J Oral Maxillofac 49:397-400.
Surg
1991
A Postextraction STEVEN D. VINCENT,
Soft-Tissue Abnormality DDS, MS,* AND LEON A. ASSAEL,
Case Presentation
nontender, friable soft tissue distal to the mandibular left first molar (Fig 1). The soft tissue measured 2 x 1.5 cm in greatest dimension and appeared to extend anteriorly, involving the gingiva on the buccal and lingual aspects of the first molar. The first molar had class II mobility and bleeding 5- to 6-mm periodontal pockets. No other lesions were noted intraorally. Periapical radiographs taken before the tooth extraction and at the time of our examination 2 months later (Figs 2 and 3) showed healing of the extraction site.
The patient, a 73-year-old alert, normally developed, white woman, in no distress, was referred for evaluation of an unusual-appearing extraction site. The mandibular left second molar had been extracted without complication because of periodontal and pulpal disease 2 months previously. No postoperative antibiotics or surgical packings were used, and subsequent healing was unremarkable, with no evidence of excessive inflammation. One month later, the patient was seen for a prosthodontic consultation, at which time the extraction site was noted to be surfaced by rough, relatively pale, asymptomatic soft tissue. At 2 months, the soft-tissue changes were noted to be persistent and the patient was referred to our clinic for evaluation. At the time of our initial evaluation the patient was taking Cardizem (Marion Laboratories, Kansas City, MO), Zantac (Glaxo Pharmaceuticals, Glaxo, NC), and ASA. She reported an allergy to penicillin characterized as urticaria. She denied past or present tobacco or ethanol use. She was currently under the care of a physician for occasional angina and a hiatal hernia. She had a partial left arm paralysis as the result of a vertebral injury 29 years ago.. She had undergone a bilateral mastectomy and left unilateral axillary node dissection 28 years ago for carcinoma of the breast. She denied all other central nervous system, respiratory, cardiovascular, gastrointestinal, genitourinary, skin, musculoskeletal, hematologic, or allergic disease or abnormality past or present. The patient had a past history of routine regular dental care. She wore no removable prosthetic appliances. Extraoral examination showed no tenderness of the masticatory muscles, temporomandibular joint, or carotid or temporal artery to palpation. There was no restriction of, or pain during, mandibular movements. No temporomandibular joint noise was auscultated during jaw movements. Tbe patient was afebrile and there was no submandibular or anterior cervical lymphadenopathy. Gross analysis of cranial nerves III-XII was within normal limits, including pinprick sensory evaluation of the left third division of the trigeminal nerve. The intraoral examination showed rough, fissured,
Differential Diagnosis Leon A. Assael, DMD The basic categories of disease that must be considered in the differential diagnosis of this postextraction soft-tissue abnormality are inflammatoryinfectious, neoplastic, and hyperplastic-reactive. A common form of inflammatory-infectious pathosis seen in such situations is simple persistence of granulation tissue in the socket. An exuberant form of this process produces a pyogenic granuloma. Granulation tissue persists when necrotic bone frag-
ments, foreign bodies such as retained calculus, or tooth fragments are present in the socket. Often they are too small to be evident on the postoperative radiograph. Periodontitis in the adjacent tooth may rarely involve the adjacent socket, and in view of the furcation involvement of the first molar, this is a definite possibility. Other unusual causes of persistent infected tissue include tuberculosis, actinomycosis, regional fungal infection such as histoplasmosis, or a pulse granuloma induced by bean protein. The history is not supportive of an inflammatoryinfectious process. The 2-month postoperative radiograph does not show a destructive process of the type produced by osteomyelitis or the presence of a sequestrum. The clinical examination did not reveal marked swelling, redness, warmth, or tenderness. Moreover, the irregular, rough, keratinized, pale surface of the lesion does not support a diagnosis of pyogenic granuloma, which generally has a smooth surface. Hence, there is scant clinical information to support the possibility that this lesion represents an inflammatory-infectious process. Neoplasia persisting in an extraction site is an occasional finding that draws every clinician’s at-
* Associate Professor, Department of Oral Pathology and Diagnosis, University of Iowa, Iowa City. t Associate Professor and Residency Program Director, Department of Oral and Maxillofacial Surgery, School of Dental Medicine, University of Connecticut Health Center, Farmington, CT. Address correspondence and reprint requests to Dr Vincent: University of Iowa, College of Dentistry DSB 356, Department of Oral Pathology and Diagnosis, Iowa City, IA 52246. 0 1991 American geons
Association
of Oral and Maxillofacial
DMDt
Sur-
0278-2391/91/4904-0012$3.00/O
397
398
A POSTEXTRACTION
SOFT-TISSUE
ABNORMALITY
FIGURE 1. A mirror image of the rough mucosa distal. buccal, and mesial to the first molar.
