Summary
Patients suffering from osteoporosis were treated with an ADFR (Activation-Depression-Free-Repeat) scheme composed of phosphate as the activator and diphosphonate as the depressor. Trabecular bone remodeling parameters were assayed and compared on undecalcified sections of iliac crest biopsies obtained from patients before and after the therapeutic reginmen. Since some patients received a composite ADFR regimen with estrogen and/or calcium supplementation during the treatment free period, the accumulated data were subdivided into two groups. Statistical analysis was performed on the comparisons of pre- and post-treatment difference in each group and between groups. The mean total trabecular volume increased significantly (p<0.05) in patients treated with pure ADFR, and increased marginally in patients treated with a composite ADFR. Other static and dynamic paramenters were not significantly different before and after the manipulation in each group. Although the comparisons of treatment effects on each parameter between the two groups were not significantly different at p<0.05 level, the mean increments to the original trabecular bone volume, trabecular diameter and thickness of trabecular interstitial lamella were greater in the pure ADFR group (91.6%, 55.12µm, 39.01µm, respectively) than that of the composite ADFR group (24.45%, 0.02µm, 5.05µm, respectively). In addition, the mean wall thickness was increased in the pure ADFR group and decreased in the composite group.
It is important that the timing of the administrations of drugs be in accordance with the phases of normal BMU' s remodeling cycles. The administration of estrogen and/or calcium during the treatment free period seemed to impair osteoblastic function. The insignificant change before and after the manipulation indicated by the static and dymanic parameters might reflect that second biopsy being taken at the similar remodeling phases as that of the first biopsy. The study suggests that the current ADFR scheme not only halts bone less, but also increases trabecular bone volume in postmenopausal osteoporosis. Eight ADFR cycles, approximately two years, were needed to significantly increase trabecular bone volume in iliac crest biopsy.
Similar content being viewed by others
References
Frost, H.M.: Tetracycline-based histological analysis of bone remodeling. Calcif Tiss Res 3, 211–237, 1969.
Parfitt, A.M.: The coupling of bone formation to resorption: A critical analysis of the concept and its relevance to the pathogenesis of osteoporosis. L Metab Bone Dis Rel Res 4, 1–6, 1982.
Frost, H.M.: The skeletal intermediary organization. A review. J Metab Bone Dis Rel Res 4, 281–290, 1983.
Frost, H.M.: The mechanostat: A proposed pathogenic mechanism of osteoporoses and the bone mass effects of mechanical and nonmechanical agents. Bone and Mineral 2, 73–85, 1987.
Parfitt, A.M.: The cellular basis of bone remodeling: The quantum concept re-examined in light of recent advances in the cell biology of bone. Calcif Tiss Int 36, S37-S45, 1984.
Richelson, L.S., Waher, H.W., Melton, L.J. III, and Riggs, B.L.: Relative contributions of aging and estrogen deficiency to postmenopausal bone loss. New Eng J Med 311, 1273–1275, 1984.
Consensus Development Conference: Prophylaxis and treatment of osteoporosis. Brit Med J 295, 914–915, 1987.
Ettinger, B., Genant, H.R., and Cann, C.E.: Postmenopausal bone loss is prevented by treatment with low-dosage estrogen with calcium. Ann Intern Med 106, 40–45, 1987.
Whedon, G.D.: Osteoporosis. New Eng J Med 305, 397–399, 1981.
Briancon, D., Meunier, P.: Treatment of osteoporosis with fluoride, calcium and vitamin D. Orthop Clin North Am 12, 629–648, 1981.
Dambacher, M.A., Ittner, J., and Rugesgger, P.: Long-term fluoride therapy of postmenopausal osteoporosis. Bone 7, 199–205, 1986.
O'Duffy, J.D., Wahner, H.W., O'Fallon, W.M., Johnson, K.A., Muhs, J.M., Beabout, J.W., Hodgson, S.F., and Riggs, B.L.: Mechanism of acute lower extremity pain syndrome in fluoride-treated osteoporotic patients. Am J Med 80, 561–566, 1986.
Frost, H.M.: The ADFR concept revisited. Calcif Tiss Int 36, 349–353, 1984.
Horwitz, N.: Coax bone to amass 10% gain in 2 years. Didronel key to manipulation. Med Tribune July 1, 13–15, 1987.
Anderson, C., Cape, R.D.T., Crilly, R.G., Hadsman, A.B., and Wolf, B.M.J.: Preliminary observations of a form of coherence therapy for osteoporosis. Calcif Tiss Int 36, 341–343, 1984.
