitors (Dkk1, Wif1) 3. Rpid trbeculr bone loss Goldrings Nture Medicine 4

5 7/24/214 Clinicl observtion Hypothesis Ptients with excess frcture t higher BMD tht postmenopusl osteoporosis ptients excess induces deteriortions of bone mteril properties in ddition to decresed bone mss Excess Decreses Elstic Modulus Around The Osteocytes Exmple of Osteocytes within the Bone Mtrix µm OVX 5 µm Position (µm) Mesured by SPM 5

6 7/24/214 Osteocyte Lcuno-Cnliculr System Contct with Cells on the Bone Surfce Excess Increses Osteocytic Gene Expression tht is Associted with the Inhibition Minerliztion nd Bone Formtion LF Bonewld Glucocorticoid Tretment results in Reduction in Elstic Modulus nd minerl round the Osteocyte Lcune from ilic crest biopsy specimen Osteocyte Network: Sclerostin, Which is Secreted by Osteocytes, Negtively Regultes Bone Formtion Mture Osteoblsts New bone X Sclerostin Pre-osteoblst lining cells X Mesenchyml stem cells Scnning Probe Microscopy Atomic Force Microscopy Osteocyte Bone Ott SM. J Clin Endocrinol Metb. 25;9: Semenov M, et l. J Biol Chem. 25;28: Semenov MV, et l. J Biol Chem. 26;281: Li X, et l. J Biol Chem. 25;28:

7 7/24/214 Do Osteocytes Contribute to bone minerl homeostsis? Osteocytic Osteolysis Revisited Osteocytes re buried in mtrix Osteocytes lcune chnge in size with clinicl clcium deficit ( hypophosphotemic rickets, glucocorticoids, during lcttion, prolonged estrogen deficiency) The osteoclst surfce my not be sufficient to mintin clcium blnce There is evidence tht osteocytes cn express MMPs, nd secete them, nd contribute to clcium nd phosphorus homeostsis Lcunr re (µm 2 ) Osteocyte Lcunr Size Increses with Lcttion John Wysolmerski nd Lynd Bonewld Virgin Lctting Lcttion 5 Virgin Lcttion Post Lcttion Lcunr re (µm 2 ) virgin lcttion post lcttion Post- virgin lcttionvirgin lcttion corticl trbeculr Corticl bone Trbeculr bone Width of Cnliculi cnliculr width (µm) Possible Explntion for Trnsient nd Permnent Chnges in Osteocyte Lcune size tht my lter bone qulity in the presence of Glucocorticoids Three Pthwys of Cell Deth Teti & Zllone Bone 28 Hotchkiss R et l. N Engl J Med 29;361:

8 7/24/214 Autophgy: Is there n ssocition with glucocorticoid use nd osteocyte utophgy? Autophgy To et oneself A mjor mechnism for mintining cellulr homeostsis. It is essentil in helping to mintin the blnce between the increse nd decrese in the number of cell popultion. It is ctive t bsl level in most cells nd contributes to the routine turnover of cytoplsmic components Process of Autophgy: Cell s response to Stress nd for Survivl 8

9 7/24/214 Gene Expression for Autophgy nd Apoptosis from Corticl Bone in vivo s Increses Osteocyte Autophgy In Vivo t low doses s Increses Osteocyte Apoptosis in Vivo t high doses Tretment Increses Osteocyte Volume Ji et l, FASEB 211 Mesured by Xtrem µct 9

10 7/24/214 Increses Osteocyte Autophgy In Vitro A GFP-LC3 Inhibition Of Osteocyte Autophgy Decreses Cthepsin K Secretion In Vitro D Con Dex 1-8 M Dex 1-6 M B C 1-8 M 1-7 M 1-5 M Dex 1-6 M % chnges from control GFP-LC M 1-7 M 1-6 M 1-5 M LC3-I LC3-II CtsK β-ctin D Con Dex 1-6 M % chnges from control E Cthepsin K ELISA 1-8 M 1-7 M 1-6 M 1-5 M Ji, FASEB Tretment of osteocytes in vitro with Hydroxychloroquine (CQ)- inhibited utolysosome formtion --3-methyldenine (3-MA) inhibits utophgosome formtion Questions Rised by These Observtions Working Hypothesis Osteocytes in the presence of s pper to be stressed nd some undergo utophgy, nd some of the cells go on to poptosis in dose nd time dependent mnner. There lso ppers to be dose dependent difference between osteocyte utophgy nd poptosis in the corticl bone comprtment which my hve clinicl rmifictions, eg induced osteonecrosis These dt require further investigtion. High Dose s Low Dose s Osteocytes poptosis Osteocytes utophgy 1. Empty lcune 2. Bone formtion Hypominerliztion of perilcunr mtrix Whole bone strength Loclized bone mteril properties Repir of bone nd recovery of bone strength No repir 1