tention to the importance of abnormal postoperative healing. Certain tumors appear to be more frequently evident in tooth sockets. These include lymphoma, myeloma, and the leukemias that may become evident in these sites because of the chronic inflammatory cells that are already present. Metastatic solid tumors are rare, but continually appear as case reports. A review of all pathologic specimens seen at Columbia Presbyterian Hospital
over a 47-year period showed only 22 cases of metastatic tumors of the mandible.* These included tumors whose primary lesions were in the breast, lung, kidney, colon, prostate, and thyroid.“4 If this lesion represented a metastatic tumor, it would likely be associated with a destructive radiographic change over the 2 months since the extraction. Although the extraction site does not appear to be full of mature bone, no destructive process is
FIGURE 2. Periapical radiograph made before extraction of the mandibular left second molar.
FIGURE 3. Periapical radiograph made 2 months following extraction of the second molar.
399
VINCENT AND ASSAEL
evident. The only area of possible increased bone loss is posterior to the distal root of the first molar. The isolated appearance of a metastasis without a known primary is an uncommon event, particularly the reappearance of breast carcinoma after 28 years. Primary neoplasms include the entire broad range of benign and malignant, odontogenic, and nonodontogenic tumors. Most of these lesions are unlikely, based on the clinical information given. It is worth noting that no widening of the periodontal ligament, as occurs in osteogenic sarcoma, is noted. Also, no central bone lesion is evident. Moreover, no preexisting tissue abnormality was noted at the time of extraction. Peripheral or central giant cell lesions may rarely present without preexisting clinical evidence after extraction. The presence of bleeding gingiva might suggest a giant cell lesion, but the pale, rough, nonexophytic surface is not typical. Hyperplastic-reactive processes are those that would induce the increased formation of nonneoplastic tissue. These include cicatricial healing, functional adaptation, or drug-induced hyperplasia. Cicatricial healing may occur if tissue loss or remnants of granulation tissue left at the time of extraction result in delayed secondary healing. Teeth that have been encompassed by fibrous connective tissue that is not removed at the time of extraction also may produce a permanent bone defect and hypet-plastic scar. Functional adaptation might produce exuberant connective tissue in the extraction site if an opposing tooth produces masticatory forces on the healing site. None of these conditions would be likely to involve the gingiva of the adjacent tooth. There is no clinical evidence in this case that previous disease, the operative procedure, or functional forces have been causal in the development of this postextraction soft-tissue abnormality. Drug-induced hyperplasia of the gingiva produces a connective tissue and gingival overgrowth that distorts the normal architecture. Drug-induced hyperplasia of the gingiva was first reported with the use of phenytoin (Dilantin, Parke-Davis, Morris Plains, NJ). In recent years, gingival hyperplasia also has been reported with the use of other drugs, including diltiazem (Cardizem), which this patient is taking.’ The history and clinical appearance of the lesion in this patient show marked similarity to reported diltiazem-induced gingival hyperplasia. The gingival lesion extends at least as far forward as the premolar. If this were drug-induced gingival hyperplasia, however, there would be an expectation of other areas of hyperplasia. These are usually most evident in areas of chronic gingival inflammation. Based on the clinical information provided, the
