Asymptomatic hepatocellular carcinoma metastatic to the mandible

Asymptomatic hepatocellular carcinoma metastatic to the mandible Report

of a case

Gerald Goveia, D.M.D., Corm.

and Saul Bahn, D.M.D.,

M.Sc.D., West Haven,

A very rare case of a hepatoma metastatic to the mandible is presented. The patient’s mandibular lesion was asymptomaticexcept for swelling, and the liver lesion was diagnosedonly after diagnosis of the mandibular lesion.

0 nly

1 per cent of all oral malignancies are metastatic lesions.’ Castigliano and Rominger,’ in their review of 176 cases in 1954, found no cases of hepatocellular carcinoma metastatic to the jaws. Clausen and Poulsen,3 in a review of the literature from 1884 to 1961, reported ninety-two cases which fulfilled their criteria for metastasis to the jaws, only one of which was a hepatocellular carcinoma. In a similar study of twenty-five cases done by Meyer and Shklar,4 there were no cases of hepatocellular carcinoma. Other reviews further confirm the rarity of the metastatic spread of this lesion to the jaws.5-’ Hepatocellular carcinoma metastatic to the mandible has been reported only four times.*-” Three other cases of metastasis to the gingival tissues have also been reported. 12-14 Hepatocellular carcinoma, arising from the parenchymal cells of the liver, is rare.8 It is seen most frequently between the ages of 45 and 60 years. Two thirds of the cases develop in patients with a previous history of cirrhosis, hemochromatosis, parasitosis (Schistosomiasis or Clonorchiasis), or clinical toxicity. Intrahepatic metastasis of hepatocellular carcinoma often occurs early. Fifty per cent of these tumors give rise to extrahepatic metastasis, usually to the lung or regional lymph nodes.8 This article presents a case of hepatocellular carcinoma metastatic to the mandible, which was first diagnosed on the basis of the histopathologic features of the mandibular lesion. CASE REPORT The patient, an 82-year-old male Caucasian, was admitted to the hospital on March 18, 1977, with a chief complaint of jaundice and an enlarged abdomen of 1 month’s duration. He had been 424

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1978 The C. V. Mosby

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Fig. 1. Full-face, frontal view of patient showing the swelling of the left periauricular area

experiencing pain in the left upper quadrant and anorexia for I week prior to admission, and reported a IO-pound loss of weight during the previous month, with nausea and vomiting. The urine had been dark brown for 3 days. The past medical history was negative for gallbladder or liver disease, peripheral vascular disease, intravenous injections, hepatitis, or allergy. The patient had last travelled outside of Connecticut about 50 years prior to hospitalization. His intake of alcohol was only 2 or 3 ounces per week, and he had not smoked for 20 years. He had been taking Maalox for 5 days prior to admission, with no relief of symptoms. The only previous hospitalization had been 1968, for bilateral iridectomy. The physical examination, performed by several medical residents, disclosed a well-developed, obese man who appeared to be 10 years younger than his stated age. The blood pressure was 150/88 mm. Hg, pulse was 96 and regular; oral temperature was 101” F.; and respirations were 25 per minute. Initial examination of the head and neck was unremarkable as documented by the four medical residents. The face was symmetrical in appearance. The abdomen was distended and there was a liver span of 12 cm. The liver was not palpable below the costal margin because of voluntary guarding by the patient. A left inguinal hernia and a four-plus prostatic enlargement was found during the admission physical examination. The chest radiograph revealed the presence of atelectasis of the lower lobe of the left lung. The laboratory data were as follows, with the abnormal findings given in italics: hematocrit, 48 per cent; hemoglobin, 16.9 Gm. per cent; white blood cell count, 12,500; remainder of the complete blood count was within normal limits; chloride, 99 mEq./liter; carbon dioxide, 30mEq./ 1; potassium, 4mEq.!l; blood urea nitrogen, 26 mg./lOO ml.; glucose, 140 mg./lOO ml.; bilirubin, 15.5 mg.1100 ml.; serum gluramic oxaloaceric acid, 470 units/ml.; alkaline phosphatase, 348 I.U.iml.; lactic dehydrogenase, 266 I.U. /ml. and amylase, 150 Somogyi U/ 100 ml. Prothrombin and partial

thromboplastin times were within normal limits. The urinalysis showed a specific gravity of 1.029; pH, 5.0; 3 + protein; 2 to 3 white blood cells, and a large amount of bile. No organisms were found on Gram stain. The initial impression was that of jaundice, fever, anorexia, left-upper-quadrant pain with probable obstruction secondary to bilary stones, and atelectasis due to guarding. The patient was placed on ampicillin, clear liquids, and intravenous fluids. He was followed by the medical service, and on March 21, was noted to be afebrile, with the values for the liver function tests considerably decreased, as follows: bilirubin, 2.3 mg.//OO ml.; serum glutamic oxaloacetic acid, 66 lJ.lml.; alkaline phospharase, 158 I.U.lml.; lactic dehydro-

