Fatal Staphylococcus aureus infective endocarditis: the dental implications.
Younessi OJ. Walker DM. Ellis P. Dwyer DE.
Department of Oral and Maxillofacial Surgery, Westmead Hospital Dental Clinical School, NSW, Australia.
Infective endocarditis remains an important and life-threatening infection despite improvements in diagnosis and management. There is currently a greater role for nosocomial acquisition of organisms and immunosuppression in the pathogenesis of this disease and emergence of a broader spectrum of infective organisms including those not commonly isolated from the mouth such as staphylococci. We report a case of infective endocarditis caused by Staphylococcus aureus in which the patient developed disseminated intravascular coagulation and multiple septic infarcts resulting in a frontal lobe brain abscess. Multiple dental extractions were complicated by delayed postextraction hemorrhage and the immediate cause of death was abdominal hemorrhage. The dental management in infective endocarditis should be planned in consultation with the attending physician, and should take into account both the causative organism and the presence of complications. When the oral cavity cannot be proven as the bacterial source for infective endocarditis, the immediate dental management should be directed toward improving the patient's oral hygiene and providing pain relief. Definitive long-term treatment, including any extractions, is ideally delayed until the patient has fully recovered from the infective endocarditis and its attendant complications.
Preliminary investigation of the association of oral lichen planus and hepatitis C.
Bagan JV. Ramon C. Gonzalez L. Diago M. Milian MA. Cors R. Lloria E. Cardona F. Jimenez Y.
Department of Stomatology, Valencia University General Hospital, Spain.
OBJECTIVE: The aim of this investigation was to determine if an association exists between hepatitis C virus and oral lichen planus. STUDY DESIGN: Three groups of subjects were selected: 505 patients with hepatitis C virus infection (group 1), 100 patients with oral lichen planus (group 2), and a randomly selected control group (age- and gender-matched) of 100 healthy subjects (group 3). The prevalence of oral lichen planus was determined in groups 1 and 3, and the prevalence of hepatitis C virus infection was established in groups 2 and 3. RESULTS: The prevalence of oral lichen planus was 3.36% (n = 17) in group 1 and 1% (n = 1) in the control group; the prevalence of hepatitis C virus infection was 23% (n = 23) in group 2, and 5% (n = 5) in the control group. No significant differences were observed in the incidence of oral lichen planus in group 1 between those patients who received interferon and those who did not. The 17 patients in group 1 who manifested oral lichen planus and hepatitis C virus infection simultaneously exhibited a marked tendency to have only reticular lesions (70.6%), with involvement of the buccal mucosa in 88.2% of these patients, the tongue in 29.4%, and the gingiva in 11.8%. Analyzing a randomized subgroup of 143 patients from group 1 (subgroup 1) that was matched by age and gender with groups 2 and 3, we found that the incidence of oral lichen planus in patients with hepatitis C virus infection (subgroup 1) was greater than in the control group (5.59% vs 1%), though this was not statistically significant (chi2 = 0.119; p = 0.06). In contrast, group 2 exhibited a statistically significant higher incidence of hepatitis C virus infection (23%) than the controls (5%; chi2 = 0.259, p = 0.0002). CONCLUSIONS: The prevalence of hepatitis C virus infection in patients with oral lichen planus was greater than in the control series. In our opinion this observation warrants the investigation of potential concomitant hepatitis C virus infection in patients with oral lichen planus.