most likely cause of this postextraction soft-tissue abnormality is a drug-induced hyperplasia secondary to diltiazem (Cardizem). SUBSEQUENT CLINICAL COURSE Under local anesthesia, an incisional biopsy was performed and submitted to the Surgical Oral Pathology Service. Microscopic evaluation showed hyperparakeratotic,
acanthotic, stratified squamous epithelium that formed bulbous elongated rete ridges (Fig 4). The papillary surface showed keratotic plugging. The individual cells showed no remarkable dysplasia, although occasional suprabasillar mitotic figures were noted (Fig 5). The acanthotic rete ridges appeared to extend into the subjacent connective tissues beyond the level of adjacent normal parakeratinized epithelium. The underlying connective tissue was unremarkable except for a focally moderate infiltrate of chronic inflammatory cells, including lymphocytes and plasma cells. Based on these findings, a diagnosis of verrucous carcinoma was rendered. The patient was treated surgically under general anesthesia. The mucosa of the buccal and lingual vestibules was reflected and the periosteum overlying the body of the mandible was elevated. The gingiva, attached alveolar mucosa, first molar, second premolar, alveolar bone and body of the mandible superior to the mandibular canal were excised from mesial of the second premolar to the retromolar region. Microscopic examination of frozen sections of the margins revealed tumor involvement of the anterior border. Therefore, the first premolar was extracted and the block resection extended anteriorly. The wound was closed, and healing occurred without significant complications. Final diagnosis was a Tl, NO, MO verrucous carcinoma. The patient is now awaiting prosthetic reconstruction.
Discussion Verrucous carcinoma is an entity first described by Ackerman in 1948.’ These lesions have since been described in the upper aerodigestive tract, skin of the external ear, penis, scrotum, and mu-
FIGURE 4. Incisional biopsy of the lesion showed bulbous budding rete ridges with hyperparakeratotic “plugging.” The rete ridges extended down into the submucosa (hematoxylineosin stain. original magnification X2.5).
A POSTEXTRACTION
FIGURE 5. Cellular features of the rete ridges showed minimal evidence of dysplasia (hematoxylin-eosin stain, original magnification x63).
cosa of the vulva, vagina, and uterine cervix. The carcinomas are found most often in people over 50, and are prevalent in males. They characteristically present as an exophytic, rough, slowly progressive, soft-tissue proliferation that is asymptomatic unless traumatized. According to Batsakis, the most common intraoral location for verrucous carcinoma is the buccal mucosa, followed by the gingiva and glossal mucosa.6 Many cases of oral verrucous carcinoma seem associated with histories of extensive use of tobacco in various forms. Eisenberg et al found cytologic features suggestive of viral infections in 15 of 17 verrucous carcinomas, and suggested a viral cofactor in the formation of these lesions.’ While the clinical and historic features are often characteristic of verrucous carcinoma, microscopic evaluation of an adequate specimen is necessary to confirm the diagnosis. The two oral lesions that most often present with clinical features similar or identical to verrucous carcinoma are verrucous hyperplasia and squamous cell carcinoma. Verrucous hyperplasia was first described by Ackerman and McGavran in 1958.* This lesion is characterized by clinical and microscopic features that mimic verrucous carcinoma, and the two are often found together in the same oral lesion. Shear and Pindborg described 68 cases, finding a slight female predominance, with oral lesions found most often on gingiva, and buccal and glossal mucosa.’ Microscopically, the best way to distinguish verrucous hyperplasia from verrucous carcinoma is that in the former lesion, the verrucous proliferation is almost entirely exophytic and superficial to adja-
