The Toothbrush, Kaposi's Sarcoma and AIDS: A Case demonstrating interesting associations
IntroductionEarly in 1994, one of the authors (RTG) published a blinded study on the possibility of finding HIV (Human Immunodeficiency Virus) pro-viral DNA on toothbrush bristles of AIDS patients. The study demonstrated that HIV pro-viral DNA could be found on the toothbrushes of AIDS patients. Even though it is well recognized that saliva is protective against transmission of the HIV, the toothbrush collects and retains blood epithelial cells from infected gingiva of AIDS patients and can thus be a ready source of the virus 2,3,4. Several months earlier, two articles had appeared which described HIV transmission between two sets of brothers with the most likely mode of transmission being the toothbrush. Similarily, multiple studies have confirmed the importance of the toothbrush in transmitting a wide range of microbial diseases. For this reason, AIDS patients presented to the clinics of the University of Oklahoma, College of Dentistry are given specific toothbrush instructions which take into account the severity of the patient's dental disease and the overall extent of the AIDS along with their CD4+ cell count. A case is presented which shows unique response to this toothbrush hygiene and underscores the importance of considering lifestyle-related transmissions of disease.
Case ReportThe patient is a 29-year-old Caucasian male who referred by his family physician to an oral pathologist (RTG) at the University of Oklahoma, College of Dentistry with a chief complaint of rapidly enlarging vascular lesions of the anterior maxillary gingiva and the right hard palate. He had no other oral manifestations of AIDS; had no other vascular lesions anywhere else; and had no other systematic manifestations of AIDS. The patient was HIV positive with a CD4+ cell count at the time of presentation of 181 cells/m3. He had initially tested HIV positive six years prior to presentation, however, a repeat of that test revealed he was HIV negative. He had yearly HIV tests after first battery, but was always found negative until just before presentation. He was taking zidovudine (AZT), 500mg/day, and trimethoprim/sulfamethoxazole (Bactrim), 320mg/1600mg/day. He was a non-smoker and had an occasional alcoholic beverage. Physical examination at the time of presentation revealed a well nourished 29-year-old Caucasian male in no acute distress. His vital signs were; blood pressure = 143/74 mm Hg; pulse = 99/min; respiration's = 21/min; and temperature (oral) = 97.9 F. His neck was negative for lymphadenopathy and other masses. The oral examination revealed a 3.5 cm ? 2.6cm ? 2.3cm, deep purple lesion of the anterior maxilla which involved the attached gingiva and extended into the unattached gingiva and extended into the unattached gingiva to near the vestibule. The lesion also extended posterior through the interdental papilla onto the anterior hard palate. A second lesion 2.0 cm ? 1.5 cm ? >0.5 cm, was found on the right hard palate at the molar region. Neither lesion was pulsatile and neither lesion hemorrhaged. There was generalized mild gingivitis associated with moderate calculus accumulation. The only other finding of note was a generalized xerostomia. X-ray examination revealed an impacted lower right third molar, but no evidence of boney involvement by either vascular lesion. He was immediately referred to an oral surgeon for biopsy of both vascular lesions. He was also seen by a dental hygienist (VA) for oral prophylaxis and sulcular toothbrushing instructions. He was instructed (by RTG) to use two toothbrushes/day, placing each in the dishwasher after use and to change both toothbrushes weekly; all toothbrushes were two rows and soft. The biopsies showed essentially the same histology: a vascular proliferative process with extravasated red blood cells and hemosiderin. The gingival lesion showed a moderated infiltrate of both lymphocytes and plasma cells, while the palatallesion showed basically no inflammatory response. Both biopsies were stained with Warthin-Starry stain and were reacted immunocytochemically with antibodies against Rochalimaea henselae. Both special stains were negative for microorganisms and a diagnosis of Kaposi's Sarcoma (KS) was rendered. After explanation of the biopsy findings and the presentation of treatment options, the patient elected to simply have the lesions observed monthly for a period of three months and to decide on a treatment course after that period of time. The patient returned in one month for routine follow-up while the palatal lesion had increased in size by 1.0 cm in two dimensions. During this period, the patient took additional prescription drugs, but did take a multivitamin. The only lifestyle change (other than his oral hygiene and toothbrushing habits) was improvement of diet. Over the next three months, the palatal lesion continued to slowly increase in size while the gingival lesion nearly disappeared. The patient continued to be seen on a regular basis and continued to have growth of the palatal lesion with basically no change in the gingival lesion. Six months after his initial presentation, his CD4+ cell count dropped to 110 cells/mm3. After the six-month appointment, the patient requested and was tried on a regimen of erythromycin (2 gm/day) and when this regimen was unsuccessful in producing results, he was requested in a regimen of Vibramycin (doxycycline 100 mg/day). Neither regimen produced a change in either lesion and the drugs were discontinued. One year after presentation, the palatal lesion had doubled in size and the election was made by the patient to have radiation therapy to the lesion; the anterior maxillary gingival lesion continued unchanged. Even though several small residual foci of vascular process remained, the elections were not to biopsy or exercise this tissue.
DiscussionA case is presented which demonstrates the importance of factors such as toothbrush care, which often are overlooked when treating AIDS patients. Clearly, if a microorganism like Rochalimaea henselae had caused either lesion, toothbrush transmission to other parts of the oral cavity and/or re-infection of an existing lesion would have been important. In the present case, because neither lesion had a demonstrable microbial cause, the association between the toothbrush and the lesions is more difficult to make. Two groups have recently demonstrated some interesting findings, which may shed some insight into the apparent disparity between the palatal KS and anterior maxillary gingival KS. Mallery et al have shown that AIDS-KS cells grown in tissue culture have an increased growth rate in response to increased oxygen levels such as those found infections. Regezi and his co-workers found that a number of cytokines released inflammatory processes such as periodontal disease in AIDS patients have the effect of promoting KS growth. Gingival disease was found in our patient and is common finding in AIDS patients, in general. Recently, gingival disease has been found to indicate a decreasing number of CD4+ cells. The possible association between the toothbrush and the resolution of the anterior maxillary gingival lesion may have been in the reduction of inflammation and the lack of microbial reintroduction by the lack of microbial reintroduction by the toothbrush, therefore altering the oxygen levels and cytokine levels, inhibiting KS growth. All of this in the presence of a decreasing CD4+ cell counts (181 cells/mm3 to 110 cells/mm3). In contrast was the palatal lesion, which did not have the same factors, involved and continued to grow.
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