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“We have previously shown that [2′-32P]-2-azido-NADP+ is an effective probe of the NADP-(H) binding site of rat liver microsomal 5 alpha-reductase (5 alpha R-1) [Bhattacharyya et al. (1994) Steroids 59, 634-641]. PEG-fractionated (6.5%) detergent-solubilized preparations (40 mg) containing 5 alpha R-1 activity were UV-photolyzed with [32P]-2-azido-NADP+ and subjected to preparative gel electrophoresis on 8% SDS-PAGE. Fractions corresponding to the second major [32P]-labeled peak following the dye-front were analyzed by 10% SDS-PAGE and showed a single [32P]-labeled species with an apparent molecular mass of approximately 26 kDa (5 alpha R-1). TCA precipitation (13.6%) of the labeled fractions resulted in recovery of > 70% of the total radioactivity in the protein pellet. Trypsin digestion of the resuspended pellet followed by immobilized-Al3+ affinity chromatography indicated that > 90% of the radioactivity remained bound to the affinity column. The [32P]-2N3-NADP(+)-labeled peptide was eluted with potassium phosphate, concentrated, and further purified by reverse-phase (C8) HPLC. Sequence analysis of the purified peptide indicated that it consisted of 11 amino acids with the sequence N-L-R-K-P-G-E-T-G-Y-K, corresponding to residues 170-180 of the rat 5 alpha R-1 sequence [Andersson et al. (1989) J. Biol. Chem. 264, 16249-16255].”

PURPOSE:

To evaluate the dimension and duration of pain reduction in patients with facial neuralgias after localization, decortication, and curettage of histologically confirmed inflammatory jawbone lesions of the newly identified form of alveolar avascular osteonecrosis called neuralgia-inducing cavitational osteonecrosis (NICO).
MATERIALS AND METHODS:

One hundred ninety patients who could be located retrospectively and who had histories of jawbone curettage for chronic “idiopathic” facial pain, either trigeminal neuralgia (TN) or atypical facial neuralgia/pain (AFN), were identified through surgical pathology reports from four institutions. To assess pain reduction after jawbone surgery, these patients were mailed a modified McGill Pain Survey by investigators with whom they had had no previous professional contact. Patient demographics and clinicopathologic characteristics were also reviewed through surgical pathology specimens and reports.
RESULTS:

More than two thirds of the respondents to whom the questionnaire was mailed experienced complete or almost complete disappearance of neuralgic pain immediately or shortly after curettage of jawbone osteonecrosis (NICO), regardless of whether they had previously been diagnosed with TN or AFN. Thirty percent, however, experienced local recurrence of jaw inflammation and facial pain, and one third developed at least one and as many as 12 additional foci of histologically confirmed osteonecrosis. Despite this, however, the long-term (average, 4.6 years) abatement of neuralgic pain was total or almost total in 74% of treated patients.
CONCLUSIONS:

Neuraglia-inducing cavitational osteonecrosis appears to be associated with at least some cases of facial neuralgia, or with a pain so similar as to be clinically indistinguishable. Decortication and curettage dramatically reduces or eliminates this intense pain in two of every three patients, although multiple surgeries may be required, and additional sites of osteonecrosis may occur. It is recommended that NICO be included in the differential diagnosis of idiopathic facial pain syndromes.

Bacterial endotoxic reactions can cause osteonecrosis in humans by disseminated intravascular coagulation. The authors first used a combination of the Shwartzman reaction and corticoid injections in rabbits to develop a new animal model of osteonecrosis. This model showed a significantly higher incidence and wider area of osteonecrosis in the femur and humerus than that found in rabbits with either Shwartzman reaction or steroid injection alone. Osteonecrosis was observed in several foci that were distributed from the diaphysis to the epiphysis in both bones. Histologically, the bone marrow cells underwent necrosis, whereas the bone trabeculae demonstrated either empty lacunae or pycnotic nuclei of osteocytes. Exogenous steroids appeared to potentiate the Shwartzman reaction and the magnitude of osteonecrosis, perhaps by increasing endothelial damage and hypercoagulability of those intraosseous and extraosseous vessels that subsequently thrombosed. This model may not only be useful in clarifying the etiology and early pathogenesis of human osteonecrosis after corticoid therapy, but also in designing pharmaceuticals for prevention and early treatment.

“We have found that EDTA and EGTA complexes of Hg2+, which conventional wisdom has assumed are biologically inert, are potentially injurious to the neuronal cytoskeleton. Tubulin, a major protein component of the neuronal cytoskeleton, is the target of multiple toxicants, including many heavy metal ions. Among the mercurials, inorganic mercuric ion (Hg2+) is one of the most potent inhibitors of microtubule polymerization both in vivo and in vitro. In contrast to other heavy metals, the capacity of Hg2+ to inhibit microtubule polymerization or disrupt formed microtubules cannot be prevented by the addition of EDTA and EGTA, both of which bind Hg2+ with very high affinity. To the contrary, the addition of these two chelating agents potentiates Hg2+ inhibition of tubulin polymerization. Results herein show that HgEDTA and HgEGTA inhibit tubulin polymerization by disrupting the interaction of GTP with the E-site of brain beta-tubulin, an obligatory step in the polymerization of tubulin. Both HgEDTA and HgEGTA, but not free Hg2+, prevented binding of [32P]8N3GTP, a photoaffinity nucleotide analog of GTP, to the E-site and displaced bound [32P]8N3GTP at low micromolar concentrations. This complete inhibition of photoinsertion into the E-site occurred in a concentration- and time-dependent fashion and was specific for Hg2+ complexes of EDTA and EGTA, among the chelating agents tested. Given the ubiquity of Hg2+ in the environment and the widespread use of EDTA in foodstuffs and medicine, these mercury complexes may pose a potentially serious threat to human health and play a role in diseases of the neuronal cytoskeleton.”