SOFT-TISSUE
ABNORMALITY
cent normal epithelium; whereas in the latter, the acanthotic, broad rete ridges seem to push down into the connective tissue to a level much deeper than adjacent normal epithelium. Because the histologic features of verrucous carcinoma and verrucous hyperplasia may be found concurrently in the same lesion, some investigators feel verrucous hyperplasia is a precursor of verrucous carcinoma. Some cases of oral squamous cell carcinoma may be clinically identical to verrucous carcinoma, but most cases are readily distinguished microscopically. Even well-differentiated squamous cell carcinoma will characteristically show a significantly greater degree of cellular dysplasia and anaplasia. Therapy for verrucous carcinoma most often consists of wide surgical excision. Early reports of anaplastic recurrences following treatment of verrucous carcinoma with radiation have caused many treatment centers to avoid radiotherapy. However, recent evidence suggests that radiotherapy alone, or possibly in combination with surgery, may be a viable therapeutic option.” This case is somewhat unusual in that the lesion apparently originated in the healing mucosa of an uncomplicated extraction site. The lesion clinically was rough, but not as white or exophytic as most oral verrucous carcinomas. In addition the patient had no history of verrucous carcinoma “risk factors” such as ethanol or tobacco usage. References 1. Bowman J, Levy B, Grubb R: Gingival overgrowth induced by diltiazem: A case report. Oral Surg 65: 183, 1988 2. Schwartz M, Baredes S: Metastatic disease to the mandible. Laryngoscope 98270, 1988 3. Pick J, Wagner R: Initial appearance of renal cell carcinoma as a metastatic mass in the mandible. J Am Dent Assoc 113:759, 1987 4. Batsakis J: Tumors of the Head and Neck, Clinical and Pathological Considerations (ed 2). Baltimore, MD, Williams & Wilkins, 1979, p 241 5. Ackerman LV: Verrucous carcinoma of the oral cavity. Surgery 23:670, 1948 6. Batsakis JG, Hybels R, Chrissman JD, et al: The pathology of head and neck tumors, part 15. Verrucous carcinoma. Head Neck Surg 5:29, 1982 7. Eisenberg E, Rosenberg B, Krutchkoff D: Verrucous carcinoma: A possible viral pathogenesis. Oral Surg Oral Med Oral Pathol 59:52, 1985 8. Ackerman LV, McGavran MH: Proliferating benign and malignant epithelial lesions of the oral cavity. J Oral Surg 16:400. 1958 9. Shear M, Pindborg JJ: Verrucous hyperplasia of the oral mucosa. Cancer 46:1855, 1980 10. Nair MK, Sankaranarayanan R, Padmanabhan TK, et al: Oral verrucous carcinoma. Treatment with radiotherapy. Cancer 61:458, 1988
Surg
1991
A Postextraction STEVEN D. VINCENT,
Soft-Tissue Abnormality DDS, MS,* AND LEON A. ASSAEL,
Case Presentation
nontender, friable soft tissue distal to the mandibular left first molar (Fig 1). The soft tissue measured 2 x 1.5 cm in greatest dimension and appeared to extend anteriorly, involving the gingiva on the buccal and lingual aspects of the first molar. The first molar had class II mobility and bleeding 5- to 6-mm periodontal pockets. No other lesions were noted intraorally. Periapical radiographs taken before the tooth extraction and at the time of our examination 2 months later (Figs 2 and 3) showed healing of the extraction site.
