Osteitis

Pa.g et s Disease of Bone. Paget s disease, osteitis deformans, occurs mainly ia people over 40. About twice as many men as women are affected. The disease, caused by faulty utilisation of may be mild and asymptomatic requiring Httle or no treatment. Clinical signs are high alkaline phosphatase and high urine hydroxyproline as weU as abnormal bone stmcture which usually goes unrecognised until discovered accidentally by routine x-ray examination (32). 

Osteitis fibrosa cystica Renal osteodystrophy Osteosclerosis Anticonvulsant treatment... 

Brekke, J. H., Bresner, M., and Reitman, M. J., Effect of surgical trauma and polylactate cubes and granules on the incidence of alveolar osteitis in mandibular third molar extraction wounds, Can. Dent. Assoc. J., 52, 315, 1986. 

The answer is c. (Hardman, pp 1536-1537.) Calcitonin is useful in the therapy of Paget s disease of bone (osteitis deformans) Calcitonin ther-... 

ROD progresses insidiously for several years before the onset of symptoms such as bone pain and fractures. Skeletal complications include osteitis fibrosa cystica (high bone turnover), osteomalacia (low bone turnover) and adynamic bone disease. When ROD symptoms appear, the disease is not easily amenable to treatment. 

Staphylococcus aureus is an important human pathogen that causes a variety of clinical manifestations, ranging from benign skin infections to life-threatening infections such as septicemia, endocarditis, osteitis, and toxic shock syndrome. The virulence has been ascribed to a coordinated production of a large set of different toxins,... 

Renal osteodystrophy is a complex disorder with several pathogenic factors. Histological evidence of bone disease is common in early renal failure and deficits in calcitriol synthesis seems to be an important factor in the pathogenesis of secondary hyperparathyroidism in early CRF. The most common component is osteitis fibrosa manifested as subperiosteal resorption of bone. This is due to decreased excretion as well as increased secretion of parathyroid hormone. In CRF small increments of serum phosphorus cause small decreases in serum calcium. 

Contraindications Primary or secondary hyperparathyroidism, including hypercalci-uria (renal calcium leak), hypomagnesemic states (serum magnesium less than 1.5 mg/dl), bone disease (osteoporosis, osteomalacia, osteitis), hypocalcemic states (e.g., hypoparathyroidism, intestinal malabsorption), normal or low intestinal absorption and renal excretion of calcium, enteric hyperoxaluria, and patients with high fasting urinary calcium or hypophosphatemia. 

Osteitis fibrosa does not occur, as in renal osteodystrophy. The common features that appear to be important in this group of diseases are malabsorption of calcium and malabsorption of vitamin D. Liver disease may, in addition, reduce the production of 25(OH)D from vitamin D, although its importance in all but patients with terminal liver failure remains in dispute. The malabsorption of vitamin D is probably not limited to exogenous vitamin D. The liver secretes into bile a substantial number of vitamin D metabolites and conjugates that are reabsorbed in (presumably) the distal jejunum and ileum. Interference with this process could deplete the body of endogenous vitamin D metabolites as well as limit absorption of dietary vitamin D. 

There were some early reports of localized mandibular osteitis in women using oral contraceptives subsequent to surgery of the mandibular molar teeth (SEDA-2, 316). It has been suggested that changes in the hemostasis could be the cause. 

The major problems of chronic renal failure that impact on bone mineral homeostasis are the loss of l,25(OH)2D and 24,25(OH)2D production, the retention of phosphate that reduces ionized calcium levels, and the secondary hyperparathyroidism that results. With the loss of l,25(OH)2D production, less calcium is absorbed from the intestine and less bone is resorbed under the influence of PTH. As a result hypocalcemia usually develops, furthering the development of hyperparathyroidism. The bones show a mixture of osteomalacia and osteitis fibrosa. 

The choice of vitamin D preparation to be used in the setting of chronic renal failure in the dialysis patient depends on the type and extent of bone disease and hyperparathyroidism. No consensus has been reached regarding the advisability of using any vitamin D metabolite in the predialysis patient. l,25(OH)2D3 (calcitriol) will rapidly correct hypocalcemia and at least partially reverse the secondary hyperparathyroidism and osteitis fibrosa. Many patients with muscle weakness and bone pain gain an improved sense of well-being. 

Carmichael KA, Fallon MD, Dalinka M, et al. 1984. Osteomalacia and osteitis fibrosa in a man ingesting aluminum hydroxide antacid. Am J Med 76 1137-1143. 

Anticonvulsant treatment Fibrogenes imperfecta ossium Osteitis fibrosa cystica Osteomalacia Osteoporosis Osteopenia Osteosclerosis Renal osteodystrophy Rickets... 

OH)2D3 concentrations. Low l,25-(OH)2D3 results in little to no intestinal calcium absorption for soft tissue needs. Thus, blood calcium can be low and secondary hyperparathyroidism develops. The inability to regulate renal handling of phosphate by PTH leads to phosphate-mediated repression of ionized calcium. Serious osteodystrophic lesions occur because of high PTH activity on bone resorption resulting in osteitis fibrosa and osteosclerosis. 

