Black hairy tongue.

In this disorder, the filiform papillae on the dorsum of the tongue are
hyperplastic and dark black. The pigmentation may be the result of trapped chromogenic
bacteria, food, coffee, or tobacco.. Black hairy tongue (lingua villosa nigra) may be
associated with the presence of chromogenic organisms (e.g., C. albicans) and the use
of certain medications (e.g., doxycycline and bismuth). The pathophysiology is thought
to be due to proliferation of the filiform papillae of the tongue, which stain black with
porphyrin-producing chromogenic bacteria or yeast, treated with a short course of
fluconazole. The black discoloration and hairy appearance of the tongue resolved in 3
days.

Figure 1. Clinical, Pathological, and Molecular Progression of Oral Cancer.

Panel A shows a typical clinical presentation of oral cancer. Benign squamous

hyperplasia can often appear similar to normal mucosa. Novel molecular approaches
have yielded considerable understanding of the field-cancerization hypothesis originally
proposed by Slaughter and colleagues.23 In most patients, cellular repopulation in
geographically distinct areas gives rise to multiple clinical lesions. Although these lesions
may have different histopathological patterns, as shown, they are often clonally related,
arising from the same cell. The progression from normal-appearing mucosa to invasive
cancer is depicted in Panel B. Normal-appearing mucosa already harbors early genetic
changes (Panel C), often with loss of 9p21 and inactivation of p16. Further clinical
progression through dysplasia is associated with further genetic changes. Carcinoma in
situ often harbors most of the genetic changes described in invasive carcinoma. LOH
denotes loss of heterozygosity. (Courtesy of Joseph A. Califano.)
Figure 1. Progression from Leukoplakia to Cancer of the Oral Cavity.

The top panels show the clinical progression of a patient's oral leukoplakia lesion (left-
hand panel) to an oral cancer (right-hand panel), which developed three years after the
complete resection of the leukoplakia. The middle panels show histologic progression
from hyperplasia to cancer (hematoxylin and eosin, x40). The transition from severe
dysplasia to an early stage of oral cancer can be seen in the far-right-hand panel. The
model of molecular progression shown in the bottom panels of the figure indicates where
certain losses of heterozygosity can occur; the cumulative number of genetic alterations
is more important than the order in which they occur. A low risk is correlated with no loss
of heterozygosity at 3p or 9p; an intermediate risk with loss at 3p, 9p, or both; and a high
risk with loss at 3p, 9p, or both plus losses at any of the other chromosomes.

Fig. Lichen plan

Figure 1. Photographs of the Patient's Lips (Panel A), Tongue (Panel B), and Palate and
Buccal Mucosa (Panel C). The lips are erythematous, with erosions. The mucosa of the
tongue is denuded, with areas of white, fibrinous exudate. There are diffuse erosions
with white exudate on the palate and buccal mucosa.

Figure 1. Oral Mucositis after Chemoradiotherapy in a Patient with Leukemia, Who Was
Later Treated with Bone Marrow Transplantation.

The principal clinical manifestations of HIV infection or AIDS in the oral cavity:
candidiasis, salivary-gland disease, Epstein–Barr virus and hairy leukoplakia, Kaposi's
sarcoma, oral ulcers, and HIV-associated periodontal conditions. Other chapters deal
with HIV infection in children, occupational safety in the dental environment, and systems
for providing dental health care to patients with HIV infection or AIDS.

Figure 1. Development and Resolution of a Kaposi's Sarcoma Lesion after Oral Surgery
in a Patient with Human Immunodeficiency Virus Infection.

Fig. 2. Oral ulceration in a person with acute HIV-1 infection who also presented with
thrush.
Major Aphthous Ulcer in Acquired Immunodeficiency Syndrome (AIDS).

Figure 3. Clinical Findings in Epstein–Barr Virus (EBV) Infection.