The patient, a 73-year-old alert, normally developed, white woman, in no distress, was referred for evaluation of an unusual-appearing extraction site. The mandibular left second molar had been extracted without complication because of periodontal and pulpal disease 2 months previously. No postoperative antibiotics or surgical packings were used, and subsequent healing was unremarkable, with no evidence of excessive inflammation. One month later, the patient was seen for a prosthodontic consultation, at which time the extraction site was noted to be surfaced by rough, relatively pale, asymptomatic soft tissue. At 2 months, the soft-tissue changes were noted to be persistent and the patient was referred to our clinic for evaluation. At the time of our initial evaluation the patient was taking Cardizem (Marion Laboratories, Kansas City, MO), Zantac (Glaxo Pharmaceuticals, Glaxo, NC), and ASA. She reported an allergy to penicillin characterized as urticaria. She denied past or present tobacco or ethanol use. She was currently under the care of a physician for occasional angina and a hiatal hernia. She had a partial left arm paralysis as the result of a vertebral injury 29 years ago.. She had undergone a bilateral mastectomy and left unilateral axillary node dissection 28 years ago for carcinoma of the breast. She denied all other central nervous system, respiratory, cardiovascular, gastrointestinal, genitourinary, skin, musculoskeletal, hematologic, or allergic disease or abnormality past or present. The patient had a past history of routine regular dental care. She wore no removable prosthetic appliances. Extraoral examination showed no tenderness of the masticatory muscles, temporomandibular joint, or carotid or temporal artery to palpation. There was no restriction of, or pain during, mandibular movements. No temporomandibular joint noise was auscultated during jaw movements. Tbe patient was afebrile and there was no submandibular or anterior cervical lymphadenopathy. Gross analysis of cranial nerves III-XII was within normal limits, including pinprick sensory evaluation of the left third division of the trigeminal nerve. The intraoral examination showed rough, fissured,
Differential Diagnosis Leon A. Assael, DMD The basic categories of disease that must be considered in the differential diagnosis of this postextraction soft-tissue abnormality are inflammatoryinfectious, neoplastic, and hyperplastic-reactive. A common form of inflammatory-infectious pathosis seen in such situations is simple persistence of granulation tissue in the socket. An exuberant form of this process produces a pyogenic granuloma. Granulation tissue persists when necrotic bone frag-
ments, foreign bodies such as retained calculus, or tooth fragments are present in the socket. Often they are too small to be evident on the postoperative radiograph. Periodontitis in the adjacent tooth may rarely involve the adjacent socket, and in view of the furcation involvement of the first molar, this is a definite possibility. Other unusual causes of persistent infected tissue include tuberculosis, actinomycosis, regional fungal infection such as histoplasmosis, or a pulse granuloma induced by bean protein. The history is not supportive of an inflammatoryinfectious process. The 2-month postoperative radiograph does not show a destructive process of the type produced by osteomyelitis or the presence of a sequestrum. The clinical examination did not reveal marked swelling, redness, warmth, or tenderness. Moreover, the irregular, rough, keratinized, pale surface of the lesion does not support a diagnosis of pyogenic granuloma, which generally has a smooth surface. Hence, there is scant clinical information to support the possibility that this lesion represents an inflammatory-infectious process. Neoplasia persisting in an extraction site is an occasional finding that draws every clinician’s at-
* Associate Professor, Department of Oral Pathology and Diagnosis, University of Iowa, Iowa City. t Associate Professor and Residency Program Director, Department of Oral and Maxillofacial Surgery, School of Dental Medicine, University of Connecticut Health Center, Farmington, CT. Address correspondence and reprint requests to Dr Vincent: University of Iowa, College of Dentistry DSB 356, Department of Oral Pathology and Diagnosis, Iowa City, IA 52246. 0 1991 American geons
Association
of Oral and Maxillofacial
DMDt
Sur-
0278-2391/91/4904-0012$3.00/O
397
398
A POSTEXTRACTION
SOFT-TISSUE
ABNORMALITY
FIGURE 1. A mirror image of the rough mucosa distal. buccal, and mesial to the first molar.
tention to the importance of abnormal postoperative healing. Certain tumors appear to be more frequently evident in tooth sockets. These include lymphoma, myeloma, and the leukemias that may become evident in these sites because of the chronic inflammatory cells that are already present. Metastatic solid tumors are rare, but continually appear as case reports. A review of all pathologic specimens seen at Columbia Presbyterian Hospital
over a 47-year period showed only 22 cases of metastatic tumors of the mandible.* These included tumors whose primary lesions were in the breast, lung, kidney, colon, prostate, and thyroid.“4 If this lesion represented a metastatic tumor, it would likely be associated with a destructive radiographic change over the 2 months since the extraction. Although the extraction site does not appear to be full of mature bone, no destructive process is
FIGURE 2. Periapical radiograph made before extraction of the mandibular left second molar.