11 7/24/214 Intervention Study PTH bone ctive gent (5ug/kg, 5x/wk) Risedronte- nti-resorptive gent (5ug/kg, 2x/wk) Both PTH And RIS Restored -induced Bone Loss 3 % Trbeculr bone volume of the DFM (% chnges from dy ) Intervention begn PTH +Ris Dys b. Three-dimensionl imges from DFM tken t dy 56 +PTH +Ris c 5th-LVB Bone Volume (%) b b +PTH +Ris b d. Three-dimentionl imges from the LVB t dy D56 Y +PTH +Ris PTH And RIS Restored Trbeculr Bone Loss Through Different Mechnisms + PTH + Ris Select gene expression chnges with nd +PTH or Risedronte, Effects on select Wnt-signling inhibitory gene expressions BFR/BS (um 3 /um 2 /d)) +PTH +Ris b 3 2 OcS/BS (%) +PTH +Ris 5 µm b Dkk1 b Sost +PTH +Ris = p<.5 from b=p<.5 from b Wif1 b, Effects on select genes tht inhibit minerliztion b 1 D28 D56 D28 D Dmp1 Phex +PTH +Ris Spp1 11

12 7/24/214 PTH Tretment Reduce Osteocyte Autophgy nd Sclerostin Production in Corticl Bone in Treted Mice Pthophysiology of Glucocorticoid-Induced Osteoporosis Glucocorticoids Osteoblst bone formtion Apoptosis Lifespn Function Urinry clcium excretion Estrogen GI clcium bsorption Testosterone Adrenl ndrogens Clcium Osteoclst bone resorption Osteoporosis -modest rpid chnges hpth 1-84, -to increse 1,25 D nd FGF23 to decrese serum P Clcium nd Vitmin D Lumbr Spine Femorl Neck Trochnter 2 Clcium + D 1 Plcebo Buckley, et l. Ann Int Med, 1996: GIOP, Chnge in Lumbr Spine BMD with Alendronte 7mg week vs. Plcebo J Rheumtology 29 12

13 7/24/214 Zolendronic Acid vs. Risedronte: Tretment & Prevention Sub-Popultions GIOP Bisphosphonte Trils: Frcture Rte % Chnge from Bseline Tretment sub-popultion 5 [1.36] [1.4] 4 4.1% Time (months) 2.7% Risedronte % Chnge from Bseline Prevention sub-popultion 5 4 [1.72] [1.96] 3 2.6% 2 1.6% Time (months) ZOL 5 mg Reid DM, et l. Lncet 29 Frcture Rte (%) P < % risk reduction 1 yer (Adchi 97) Bseline Plcebo Etidronte Risedronte Etidronte 4 mg Cyclicl Risedronte 5 mg Alendronte 5 mg, 1 mg Alendronte Ext 2.5 mg, 5 mg, 1 mg 7% risk reduction 1 yer (Reid 98 - Abstrct) 4% risk reduction 1 yer (Sg 98) 2 yer (Sg 98 - Abstrct) Alendronte 9% risk reduction 13

14 7/24/214 Effect of 1 yer of PTH+HRT vs. HRT lone for Glucocorticoid-Induced Osteoporosis % chnge in BMD Spine QCT Spine DXA Hip Rdius How does PTH compre to Bisphosphontes for the tretment of GIOP????? Lne, JCI 1998;12:1627 Percent Chnge in Bone Minerl Density t the Lumbr Spine nd Totl Hip from Bseline to 18 Months Incident Frcture Dt t 18 months of the Study Site Alendronte rhpth 1-34 Vertebrl 1/165 1/171 (6.1%) (.6) P vlue.4 Sg K et l. N Engl J Med 27;357: Sg, et l NEJM 27 14

15 7/24/214 ACR Recommendtions for GIOP 1. Counsel nd ssess risk fctors of those strting or on GL therpy 2. Determine Ptient Risk Ctegory ( eg FRAX score) 3. Low Risk tretment 1. s < 7.5mg/dy no Phrmcologic Rx Recommended 1. s > 7.5mg/dy: Bisphosphontes (Aln, Ris or ZA) 4. Medium Risk 1. s < 7.5mg/dy: Bisphosphontes ( Aln, Ris) 2. s > 7.5mg/dy: Bisphosphontes ( Aln, Ris, or ZA) 5. High Risk 1. s < 5mg/dy for <1 month: Bisphosphontes (Aln, Ris, ZA) 2. s > 5mg/dy for > 1month: Bisphosphontes (Aln, Ris, ZA) or PTH 6. Monitor Ptients on prevlent Rx Expecttion for Low nd Medium risk ptients tht durtion of Anticipted to be up to 3 months Uncertinties in the Prevention nd Tretment of GIOP The Criticl Timing of Bone Protective Therpy The Durtion of the Bone Protective Therpy The Tretment of Premenopusl Women The Use of Hormone Therpy for both women nd men ACR 21 Hnsen et l JBMR Sept. 211 Thnk You to My Collbortors UCSF/UCD Wei Yo Guive Blooch Mehdi Blooch Kuo Lin Rvi Nll Clude Arnud Mohmmd Shhnzri Weiwei Di Junjing Ji Min Gun LLNL/UCSF John Kinney Dvid Hupt Proctor nd Gmble Roger Phipps Merck nd Co Donld Kimmel Univ of Missouri t KC Lynd Bonewld UC Berkeley Robert Ritchie, Joel Ager Southwest Reserch Institute Dniel Nicolell 15

16 7/24/214 Acknowledgements Funding NIAMS-K24-AR4884 NIAMS-R21AR57515 BIRCWH-1K12HD NIAMS- R1AR4352 Thnk you for your ttention 16

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