Luisetto, G., Ziliotto, D., Zangari, M., and Tizian, L.: Coherence therapy versus calcitonin in the treatment of postmenopausal osteoporosis. International Symposium on Osteoporosis, September 27–October 2, Aalborg, Denmark. Abstract No. 352, 1987.
Mallette, L.E., and LeBalnc, A.: Cyclic therapy of osteoporosis: Use of brief, high-dose pulse of etidronate as a terminator of osteoclast activity. International Symosium on Osteoporosis, September 27–October 2, Aalborg, Denmark. Abstract No. 353, 1987.
Reginster, J.Y., Denis, D., Albert, A., and Franchimont, P.: Preliminary results of an ADSFR regimen as late preventive treatment of postmenopausal osteoporosis. International Symposium on Osteoporosis, September 27–October 2, Aalborg, Denmark. Abstract No.362, 1987.
Rittinghaus, E.F., Busch, U., Prokop, M., Delling, G., and Hesch, R.D.: Dramatic increase of bonemass and turn-over in osteoporosis by combined 1–38 hPTH and calcitonin therapy. International Symposium on Osteoporosis, September 27–October 2, Aalborg, Denmark. Abstract No. 365, 1987.
Marie, P.J., and Caulin, F.: Mechanisms underlying the effects of phosphate and calcitonin on bone histology in postmenopausal osteoporosis. Bone 7, 17–22, 1986.
Aloia, J.F., Vaswani, A., Meuner, P.J., Edouard, C.M., Arlot, M.E., Yeh, J.K., and Cohn, S.H.: Coherence treatment of postmenopausal osteoporosis with growth hormone and calcitonin. Calcif Tiss Int 40, 253–259, 1987.
Reiss, E., Canterbury, J.M., Bercovitz, M.A., and Kaplan, E.L.: The role of phosphate in the secretion of parathyroid hormone in man. J Clin Invest 49, 2146–2149, 1970.
Goldsmith, R.S., Jowsey, J., Dube, W.J., Riggs, B.L., Arnaud, C.D., and Kelly, P.J.: Effect of phosphorus supplementation on serum parathyroid hormone and bone morphology in osteoporosis. J Clin Endocrinol & Metab 43, 523–532, 1976.
Fleisch, H.: Bisphosphonates — History and experimental basis. Bone 8 (suppl) 1, S23-S28, 1987.
Chambers, T.J.: Diphosphonates inhibit bone resorption by macrophagesin vitro. J Pathol 132, 255–262, 1980.
Cecchini, M.G., Felix, R., Fleisch, H., and Cooper, P.H.: Effect of bisphosphonates on proliferation and viability of mouse bone marrow-derived macrophages. J Bone Min Res 2, 135–142, 1987.
Malluche, H.H., Sherman, D., Meyer, W., and Massry, S.C.: A new semi-automatic method for quantitative static and dynamic bone histology. Calcif Tiss Int 34, 439–448, 1982.
Kragstrup, J., Melsen, F., and Mosekilde, L.: Thickness of bone formed at remodeling sites in normal human iliac trabecular bone: Variations with age and sex. Metab Bone Dis & Rel 5, 17–21, 1983.
Snow, G.R., and Anderson, C.: The effects of 17-beta-estradiol and progestogen on trabecular bone remodeling in oophorectomized dogs. Calcif Tiss Int 39, 198–205, 1986.
Brown E.M.: Set-point for calcium: Its role in normal and abnormal parathyroid secretion. in: Hormonal Control of Calcium Metabolism (D.V. Cohn, R.V. Talmage and J.L. Matthews eds.), Excerpta Medica, Amsterdam, pp 35–43, 1981.
Parfitt, A.M., Drezner, M.K., Glorieux, F.H., Kanis, J.A., Malluche, H., Meunier, P.J., Ott, S.M., and Recker, R.R.: Bone histomorphometry: Standardization of nomenclature, symbols and units. Report of the ASBMR Histomorphometry Nomenclature Committee. J Bone and Mineral Res 2, 595–610, 1987.
Author information
Authors and Affiliations
About this article
Cite this article
Shin, MS., Anderson, C. Coherence therapy for postmenopausal osteoporosis: A histomorphometric study. J Bone Miner Metab 8, 26–33 (1990). https://doi.org/10.1007/BF02377310
Issue Date:
DOI: https://doi.org/10.1007/BF02377310