FIGURE 3. Periapical radiograph made 2 months following extraction of the second molar.
399
VINCENT AND ASSAEL
evident. The only area of possible increased bone loss is posterior to the distal root of the first molar. The isolated appearance of a metastasis without a known primary is an uncommon event, particularly the reappearance of breast carcinoma after 28 years. Primary neoplasms include the entire broad range of benign and malignant, odontogenic, and nonodontogenic tumors. Most of these lesions are unlikely, based on the clinical information given. It is worth noting that no widening of the periodontal ligament, as occurs in osteogenic sarcoma, is noted. Also, no central bone lesion is evident. Moreover, no preexisting tissue abnormality was noted at the time of extraction. Peripheral or central giant cell lesions may rarely present without preexisting clinical evidence after extraction. The presence of bleeding gingiva might suggest a giant cell lesion, but the pale, rough, nonexophytic surface is not typical. Hyperplastic-reactive processes are those that would induce the increased formation of nonneoplastic tissue. These include cicatricial healing, functional adaptation, or drug-induced hyperplasia. Cicatricial healing may occur if tissue loss or remnants of granulation tissue left at the time of extraction result in delayed secondary healing. Teeth that have been encompassed by fibrous connective tissue that is not removed at the time of extraction also may produce a permanent bone defect and hypet-plastic scar. Functional adaptation might produce exuberant connective tissue in the extraction site if an opposing tooth produces masticatory forces on the healing site. None of these conditions would be likely to involve the gingiva of the adjacent tooth. There is no clinical evidence in this case that previous disease, the operative procedure, or functional forces have been causal in the development of this postextraction soft-tissue abnormality. Drug-induced hyperplasia of the gingiva produces a connective tissue and gingival overgrowth that distorts the normal architecture. Drug-induced hyperplasia of the gingiva was first reported with the use of phenytoin (Dilantin, Parke-Davis, Morris Plains, NJ). In recent years, gingival hyperplasia also has been reported with the use of other drugs, including diltiazem (Cardizem), which this patient is taking.’ The history and clinical appearance of the lesion in this patient show marked similarity to reported diltiazem-induced gingival hyperplasia. The gingival lesion extends at least as far forward as the premolar. If this were drug-induced gingival hyperplasia, however, there would be an expectation of other areas of hyperplasia. These are usually most evident in areas of chronic gingival inflammation. Based on the clinical information provided, the
most likely cause of this postextraction soft-tissue abnormality is a drug-induced hyperplasia secondary to diltiazem (Cardizem). SUBSEQUENT CLINICAL COURSE Under local anesthesia, an incisional biopsy was performed and submitted to the Surgical Oral Pathology Service. Microscopic evaluation showed hyperparakeratotic,
acanthotic, stratified squamous epithelium that formed bulbous elongated rete ridges (Fig 4). The papillary surface showed keratotic plugging. The individual cells showed no remarkable dysplasia, although occasional suprabasillar mitotic figures were noted (Fig 5). The acanthotic rete ridges appeared to extend into the subjacent connective tissues beyond the level of adjacent normal parakeratinized epithelium. The underlying connective tissue was unremarkable except for a focally moderate infiltrate of chronic inflammatory cells, including lymphocytes and plasma cells. Based on these findings, a diagnosis of verrucous carcinoma was rendered. The patient was treated surgically under general anesthesia. The mucosa of the buccal and lingual vestibules was reflected and the periosteum overlying the body of the mandible was elevated. The gingiva, attached alveolar mucosa, first molar, second premolar, alveolar bone and body of the mandible superior to the mandibular canal were excised from mesial of the second premolar to the retromolar region. Microscopic examination of frozen sections of the margins revealed tumor involvement of the anterior border. Therefore, the first premolar was extracted and the block resection extended anteriorly. The wound was closed, and healing occurred without significant complications. Final diagnosis was a Tl, NO, MO verrucous carcinoma. The patient is now awaiting prosthetic reconstruction.
