In the first part of our review, biochemical aspects of the biomedicinal chemisty of fluorinated compounds will be covered. Medicinal aspects of this field are then discussed, with emphasis on drugs that have been recently marketed, or are in the final phases of testing.
The concentrations of mercury in saliva and feces and the resistance pattern of the gastrointestinal microflora were investigated for 20 subjects. Ten patients, with a mean number of 19 amalgam surfaces, had all amalgam fillings removed during one dental session. Ten subjects without amalgam fillings served as a control group. Saliva and fecal samples were collected before amalgam removal and 2, 7, 14, and 60 days afterward. Mercury levels in saliva and feces correlated significantly with the number of amalgam surfaces. No differences in the resistance pattern of the oral microflora were detected between the two groups. In the amalgam group there was an increase in the relative number of intestinal microorganisms resistant to mercury, ampicillin, cefoxitin, erythromycin, and clindamycin on days 7-14. This was not statistically significant in light of the normal variations of the control group. A significant correlation between the prevalence of mercury resistance and multiple antimicrobial resistance in intestinal bacterial strains was observed.
However, these mercury deposits, which commonly occur in such cases, were successfully eliminated by the oral intake of 100 mg tablet of Chinese parsley (Cilantro) 4 times a day (for average weight adults) with a number of drug-uptake enhancement methods developed by the 1st author, including different stimulation methods on the accurate organ representation areas of the hands (which have been mapped using the Bi-Digital O-Ring Test), without injections of chelating agents. Ingestion of Chinese parsley, accompanied by drug-uptake enhancement methods, was initiated before the amalgam removal procedure and continued for about 2 to 3 weeks afterwards, and ECGs became almost normal. During the use of strong bluish curing light to create a photo-polymerization reaction to solidify the synthetic filling material, the adjacent gingiva and the side of the tongue were inadvertently exposed. This exposure to the strong bluish light was found to produce pre-cancerous conditions in the gingiva, the exposed areas of the tongue, as well as in the corresponding organs represented on those areas of the tongue, and abnormally increased enzyme levels in the liver. These abnormalities were also successfully reversed by the oral intake of a mixture of EPA with DHA and Chinese parsley, augmented by one of the non-invasive drug-uptake enhancement methods previously described by the 1st author, repeated 4 times each day for 2 weeks.
OBJECTIVE AND STUDY DESIGN:
Forty-nine consecutive patients with clinically diagnosed oral lichenoid reactions in contact with amalgam fillings were studied clinically and histologically. The long-term effect of replacement of these fillings was also examined.
RESULTS:
Seventeen (35%) patients showed positive reactions to mercury at the epicutaneous patch test that was carried out before treatment. After treatment, total regression of the lesions was found clinically in 33 (69%) and histologically in 26 (55%) patients. Most of the remaining lesions changed clinically and histologically to a less pronounced tissue reaction. Lesions in direct contact with amalgam fillings (group I) showed significantly better healing results than lesions that exceeded the contact area (group II). No difference in healing capacity was noted in the two groups between patients with positive patch reactions to mercury compared with those with negative reactions. Lesions that histologically were classified as benign oral keratosis showed a similar healing pattern as those classified as oral lichen planus.
CONCLUSION:
In group I all lesions changed histologically and clinically to a normal mucosa or to a less affected tissue reaction. In group II this change was less pronounced, which suggests that the fillings themselves were not the only factor involved in the cause of these lesions. The results suggest that various etiologic factors are involved in lichenoid reactions and that the effect of removal of amalgam fillings cannot be predicted by epicutaneous patch testing and biopsies.