The disorder termed osteocavitation lesion has been described in the literature since at least 1976. This disorder has often been misdiagnosed as trigeminal neuralgia or atypical facial pain, and, unfortunately, patients have either continued to suffer or inappropriate treatment or treatments have been prescribed in an attempt to rid the patient of this terrible pain disorder. These symptoms, which can be misinterpreted as trigeminal neuralgia, include a history of undiagnosed facial pain, a history of tooth extraction, the presence of trigger areas and normal radiographic findings. A confirmed diagnosis of osteocavitation lesion can be treated only with surgery.

While not as attention-grabbing as some of the infections ofour time, we appear to be in danger ourselves of forgetting that the mouth constitutes a major portal of entry for a wide range of micro-organisms, whether inherently oral commensals or direct pathogens, the effects of which may be merely troublesome, as with the common oral infectious diseases, or more serious. There is an analogy with oral neoplasia which, though it may be as prevalent as cervical cancer, does not attract anything like the attention ofthe latter. One wonders why. Ever since the original concept of focal infection led to an excess of extractions over 70 years ago, the theory has been in relative disrepute. And yet to ignore focal infection is to refuse to recognize an abundant literature, all of medical significance.

Focal infection of oral origin may derive from closed or open sites. Open foci include caries lesions, periodontal pockets, and extraction sockets; closed foci, infection around root apices, unerupted but infected teeth, and infected pulps (Newman, 1968). Focal infection leading to infective endocarditis can even occur via a dens in dente (Whyman and MacFadyen, 1994). From the oral foci, microorganisms- bacterial, viral, or other-or their products may gain entry to the deeper tissues directly, by spreading along fascial planes, through bony cavities, or even along blood or lymph vessels or nerves, or via salivary gland mucous surfaces. Can one die of such simple chronic infection? One may cite the coroner’s court, but there is also extensive literature evidence.

The influence of various factors that may affect the outcome of root canal therapy was evaluated in 356 patients 8 to 10 yr after the treatment. The results of treatment were directly dependent on the preoperative status of the pulp and periapical tissues. The rate of success for cases with vital or nonvital pulps but having no periapical radiolucency exceeded 96%, whereas only 86% of the cases with pulp necrosis and periapical radiolucency showed apical healing. The possibility of instrumenting the root canal to its full length and the level of root filling significantly affected the outcome of treatment. Of all of the periapical lesions present on previously root-filled teeth, only 62% healed after retreatment. The predictability from clinical and radiographic signs of the treatment-outcome in individual cases with preoperative periapical lesions cases was found to be low. Thus, factors which were not measured or identified may be critical to the outcome of endodontic treatment.

The lymphocyte transformation test (LTT) was used to elucidate whether certain side effects induced by radiographic contrast media have an immunologic etiology. Groups studied were: 8 patients who had previously experienced adverse reactions in association with urography, 6 patients who underwent urography without notable side reactions, 17 occupationally exposed nurses, and 9 unexposed controls. The lymphocytes from 2 hypersensitive patients and from 11 nurses exhibited a positive proliferative response to amidotrizoate. Five nurses who had shown a positive response, had a previous history of hypersensitivity reactions when handling contrast media, whereas the remaining 6 were free of symptoms. Amidotrizoate-specific memory cells were absent in patients who underwent urography without signs of hypersensitivity and in 7/9 of unexposed control subjects. Lymphocytes from patients sensitive to amidotrizoate cross-reacted to structurally related ionic contrast media while non-ionic contrast agents did not induce proliferation of the lymphocytes. Thus, ionic radiographic contrast agents have antigenic properties in man. Irradiated mixtures of radiographic contrast media and serum proteins were, in general, not effective in inducing an LTT response.

The overwhelming majority of all root canal fillings in Sweden today are made with gutta-percha. A
number of different gutta-percha brands contains 0,6-0,7% cadmium, probably due to cadmium-based
color pigment. Cadmium-pigments are prohibited in Sweden since 1982. In a special regulation the
Naturvårdsverket has made an exception for dental materials. In this kind of endodontic therapy based on gutta-percha, chloroform is used both as an ingredient in a so called sealer and as a solvent for the gutta-percha itself. No drugs sold in Sweden contains chloroform. In the USA the use of chloroform is
prohibited in both drugs and cosmetics due to its canceroginity.