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Notes: Abstract The value of a new computerized radiogrammetric method of assessment of the second metacarpal has been evaluated, and its results have been compared with those of single (SPA) and dual photon absorptiometry measurements (forearm and spine) in 74 and 79 postmenopausal women, respectively. Standard hand X-rays were digitized by a video-camera connected to a microcomputer. The combined cortical thickness (CCT) was automatically calculated in a zone of 10 mm around the midpart of the second metacarpal. The intra- and interobserver coefficients of variation were close to 1%. The correlation between CCT and SPA of the proximal and midforearm (with a significant amount of cortical bone) was satisfactory (r=0.62 and 0.50, respectively; P〈0.001). The correlation between CCT and osteodensitometry of sites comprising more trabecular bone were not so good (0.50 for lumbar and 0.44 for distal forearm bone mineral density, respectively), but still significant (P〈0.001). Radiogrammetry proved unaffected by a change of X-ray apparatus, as measurements of 48 metacarpals radiographed by two different kinds of X-ray apparatus were not significantly different. Radiogrammetry is by no means the best method to evaluate bone mass. Its automation did not improve the correlation with osteodensitometric values. Radiogrammetry is still of interest in mass screening, particularly when other more expensive techniques such as osteodensitometric methods of bone mass measurement are not readily available. Its automation makes it simpler, faster, and more precise, rendering its use easier on a larger scale.

Notes: Summary Subcutaneous and periarticular dystrophic calcifications are well known to be associated with progressive systemic sclerosis (PSS). On the other hand, calcifications inside the joints are very rarely reported. We report a new case of this unusual complication of PSS. The observation of the complete radiological follow-up led us to propose a mechanical rather than a purely inflammatory pathogenetic mechanism of this complication.

Notes: Summary Sodium Fluoride (NaF) is the only medication so far clinically available with a bone formation stimulating property, through its peculiar mitogenic dose-dependent action on the osteoblast cell line. Bone strength is commensurate to bone mass, and in a condition with fragility fractures, like osteoporosis, it seems logical to restore bone mass without weakening bone strength. However, as with any active drug, NaF therapy requires adhesion to elementary rules if drawbacks are to be prevented. A first mandatory rule is not to prescribe NaF without calcium supplementation, if bone loss at the appendicular skeleton is to be avoided; to prevent this, the availability of monofluorophosphate (MEP), containing the fluoride and calcium salts in the same preparation has enhanced the compliance to calcium supplementation. A second rule is not to give supraphysiological doses of vitamin D, for the same reason. Third, if one wants to avoid a calcium shift from cortical to trabecular bone and osteomalacia, one should use small doses of NaF, of the order of 50 mg/day. With this in mind, the bioavailability of the drug has to be taken into account, particularly its gastrointestinal abosorption which is dramatically enhanced if a plain non entericoated (EC) capsule is used, as compared to that of an EC tablet with the same face value. Too much NaF is deleterious to bone, a fact known for years. Already in 1972, it was noted that in all patients receiving 60 mg or more of NEC NaF, daily, morphologically abnormal bone developed and which appeared irregular and contained areas of incompletely mineralized bone. The bone was histologically and microradiographically normal in patients receiving 45 mg or less of NEC NaF/day. Fourth, NaF therapy is contraindicated in renal insufficiency owing to an enhanced retention in the skeleton. NaF is, however, by no means the ideal medication, because its therapeutic window is narrow. It has many bothersome drawbacks, and notably it is irritating for the gastric mucosa, a hazard which may be partly circumvented by the use of an Ec or slow release tablet. Furthermore, peripheral stress fractures may occur, and, in our experience, they were seen in 17% of patients, almost exclusively in females with a low lumbar BMD. Their occurrence should be curtailed by not allowing an increase in alkaline phosphatase activity of more than 50%. This is a relatively benign complication, because no stress fracture degenerated into a complete fracture. In all cases, the stress fractures healed after a transitory drug discontinuation. If there is some concern about cortical bone, NaF therapy may be associated with an antiresorber like estrogens which will prevent any further bone loss, and does not impair the response to NaF. NaF therapy should be reserved for patients suffering chiefly from trabecular osteoporosis and shoud be avoided in senile osteoporosis, because of a frequently imparied renal function. Currently, we would recommend in clinical practice a daily dose of 50 mg EC-NaF or 150 mg Ca-MFP as the therapy of involutional osteoporosis in women, reserving the dose of 75 mg EC-NaF or 200 mg MFP for males or female patients resistant to lower dose. The therapy should be maintained for 2 to 3 years, or more, according to the bone response, taking into account that patients with the vertebral crush fracture syndrome have lost on average 30%, as compared to the young adult mean.