Panel A shows petechiae of the eyelids with periorbital edema, and Panel B shows
tonsillar enlargement in a patient with infectious mononucleosis. Panel C shows macular
rash after ampicillin therapy in a patient with infectious mononucleosis. Panel D shows
oral hairy leukoplakia in a patient with AIDS. Photographs courtesy of Maria Turner, M.D.

Figure 3. Oral Ulcers Caused by Conditions Other Than Aphthous Stomatitis.

Panel A shows lichen planus with a superficial irregular erosion on the lip (arrowhead).
Panel B shows pemphigus on the buccal mucosa, with irregular ulceration (arrowhead).
Panel C shows pemphigoid on the gingiva (arrowhead), causing erosion. Panel D shows
lupus erythematosus with irregular ulceration on the buccal mucosa (arrowhead). Panel
E shows squamous-cell carcinoma on the buccal mucosa in the form of a mass that has
ulcerated (arrowhead).
Sifilis – manifestari orale

Physical examination revealed pseudomembranous lesions and erosions of the tongue,

the hard and soft palate, and tonsils, as well as generalized lymph-node enlargement.
Condylomata lata, macular skin lesions, and alopecia were absent. Titers of Treponema
pallidum were 1:81,920 on hemagglutination assay, and a fluorescent treponemal
antibody absorption test was positive. A serologic test for human immunodeficiency virus
infection was negative. The patient was treated with intramuscular penicillin G
benzathine (2.4 million U), with full resolution of the oral lesions within two weeks.

Culture of the lesions showed herpes simplex virus type 1 (HSV-1). Differing from
herpetic vesicles on the skin, round, discrete areas of ulceration are the typical
presentation of herpetic glossitis.

An eight-year-old girl had a four-month history of painful mouth lesions,

resulting in decreased oral intake and weight loss, and a one-year history of intermittent
abdominal pain and irregular bowel movements. On examination, she had cheilitis,
redness and swelling of the gingiva, and oral ulcerations (Panels A and B), as well as
tenderness of the right lower quadrant and a perianal fissure. Colonoscopy with multiple
biopsies revealed findings consistent with the presence of Crohn's disease. Five weeks
after the initiation of treatment with 40 mg of oral prednisone daily (2 mg per kilogram of
body weight), the patient's cheilitis had greatly improved (Panel C), as had the
gastrointestinal symptoms. The gastrointestinal disease relapsed when prednisone
therapy was tapered and then stopped. During the following 3 1/2 years the patient
continued to have active disease despite treatment with prednisone and azathioprine,
but the lip and oral lesions did not recur. Intestinal obstruction and peritonitis developed
and required resection of the ileocecal region and anastomosis of the ileum to the
ascending colon. The doses of prednisone and azathioprine were reduced gradually, and
at the most recent follow-up visit, the patient was in remission while taking 25 mg of
azathioprine three times daily.

61-year-old man presented for evaluation of increasing abdominal pain of eight months'
duration. The patient reported having worked in a lead-smelting company for the past 30
years. The physical examination showed a bluish discoloration of the gums (Panel A).
The blood level of lead was 130 µg per deciliter (6.3 µmol per liter [reference range, <20
[1.0 µmol per liter]). His hemoglobin level was 11.5 mg per deciliter, and basophilic
stippling was evident in some erythrocytes on a blood smear stained with May–
Grunwald–Giesma stain (Panel B). The patient was given a diagnosis of chronic lead
poisoning.

Contact stomatitis la bifosfonat. Pentru excludere citodiagnostic and microbiologic

evaluations, including those for cancer, herpesviruses, and Treponema pallidum, were
unrevealing.
Physical examination revealed mild hyperreflexia, Chvostek's sign, and Trousseau's sign,
as evidenced by changes in the patient's right hand (Panel A) 90 seconds after insufflation
of the blood-pressure cuff to 10 mm Hg above systolic pressure (Panel B). Laboratory
studies showed hypocalcemia, hypomagnesemia