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Fig. 2. Posterior view of patient illustrating the swelling below the left ear.

genase, 194 I.U./ml. The blood urea nitrogen was 11 mg./lOO ml., andglucose was 1.50mg.//OO ml.; rheumatoid factor was negative, HAA was negative, and ANA was negative. The serum amylase, however, was elevated to 230 U./ml. The assessment was “probable gallbladder disease with questionable passage of small stones.” A liver scan showed a filling defect of the right upper lobe. The findings on an echogram of the liver and gallbladder were normal, but a cystic mass in the midline of the epigastrium was noted. An assessment of “questionable pancreatic pseudocyst or ruptured duodenal ulcer with abscess was recorded.” A repeat of the echogram confirmed the gallstones and the cystic mass suspected to be a liver abscess. On March 28, 1977, the patient complained of dysuria. The results of laboratory tests showed that the patient’s condition was stable and the jaundice was resolving. The patient was transferred to the surgical service on April 1, 1977, and scheduled for exploratory laparotomy in order to rule out a perforated duodenal ulcer with abscess, and cholecystectomy. The surgeon’s physical examination revealed an enlarged, nontender liver 5 cm. below the right costal margin. The HEENT examination gave negative findings. An intravenous cholangiogram on April 4 showed gallstones, and on scan there was a cold nodule in the right lateral lobe of the liver. An operation was scheduled for April 15. On April 12, the patient presented to the dental clinic for his routine oral examination. At this time a swelling 2.0 by 4.0 cm., of the left preauricular area was noted (Figs. 1 and 2). When questioned, the patient related that his wife had noticed the swelling just that morning. It was not painful and there was no paresthesia or other symptoms. The 3.0 cm. thick mass had a rubbery consistency when palpated, and a fluid-like wave could be felt intraorally when the lesion was depressed extraorally (Fig. 3). It appeared that both medial and lateral cortices of the mandible were clinically involved. The panoramic radiograph showed a radiolucency 2.5 by 4.0 cm., of the left ascending ramus of the mandible which was well circumscribed but showed opaque specks toward the inferior border and angle of the mandible (Fig. 4). Differential diagnoses included calcifying

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Fig. 3. Intraoral view showing the swelling of the left retromolar area and anterior tonsillar pillar with recent

needle biopsy sites.

Fig. 4. Radiographof left ascendingramusof the mandible illustrating circumscribed, diffuse radiolucency with opaque specks near the inferior border.

epithelial odontogenic tumor, residual cyst, ameloblastoma, hemangioma, aneurysmal bone cyst, metastasis, or primary malignant tumor. This was reported to the surgical service, and a request for approval to aspirate and needle biopsy was made. On April 1.5, a cholecystectomy, exploration of the common bile duct, and biopsy of the liver cyst were performed in the operating room with the patient under general anesthesia. The findings were multiple large stones in the gallbladder and common bile duct, adhesions, a healed duodenalulcer perforation, cyst of the right lobe of the liver, and lobulated liver. It was reported that the biopsy site of the cyst of the liver bled excessively and was still oozing on closure. The patient’s recovery was uneventful.

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Fig. 5. Photomicrographof the mandibular lesion demonstratinglarge round nuclei with moderately anaplastic cytoplasm resembling liver tissue. (Magnification, X 100.)

The histopathologic findings were: liver cyst contents composed of blood and hepatic tissue, slightly hyperplastic liver tissue from a biopsied liver nodule, cholelithiasis, and chronic cholecystitis with a thickened wall of the gallbladder. No tumor cells were identified. On April 26, the patient was taken to the Oral Surgery Department for aspiration and biopsy of the mandibular lesion. A left inferior alveolar nerve block, by means of 2 per cent Xylocaine with 1 : 100,000 epinephrine, was administered. On aspiration of the left mandibular ramus lesion, with a 27 gauge needle, there was minimal bloody return (0.1 c.c .) but no cystic fluid. The decision was made to do a needle biopsy because of the gelatinous consistency of the tumor mass which was appreciated at the time of aspiration. A biopsy with the use of a Vim-Silverman needle was performed. The gross specimen was of soft consistency, and minimal bleeding followed the removal of the tissue core. Because the lesion appeared to have grown since initial observation of it on April 12, a metastatic malignant tumor was suspected. The histopathologic features of the mandibular lesion were read as indicating hepatocellular carcinoma (Fig. 5), and a repeat biopsy was requested for ultrastmctural studies. On April 28, the needle biopsy was repeated, with the same gross findings. A part of the specimen was subjected to electron microscope studies. Histopathologically, there were large flat cells from tubular structures and cords in continuous mass with scant supporting tissue. The nuclei were large and rounded and the cytoplasm was moderately anaplastic. The tumor was abundantly vascularized. A microscopic review of the laparotomy biopsy specimens and recuts, together with reticulum stain, made it clear that the atypical liver-cell proliferation was, indeed, that of an hepatocellular carcinoma. The cells of the mandibular biopsy specimen were seen to be about four times as large and the nuclei were considerably more hypertmphic than in the liver biopsy specimen (Figs. 6 and 7). The ultrastmctural description of the needle mandibular biopsy follows: Thick sections showed large tumoral hepatocytes. Thin sections disclosed well-differentiated hepatocytes. The most prominent change was dilatation and fragmentation of RER (rough endoplasmic reticulum). There were numerous cross sections of smooth endoplasmic reticulum and RER. In general, the mitochondria were decreased in number and in size, although the best normal-looking cells showed normalappearing mitochondria as well as glycogen rosettes. Bile canaliculi were seen, reinforcing hepatic

