Abstract

HomeRadiologyVol. 78, No. 6 PreviousNext ArticlesLocalized Osteosclerosis in HyperparathyroidismArch W. Templeton, J. Richard Iaconette, Robert S. OrmondArch W. Templeton, J. Richard Iaconette, Robert S. OrmondArch W. TempletonJ. Richard IaconetteRobert S. OrmondPublished Online:Jun 1 1962https://doi.org/10.1148/78.6.955MoreSectionsPDF ToolsImage ViewerAdd to favoritesCiteTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinked In AbstractRoentgenograms showing patchy osteosclerotic changes in the skull in patients with hyperparathyroidism are not frequently seen but certainly are not rare. Osteosclerotic changes involving the lumbar spine and pelvis in cases of either primary or secondary hyperparathyroidism are, however, very unusual. Representative films demonstrating these changes and a brief discussion of possible mechanisms for their occurrence constitute this paper.Characteristic roentgenologic changes of bone mottling, decalcification, cyst formation, and granularity were first associated with hyperparathyroidism by Camp and Ochsner (3) in 1931. Recently Teng and Nathan (7) called attention to the early changes seen in hyperparathyroidism and reviewed the pathognomonic bone signs—subperiosteal and endosteal resorption of bone, subchondral resorption of the clavicle and symphysis pubis, and subperiodontal resorption of the lamina dura. The abnormalities seen in the skull have been discussed by Ellis and Hochstim (5). These vary from the more common granular, rarefied appearance to the less usual patches of bone sclerosis. Beveridge et al. (2) published a case of primary hyperparathyroidism with secondary renal failure accompanied by bone changes very similar to those found in our patients. Osteosclerotic changes associated with primary chronic renal disease, with and without parathyroid hyperfunction, have occasionally been noted (4, 9).In Figure 1 are reproduced anteroposterior and lateral lumbar spine films of a 47-year-old female with secondary hyperparathyroidism. Blood urea nitrogen of 55 mg./100 c.c. and creatinine of 7.1 mg./100 c.c. indicated significant renal damage. The serum calcium was 9.7 mg./100 c.c, but the serum phosphate was elevated to 6.3 mg./100 c.c. The roentgenograms demonstrate coarse trabeculae and increased bone density. Very small kidneys are seen on the anteroposterior spine film.Figure 2 is the lateral view of the skull of a patient with primary hyperparathyroidism. The calvarium is thickened. Many areas of sclerotic, coarse bone are seen. The serum calcium in this case was 15.1 mg./100 c.c. and the serum phosphate 1.7 mg./100 c.c. There was no laboratory evidence of renal disease. Microscopic examination of a bone specimen showed large, irregular spicules of new bone. In addition, there was increased osteoid.Figure 3 shows anteroposterior and lateral films of the lumbar spine of a 43-year-old white female with primary hyperparathyroidism. The serum calcium ranged from 12.8 to 14.2 mg./100 c.c. and the serum phosphate averaged 1.3 mg./100 c.c. The blood urea nitrogen and creatinine were normal. The roentgenograms show a marked increase in bone density characterized by a chalky appearance. A biopsy of the ilium demonstrated a very thick layer of osteoid surrounding unusually prominent trabeculae. Scattered osteoblasts were identified. A left parathyroid adenoma weighing 4.8 gm. was removed.In the cases illustrated here there were many classic bone changes of hyperparathyroidism. The distal ends of the clavicles were resorbed, the digits demonstrated subperiosteal reabsorption, and the laminae durae were absent. Yet they also demonstrate either dense areas of bone in the skull or generalized sclerosis throughout the lumbar spine and pelvis.DISCUSSIONParathyroid hormone stimulates osteoclast hyperplasia and hyperfunction with resultant resorption of bone matrix, not osteoid. In hyperparathyroidism the increased osteoclastic activity is not uniformly accelerated throughout the skeleton.Article HistoryPublished in print: June 1962 FiguresReferencesRelatedDetailsCited BySkeletterkrankungenJ.Freyschmidt2016Musculoskeletal manifestations of endocrine disordersStephanie B.Boswell, Dakshesh B.Patel, Eric A.White, Christopher J.Gottsegen, Deborah M.Forrester, SulabhaMasih, George R.Matcuk2014 | Clinical Imaging, Vol. 38, No. 4Visual VignettePaulMadaj, TheresaTran, RajeevVarma, Andrew G.Gianoukakis2010 | Endocrine Practice, Vol. 16, No. 6Skeletterkrankungen2008SkeletterkrankungenJürgenFreyschmidt1993Case report 310MartinLachmann, Morrie E.Kricun, Emanuel E.Schwartz1985 | Skeletal Radiology, Vol. 13, No. 3Handbuch der Medizinischen Radiologie Encyclopedia of Medical RadiologySusanneBosnjakovic-Büscher, H.Ellegast, F.Heuck1983 | , Vol. 5 / 5Handbuch der Medizinischen Radiologie / Encyclopedia of Medical RadiologySusanneBosnjakovic-Büscher, H.Ellegast, F.Heuck, H. W.Schneider1983Epiphyseal sclerosis in renal osteodystrophy simulating osteonecrosisPGarver, DResnick, GNiwayama, JGuerra1981 | American Journal of Roentgenology, Vol. 136, No. 6Klinische Osteologie · AH.-J.Dulce, H.Höhling, B. A.Ashton, P. P.Fietzek, H. M.Frost, B. E. E.Nordin, J. A.Parsons, Joan M.Zanelli, H. F.DeLuca, J. G.Ghazarian, I.MacIntyre, I. M. A.Evans, L. S.Galante, C. J.Hillyard1980IdentifikationHorstHunger, DieterLeopold1978Metabolic Bone DiseaseJOEL F.HABENER, JOHN T.POTTS1978Increased bone mineral content in young adults with familial hypophosphatemic vitamin D refactory ricketsJ.E.Harrison, W.A.Cumming, V.Fornasier, D.Fraser, S.W.Kooh, K.G.McNeill1976 | Metabolism, Vol. 25, No. 1Calcification and PhysiologyJ.A.PARSONS1976Calcification and PhysiologySANDY C.MARKS, DONALD G.WALKER1976Calcium Metabolism, Bone and Metabolic Bone DiseasesH. 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