[Maxillary osteonecrosis associated with bisphosphonates].
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Biomedical subjects
Publications and source records attributed to Carlos Madrid.
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About a decade ago, bisphosphonates were introduced as an alternative to hormone replacement therapies for osteoporosis and to treat osteolytic tumors. More recently, it has became evident that the bisphosphonates used intravenously such as pamidronate (Aredia; Novartis Pharmaceuticals Corp., East Hanover, NJ) and zoledronate (Zometa; Novartis Pharmaceuticals Corp.), in particular, could lead to painful refractory bone exposure (sometimes termed osteochemonecrosis or osteonecrosis) in the jaws. Patients with osteonecrosis of the jaws usually present after dental treatment with oral signs and symptoms of painful, exposed, and necrotic bone, primarily of the mandible and, to a lesser extent, the maxilla. Although the precipitating event that produces this complication may be spontaneous, there is little doubt that oral surgery and endosseous implants can be responsible. Exodontia is the main precipitant. The present postulated mechanism of osteonecrosis of the jaws is that prolonged use of bisphosphonates may suppress bone turnover to the point that the repair function of physiologic microdamage of bone is abolished. Such a mechanism could presumably interfere with the healing process after implant placement. Although, to our knowledge, there is no evidence that bone disorders are a contraindication to implants, there is evidence that bisphosphonate therapy is a contraindication. Where possible, extractions should be avoided, and it is best to avoid all elective oral surgery in patients on bisphosphonates, including endosseous implant placement, or the treatment should be performed well before commencing bisphosphonates. If surgery is essential on a patient taking bisphosphonate therapy, the patient must be counseled about the risks.
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A major concern in the management of patients under anticoagulants is the potential for excessive bleeding after dental procedures. Recommendations for the administration of oral anticoagulants in conjunction with oral surgery range from complete withdrawal of anticoagulants to the maintenance of an unchanged therapy. Rising evidences show that the alteration of anticoagulation is not necessary for patients with INR of 4 or less previous to tooth extractions. Topical antifibrinolytics as tranexamic acid control successfully alveolar bleeding. It is time to stop interrupting anticoagulant therapy for oral surgery. A theoretical risk of hemorrhage after dental surgery in patients at therapeutic levels of anticoagulation exists but it is minimal and is greatly overweighed by the risk of thromboembolism after alteration of the anticoagulant therapy.
One 53-year-old male was referred with a history of sensitive peripheral neuropathy and Raynaud disease leading to suspect a Sjögren syndrome (SS). Labial salivary gland biopsy shown the classical features of chronic lymphocytic sialadenitis. As clinical and immunologic tests were positive, we conclude to a chronic lymphocytic sialadenitis simulating SS. Enzyme immunoassay and recombinant immunoblot were positive to HCV. Circulating HCV-RNA was detected by PCR. Liver biopsy revealed chronic persistent hepatitis. In one second biopsy, RNA was extracted. PCR amplification and southern blot hybridization for HCV-RNA were performed. After a 8-month treatment by interferon alpha, HCV-RNA was no longer detected in the serum. There was an objective improvement of the Schirmer test. The detection of HCV-RNA in the salivary glands of a Sjögren like syndrome-patient suggests that a direct infection of the salivary glands by HCV could play an important role in the pathogenesis of HCV related sialadenitis.