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Figs. 6 and 7. Photomicrographsof liver biopsy specimen showing well-differentiated cells with atypical proliferation. (Fig. 6, magnification, x 100; Fig. 7, X440.) origin of these cells. The diagnosis was consistent with metastatic well-differentiated carcinoma.

evidence

of

hepatocellular

DISCUSSION

Metastasis of hepatocellular carcinoma to bone is rare. When a malignant tumor metastasizes to bone, it is usually to those osseous structures with active marrow; therefore, the ribs, sternum, vertebral bodies, pelvis, calvarium, and proximal femur are involved. The mandible also contains active marrow throughout life. The most common tumors that metastasize to bone include carcinoma of the breast, prostate, lung, colon, bladder, stomach, thyroid, and kidney.8 The usual symptoms of metastasis are local pain, swelling, paresthesia, and loosening of teeth. Pathologic fractures are rare.3 This case is unusual in that the patient was totally unaware of the jaw lesion until the

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swelling was noticed. There were no other symptoms. Although upon initial dental examination the lesion was thought to be slow growing, the rapidity of its growth was appreciated when it was observedto enlarge betweenexamination on April 12 and biopsy on April 26. It would seemreasonablethat there was no swelling of the face at the time that the patient was admitted to the hospital on March 18. In this case, becauseit was thought that the lesion might be malignant, a needle biopsy was decided upon. This was a wise decision in that previous cases have served to illustrate the propensity that metastatic hepatoma has for severe or massive hemorrhage.s* lo It is interesting to note that the disease which caused the patient’s symptoms on admission was apparently due to gallbladder obstruction secondary to stones rather than primary liver disease. The liver tumor in this patient was asymptomaticand final diagnosis was madeonly after discovery and biopsy of the mandibular lesion. This further reinforces the importance of a comprehensive examination of the oral cavity, head, and neck in all patients. SUMMARY

A very rare caseof a hepatomametastaticto the mandible is presented.The mandibular lesion was asymptomaticexcept for swelling, and the liver lesion was diagnosedonly after diagnosis of the mandibular lesion. REFERENCES

1. Bertelli, A., Costa, F., and Miziarra, J.: Metastatic Tumors of the Mandible, ORALSURG.30: 21, 1970. 2. Castigliano, A. A., and Rominger, C. J.: Metastatic Malignancy of the Jaws, Am. J. Surg. 87: 496, 1954. 3. Clausen, F., and Poulsen, H.: Metastatic Carcinomato the Jaws, Acta Pathol. Microbial. &and. 57: 361, 1963. 4. Meyer, I., and Shklar, H.: Malignant Tumors Metastatic to Mouth and Jaws, ORALSURG.20: 350, 1965. 5. Cash, C. D., Rayer, R. Q., andDahlin, D. C.: MetastaticTumors of the Jaws, ORALSURG.14: 897,196l. 6. McDaniel, R. K., Luna, M. A., and Stimson, P. G.: Metastatic Tumors in the Jaws, ORALSURG.31: 38, 1971. 7. Sachs, R. L.: Metastatic Carcinoma to the Jaw Bones, J. Dent. Res. 43: 799, 1964. 8. Yacabucci, J., Mainous, E., andKramer, H.: Hepatocellular CarcinomaDiagnosedFollowing Metastasisto the Mandible, ORAL SURG.33: 888, 1972. 9. Dick, A., Mead, S., Mensh, M., and Schatten,W .: Primary Hepatoma With Metastasisto the Mandible, Am. J. Surg. 94: 846, 1957. 10. Appenzeller, J., Weitzner, S., and Long, G.: Hepatocellular CarcinomaMetastatic to the Mandible, J. Oral Surg. 29: 668, 1971. 11. Lepesteur, J., et al.: Mandibular MetastasisFrom Hepatoma. Rev. Stomatol. Chir. Maxillofac. 74: 533, 1973. 12. Lund, B. A., and Soule, E. H.: Hepatocellular Carcinoma With Metastasisto Gingival Mucosa, J. Oral. Surg. 28: 604, 1970. 13. Radden, B. G., and Reade, P. C.: Gingival MetastasisFrom a Hematoma, ORALSURG.21: 621, 1966. 14. Lapeyrolerie, F. M., and Manhold, J. H.: HepatomaMetastaticto the Gingiva, ORALSURG.18: 365, 1964. Reprint

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Dr. Saul L. Bahn Veterans Administration Hospital West Haven. Conn. 06516