A. MICHAEL PARFITT
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Also affiliated: Cedars-Sinai Medical Center (1972); University College Hospital (1966); Royal National Hospital for Rheumatic Diseases (1977); Beth Israel Deaconess Medical Center (2001); University of Wisconsin–Madison (1992); Harvard University (2001); University of Ottawa (1986); Henry Ford Health (1976–2003); University of Cape Town (1985); University of California, Los Angeles (1972); The University of Queensland (1964–1991); Oregon Health & Science University (1987); University of Michigan (1977–1981); University of Arkansas Medical Center (1997–2004); Groote Schuur Hospital (1985); Royal National Orthopaedic Hospital (1964–1965); Henry Ford Hospital (1972–2003); Portland VA Medical Center (1987); Central Arkansas Veterans Healthcare System (2002–2012); St Mary's Hospital (1994); University College London (1966); University of Bath (1977)
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
A. M. Parfitt's research has focused on understanding microbial infections and their related disease processes. Their work includes investigating the mechanisms of microbial pathogenesis and exploring potential therapeutic interventions. Parfitt has contributed to the field through publications detailing findings in this area.
Metrics
- h-index: 86
- Publications: 301
- Citations: 40,410
Selected Publications
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Parathyroid Growth (2014)
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Skeletal Heterogeneity and the Purposes of Bone Remodeling (2013)
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Standardized nomenclature, symbols, and units for bone histomorphometry: A 2012 update of the report of the ASBMR Histomorphometry Nomenclature Committee (2012)
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For whom the bell tolls: Distress signals from long-lived osteocytes and the pathogenesis of metabolic bone diseases (2012)
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What old means to bone (2010)
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Dependence of bone yield (volume of bone formed per unit of cement surface area) on resorption cavity size during osteonal remodeling in human rib: implications for osteoblast function and the pathogenesis of age-related bone loss (2009)
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Trabecular packet-level lamellar density patterns differ by fracture status and bone formation rate in white females (2009)
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Perspective: Quantifying Osteoblast and Osteocyte Apoptosis: Challenges and Rewards (2007)
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Independent and Combined Contributions of Cancellous and Cortical Bone Deficits to Vertebral Fracture Risk in Postmenopausal Women (2006)
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Misconceptions V—Activation of osteoclasts is the first step in the bone remodeling cycle (2006)
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Osteocyte Apoptosis Is Induced by Weightlessness in Mice and Precedes Osteoclast Recruitment and Bone Loss (2006)
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Rosiglitazone Causes Bone Loss in Mice by Suppressing Osteoblast Differentiation and Bone Formation (2005)
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Differences in osteocyte and lacunar density between Black and White American women (2005)
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Drugs Used to Treat Osteoporosis: The Critical Need for a Uniform Nomenclature Based on Their Action on Bone Remodeling (2005)
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The morphological association between microcracks and osteocyte lacunae in human cortical bone (2005)
Collaboration Network
Top Collaborators
- Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone.
