Ricardo Battaglino, PhD

Dr. Battaglino's research focuses on the biology of osteoclast differentiation and activation. Osteoclasts are multinucleated cells of the monocyte-macrophage lineage that form by fusion of mononuclear precursors. This multi-step differentiation process is under the control of the bone microenvironment that includes stromal cells, osteoblasts and local factors. Bone resorption by osteoclasts (OC) is required for normal modeling and remodeling of bone. Excessive resorption is an important pathologic feature of many diseases, including osteoporosis, arthritis, periodontitis and the hypercalcemia of malignancy. Although several key regulators of osteoclast formation and activation have recently been characterized, many gaps in our knowledge still remain.

Using differential cDNA screening and gene array approaches Dr. Battaglino's lab has isolated and characterized a number of novel genes that are predominantly expressed in osteoclasts. As information from the human and mouse genome projects accrues, we seek to define the complete array of osteoclast genes using these approaches.

We have described a role for a novel gene innvolved in osteoclast development, which we call the NHAoc/NHA2. This gene regulates a previously undescribed mechanism to control osteoclast numbers and ultimately the rate of bone remodeling. We are currently studying a possible role for NHAoc/NHA2 in mitochrondrial mediated osteoclast apoptosis. We are also analyzing the bone phenotype of a NHA0c/NHA2 deficient mouse.

Recently, we have characterized a novel redox regulatory protein (PAMM) that modulates osteoclast differention in vivo and may be part of a novel mechansim mediating bone loss induced by oxidative stress.

Finally, in conjunction with researchers in the Department of Physical Medicine and Rehabilitation, Harvard Medical School, we are working to understand the severe bone loss that occurs following neurological injury, including spinal cord injury. This work has very exciting translational and clinical implication since there is no current treatment for osteoporosis in SCI patients.

Selected Publications  

Xu Y, Morse LR, da Silva RA, Odgren PR, Sasaki H, Stashenko P, Battaglino RA. (2010) PAMM: A Redox regulatory protein that modulates osteoclast differentiation. Antioxid. Redox Signal (In press)

Xu Y, Young MJ, Battaglino RA, Morse LR, Fontana CR, Pagnois TC, Kent R, Soukos NS. (2009) Endodontic antimicrobial photodynamic therapy: safety assessment in mammalian cell cultures. J. Endod. 35(11):1567-1572.

Morse LR, Giangregori L, Battaglino RA, Holland R, Craven BC, Stolzmann K, Lazzari A, Sabharwal  S, Garshick E. (2009) VA based survey of osteoporosis management in spinal cord injury.  PM R 1(3):240-244.

Morse LR, Lazzari AA, Battaglino R, Stolzmann KL, Matthess KR, Gagnon DR, Davis SA, Garshick E. (2009) Dual energy x-ray absorptiometry of the distal femur may be more reliable than the proximal tibia in spinal cord injury. Arch. Phys. Med. Rehabil. 90(5):827-831.

Morse LR, Geller A, Battaglino RA, Stolzmann K, Matthess K, Lazzari A, Garshick E. (2009) Barriers to providing dual energy x-ray absorptiometry services to individuals with spinal cord injury. Am. J. Phys. Med Rehabil. 88(1):57-60.

Morse LR, Battaglino RA, Stolzmann K, Hallett L, Waddimba A, Gagnon D, Lazzari A, Garshick E. (2009) Osteoporotic fractures and hospitalization risk in chronic spinal cord injury. Osteoporos Int. 20(3):385-392.

Morse L, Teng YD, Pham L, Newton K, Du Y, Liao WL, Kohler T, Müller R, Graves D, Stashenko P, Battaglino R. (2008) Spinal cord injury causes rapid osteoclastic resorption and growth plate abnormalities in growing rats. (SCI-induced bone loss in growing rats) Osteoporos Int. 19(3):645-652.

Morse LR, Nguyen HP, Jain N, Williams S, Tun CG, Battaglino RA, Stashenko P, Garshick E. (2008) Age and motor score predict osteoprotegerin level in chronic SCI. J. Musculoskelet. Neuronatal Interact. 8(1):50-57.

Battaglino RA, Pham L, Morse LR, Vokes M, Sharma A, Odgren PR, Yang M, Sasaki H, Stashenko P. (2008) NHA- oc/NHA2: A mitochondrial cation-proton antiporter selectively expressed in osteoclasts. Bone 42(1):180-192.

Pham L, Purcell P, Morse LR, Stashenko P, Battaglino RA. (2007) Expression analysis of nha-oc/NHA2: A novel osteoclast-specific gene. Gene Expr. Patterns 7(8):846-851.

Battaglino RA, Vokes M, Späte U, Sharma A, Graves D, Kohler T, Muller R, Yoganathan S, Stashenko P. (2007) Fluoxetine treatment increases trabecular bone formation in mice. J. Cell. Biochem.100(6):1387-1394.

Schulze-Späte U, Battaglino R, Fu J, Sharma A, Vokes M, Stashenko  P. (2007) Brn3 transcription factors control terminal osteoclastogenesis  J. Cell Biochem. 102(1):1-12.

Gyurko R, Shoji H, Battaglino RA, Boustany G, Gibson FC III, Genco CA, Stashenko P, Van Dyke TE. (2005)  Inducible nitric oxide synthase mediates bone development and P. gingivalis-induced alveolar bone loss. Bone 36(3):472-479.