Sevoflurane administration can result in increased serum inorganic fluoride ion concentrations, which have been associated with inhibition of renal concentrating ability. We measured serum fluoride levels, renal function, and recovery variables as a function of time in ASA grade I-III patients administered general anesthesia with isoflurane or sevoflurane for at least 1 h. Fifty patients were exposed to sevoflurane (< or = 2.4% inspired concentration) or isoflurane (< or = 1.9% inspired concentration) for maintenance of anesthesia as part of a multicenter trial. Blood was collected for determination of serum fluoride ion concentration, electrolytes, blood urea nitrogen, and creatinine at various time points pre- and postoperatively. Mean serum fluoride levels were significantly increased in sevoflurane versus isoflurane groups at all time points; the mean peak serum levels were 28.2 +/- 14 mumol/L at 1 h for sevoflurane and 5.08 +/- 4.35 mumol/L at 12 h for isoflurane. Sevoflurane-mediated increases in serum fluoride levels peaked at 1 h and, in general, decreased rapidly after discontinuation of the anesthesia. Three of 24 patients exposed to sevoflurane had one or more fluoride levels > 50 mumol/L. One of these patients had a serum inorganic fluoride ion level > 50 mumol/L at 12 h after sevoflurane, and an additional patient had fluoride levels > 33 mumol/L for up to 24 h after sevoflurane discontinuation. Those two patients also demonstrated an increase in serum blood urea nitrogen and creatinine at 24 h after sevoflurane administration compared with baseline. The elimination half-life of serum fluoride ion was 21.6 h. The results of this study suggest the possibility of sevoflurane induced nephrotoxicity.
In 1915, Dr. G.V. Black described a condition of bone degeneration which he termed chronic osteitis. He further described the clinical entity as localized, softened, hollowed out bone, producing various types of symptoms. Since that time, much has been learned about what is now known as NICO – Necrotizing Ischemic Chronic Osteitis – a condition also known by other names, including neuralgia-inducing cavitational osteonecrosis, Ratner bone cavity, and Robert’s bone cavity.
This report describes a patient who suffered from several complaints, which by herself were attributed to her amalgam fillings. Analysis of mercury in plasma and urine showed unexpectedly high concentrations, 63 and 223 nmol/l, respectively. Following removal of the amalgam fillings, the urinary excretion of mercury became gradually normalized, and her symptoms declined.
The aims of this study were: (1) to demonstrate how reproducible variations in incomplete anesthesia of the inferior alveolar nerve can be used as a guide to locate the etiologic sites of referred trigeminal pain emanating from the mandible; (2) to describe the salient histopathologic features of a lowgrade, nonsuppurative osteomyelitis seen in this patient population. Forty-six patients with idiopathic facial pain were subjected to a specific protocol of local anesthetic injections to sequentially block branches of the mandibular nerve to determine the effects on his/her pain. If this significantly reduced or altered the pain on three separate appointments, then exploratory surgery was conducted near identified zones of unanesthetized gingiva. Blocking (92%), bridging (4%), and divergence (4%) were observed patterns of anesthetic resistance of the mucogingival tissues used to categorize the incomplete anesthesia. A 100% correlation was found between the identified zones of unanesthetized gingiva and the discovery of intramedullary pathology. Medullary fibrosis with ischemic and degenerative changes in the cancellous bone were common findings, along with chronic inflammatory cell infiltrates and clusters of lymphocytes. It is concluded that Ratner’s method of diagnostic anesthesia be implemented when searching for occult pain producing pathology of the jaws.
On the basis of the findings of nine of our patients and our review of previously reported cases of diffuse sclerosing osteomyelitis and chronic recurrent multifocal osteomyelitis, we discuss the similarity of these two entities. Our nine patients had initially been given diagnoses of diffuse sclerosing osteomyelitis on the basis of their clinicopathologic findings. However, technetium 99m-MDP bone scans performed on four of them revealed multiple bone lesions leading to the diagnosis of chronic recurrent multifocal osteomyelitis. Furthermore, no clear difference between clinical features in the patients with multiple bone lesions and those in the patients with diffuse sclerosing osteomyelitis was found. We conclude that diffuse sclerosing osteomyelitis is an expression of chronic recurrent multifocal osteomyelitis.
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.