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin
- Osteoblast Programmed Cell Death (Apoptosis): Modulation by Growth Factors and Cytokines
- Osteocyte Apoptosis Is Induced by Weightlessness in Mice and Precedes Osteoclast Recruitment and Bone Loss
Showing 5 of 14 shared publications
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Osteoblast Programmed Cell Death (Apoptosis): Modulation by Growth Factors and Cytokines
- Osteocyte Apoptosis Is Induced by Weightlessness in Mice and Precedes Osteoclast Recruitment and Bone Loss
- Rosiglitazone Causes Bone Loss in Mice by Suppressing Osteoblast Differentiation and Bone Formation
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
Showing 5 of 10 shared publications
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Osteoblast Programmed Cell Death (Apoptosis): Modulation by Growth Factors and Cytokines
- Rosiglitazone Causes Bone Loss in Mice by Suppressing Osteoblast Differentiation and Bone Formation
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
Showing 5 of 9 shared publications
- The morphological association between microcracks and osteocyte lacunae in human cortical bone
- Reduced Iliac Cancellous Osteocyte Density in Patients With Osteoporotic Vertebral Fracture
- Age and distance from the surface but not menopause reduce osteocyte density in human cancellous bone
- Relationships between osteocyte density and bone formation rate in human cancellous bone
- Differences in osteocyte and lacunar density between Black and White American women
Showing 5 of 9 shared publications
- Effect of Vitamin D Nutrition on Parathyroid Adenoma Weight: Pathogenetic and Clinical Implications*
- Osteomalacia due to vitamin D depletion: a neglected consequence of intestinal malabsorption
- The morphological association between microcracks and osteocyte lacunae in human cortical bone
- Reduced Iliac Cancellous Osteocyte Density in Patients With Osteoporotic Vertebral Fracture
- Differences in osteocyte and lacunar density between Black and White American women
Showing 5 of 9 shared publications
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin
- Osteoblast Programmed Cell Death (Apoptosis): Modulation by Growth Factors and Cytokines
- Osteocyte Apoptosis Is Induced by Weightlessness in Mice and Precedes Osteoclast Recruitment and Bone Loss
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
Showing 5 of 8 shared publications
- The morphological association between microcracks and osteocyte lacunae in human cortical bone
- Reduced Iliac Cancellous Osteocyte Density in Patients With Osteoporotic Vertebral Fracture
- Age and distance from the surface but not menopause reduce osteocyte density in human cancellous bone
- Relationships between osteocyte density and bone formation rate in human cancellous bone
- Differences in osteocyte and lacunar density between Black and White American women
Showing 5 of 7 shared publications
- Standardized nomenclature, symbols, and units for bone histomorphometry: A 2012 update of the report of the ASBMR Histomorphometry Nomenclature Committee
- Normative data for iliac bone histomorphometry in growing children
- Static and dynamic bone histomorphometry in children with osteogenesis imperfecta
- Structural and cellular changes during bone growth in healthy children
- Deficient Bone Formation in Idiopathic Juvenile Osteoporosis: A Histomorphometric Study of Cancellous Iliac Bone
Showing 5 of 6 shared publications
- Osteocyte Apoptosis Is Induced by Weightlessness in Mice and Precedes Osteoclast Recruitment and Bone Loss
- Rosiglitazone Causes Bone Loss in Mice by Suppressing Osteoblast Differentiation and Bone Formation
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
- The Skeletal Effects of Glucocorticoid Excess Override Those of Orchidectomy in Mice
- Normative data for iliac bone histomorphometry in growing children
- Static and dynamic bone histomorphometry in children with osteogenesis imperfecta
- Structural and cellular changes during bone growth in healthy children
- Deficient Bone Formation in Idiopathic Juvenile Osteoporosis: A Histomorphometric Study of Cancellous Iliac Bone
- The bone formation defect in idiopathic juvenile osteoporosis is surface-specific
- Normative data for iliac bone histomorphometry in growing children
- Static and dynamic bone histomorphometry in children with osteogenesis imperfecta
- Structural and cellular changes during bone growth in healthy children
- Deficient Bone Formation in Idiopathic Juvenile Osteoporosis: A Histomorphometric Study of Cancellous Iliac Bone
- The bone formation defect in idiopathic juvenile osteoporosis is surface-specific
- Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone.
- Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin
- What old means to bone
- The Skeletal Effects of Glucocorticoid Excess Override Those of Orchidectomy in Mice
- Apoptosis in Bone Cells
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
- The Skeletal Effects of Glucocorticoid Excess Override Those of Orchidectomy in Mice
- Age and distance from the surface but not menopause reduce osteocyte density in human cancellous bone
- Relationships between osteocyte density and bone formation rate in human cancellous bone
- The mineralization index—A new approach to the histomorphometric appraisal of osteomalacia
- The morphological association between microcracks and osteocyte lacunae in human cortical bone
- Effects of vertebral bone fragility and bone formation rate on the mineralization levels of cancellous bone from white females
- Trabecular packet-level lamellar density patterns differ by fracture status and bone formation rate in white females
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