One female and one male patient had hyperparathyroidism with elevated serum alkaline phosphatase activities and extensive bone changes characteristic of generalized osteitis fibrosa cystica. In both instances, the serum acid phosphatase activity of the serum fell to normal values after removal of the parathyroid adenoma despite transitorily increased serum alkaline phosphatase activity. The fifth patient was a female with osteopetrosis involving the major part of the skeleton. The serum acid phosphatase was 8.7 K.A. units, the highest in the control series— yet the serum alkaline phosphatase was within normal limits. It would appear, therefore, that some patients with skeletal disease may have a slight but definitely elevated serum acid phosphatase activity, at least as determined by the Gutman method (GIO, G14), which cannot be explained by concurrent prostatic carcinoma or by a spillover of alkaline phosphatase activity to a pH of 5.0. 

Using the Bodansky (B18, 52) procedure with 8-glycerophosphate as substrate, Woodard (W8) was unable to obtain such elevations. She determined the serum acid phosphatase activities in 83 females and 342 males, or a total of 425 patients with miscellaneous diseases. Of these, 61 had various types of infectious or metabolic disorders, including 11 cases of inflammatory disease of bone and 12 cases of hepatic cirrhosis. The remainder had some type of neoplastic disease and about one-third had metastases to bone from cancer of various primary sites. There were 15 cases of osteogenic sarcoma and 32 cases of osteitis deformans. All these cases, whether their serum alkaline phosphatase activities were elevated or not, had serum acid phosphatase values that were essentially within the normal range, 0.06-0.89 Bodansky unit for females and 0.11-0.88 unit for males. In contrast to the Gutman method (GIO, G14), there-... 

BCG immunization is generally well tolerated. Locally a small papule appears which scales and ultimately leaves a scar however, abnormal reactions can occur. The most common adverse local reaction, suppurative Ijmphadeni-tis, has been reported in 0.1-10% of immunized children under 2 years of age. Faulty immunization technique is the most frequent cause of severe abnormal BCG primary reactions (35). The most serious generalized complications of BCG immunization involve disseminated infection with the BCG bacillus and BCG osteitis. Allergic reactions are unusual, but severe anaphylactic reactions can occur, especially when the product is used as an immunostimulant. 

Following a report of 10 cases of BCG osteitis in Finland (56), the medical records of 222 children with BCG osteitis registered from 1960 to 1988 in Finland were analysed (55). The most common sites of osteitis were the metaphyses of the long bones the legs were affected more often (58%) than the arms (14%). There was also osteitis of the sternum (15%) and ribs (11%). With adequate treatment, the prognosis for children with BCG osteitis was good, but six children were left with sequelae, with abnormalities of the limbs in five cases and pronounced cheloid formation in the other. 

In Czechoslovakia, BCG osteitis was not diagnosed before 1981. However, from March 1980 onwards another BCG vaccine (Moscow strain) was introduced (57), and after 1981 12 cases of BCG osteitis were diagnosed (58). Most of the cases developed between 7 and 24 months after immunization, but some occurred later. The risk of osteitis rose to 35 per million in the period 1982-85. There were 28 cases of BCG osteomyelitis during the period from 1980 to June 1985, when Russian BCG vaccine containing a higher amount of culturable particles was used, and only 11 cases during the period from July 1985-89, by which time the dose of vaccine had been halved (59). During the last 2 years of the second period there was only one case in each immunized birth cohort. Elsewhere, an infant developed BCG osteomyelitis of the upper spine, a very rare complication described only three times before (60). 

Six cases of BCG osteitis in Switzerland occurred in 1980-85 (61). Reports from various countries, for example New Zealand (62) and India (63), have emphasized the increasing knowledge of BCG osteitis. BCG osteitis has never been reported in the UK with use of the Glaxo vaccine. Table 1 shows rates of BCG osteitis in different countries (64). 

Osteitis occurred in <0.1-30/100000 vaccinees and has been reported mainly among infants immunized with BCG in the neonatal period in the Scandinavian countries. A retrospective study showed that BCG osteitis was present in Sweden from 1949 onwards. The reported incidence was one per 40000 in children bom between 1960 and 1969 (53,54). In Sweden, the reported incidence of osteitis rose to one per 3000 and one per 4000 for children vaccinated in the neonatal period during 1972-75. Compulsory notification of BCG adverse effects to the Swedish Adverse Dmg Reaction Committee was introduced at that time. 

The incidence of BCG osteitis correlates closely with the BCG vaccine used. Between 1960 and 1970, when the vaccine based on the Gothenburg strain was prepared in Sweden, the incidence of BCG osteitis was 7.3 per 100000 vaccinees. There was a significant increase to 37 per 100000 in the early 1970s, when the vaccine was prepared in Copenhagen using the... 

Bottiger M, Romanus V, de Verdier C, Boman G. Osteitis and other complications caused by generalized BCG-itis. Experiences in Sweden. Acta Paediatr Scand 1982 71(3) 471-8. 

Kroger L, Korppi M, Brander E, Kroger H, Wasz-Hockert O, Backman A, Rapola J, Launiala K, Katila ML. Osteitis caused by Bacille Calmette-Guerin vaccination a retrospective analysis of 222 cases. J Infect Dis 1995 172(2) 574-6. 

Hanimann B, Merger R, Baerlocher K, Bruimer C, Giger T, Schopfer K. BCG Osteitis in der Schweiz. [BCG osteitis in Switzerland. A report of 6 cases.] Schweiz Med Wochenschr 1987 117(6) 193-8. 

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