Discussion Verrucous carcinoma is an entity first described by Ackerman in 1948.’ These lesions have since been described in the upper aerodigestive tract, skin of the external ear, penis, scrotum, and mu-
FIGURE 4. Incisional biopsy of the lesion showed bulbous budding rete ridges with hyperparakeratotic “plugging.” The rete ridges extended down into the submucosa (hematoxylineosin stain. original magnification X2.5).
A POSTEXTRACTION
FIGURE 5. Cellular features of the rete ridges showed minimal evidence of dysplasia (hematoxylin-eosin stain, original magnification x63).
cosa of the vulva, vagina, and uterine cervix. The carcinomas are found most often in people over 50, and are prevalent in males. They characteristically present as an exophytic, rough, slowly progressive, soft-tissue proliferation that is asymptomatic unless traumatized. According to Batsakis, the most common intraoral location for verrucous carcinoma is the buccal mucosa, followed by the gingiva and glossal mucosa.6 Many cases of oral verrucous carcinoma seem associated with histories of extensive use of tobacco in various forms. Eisenberg et al found cytologic features suggestive of viral infections in 15 of 17 verrucous carcinomas, and suggested a viral cofactor in the formation of these lesions.’ While the clinical and historic features are often characteristic of verrucous carcinoma, microscopic evaluation of an adequate specimen is necessary to confirm the diagnosis. The two oral lesions that most often present with clinical features similar or identical to verrucous carcinoma are verrucous hyperplasia and squamous cell carcinoma. Verrucous hyperplasia was first described by Ackerman and McGavran in 1958.* This lesion is characterized by clinical and microscopic features that mimic verrucous carcinoma, and the two are often found together in the same oral lesion. Shear and Pindborg described 68 cases, finding a slight female predominance, with oral lesions found most often on gingiva, and buccal and glossal mucosa.’ Microscopically, the best way to distinguish verrucous hyperplasia from verrucous carcinoma is that in the former lesion, the verrucous proliferation is almost entirely exophytic and superficial to adja-
SOFT-TISSUE
ABNORMALITY
cent normal epithelium; whereas in the latter, the acanthotic, broad rete ridges seem to push down into the connective tissue to a level much deeper than adjacent normal epithelium. Because the histologic features of verrucous carcinoma and verrucous hyperplasia may be found concurrently in the same lesion, some investigators feel verrucous hyperplasia is a precursor of verrucous carcinoma. Some cases of oral squamous cell carcinoma may be clinically identical to verrucous carcinoma, but most cases are readily distinguished microscopically. Even well-differentiated squamous cell carcinoma will characteristically show a significantly greater degree of cellular dysplasia and anaplasia. Therapy for verrucous carcinoma most often consists of wide surgical excision. Early reports of anaplastic recurrences following treatment of verrucous carcinoma with radiation have caused many treatment centers to avoid radiotherapy. However, recent evidence suggests that radiotherapy alone, or possibly in combination with surgery, may be a viable therapeutic option.” This case is somewhat unusual in that the lesion apparently originated in the healing mucosa of an uncomplicated extraction site. The lesion clinically was rough, but not as white or exophytic as most oral verrucous carcinomas. In addition the patient had no history of verrucous carcinoma “risk factors” such as ethanol or tobacco usage. References 1. Bowman J, Levy B, Grubb R: Gingival overgrowth induced by diltiazem: A case report. Oral Surg 65: 183, 1988 2. Schwartz M, Baredes S: Metastatic disease to the mandible. Laryngoscope 98270, 1988 3. Pick J, Wagner R: Initial appearance of renal cell carcinoma as a metastatic mass in the mandible. J Am Dent Assoc 113:759, 1987 4. Batsakis J: Tumors of the Head and Neck, Clinical and Pathological Considerations (ed 2). Baltimore, MD, Williams & Wilkins, 1979, p 241 5. Ackerman LV: Verrucous carcinoma of the oral cavity. Surgery 23:670, 1948 6. Batsakis JG, Hybels R, Chrissman JD, et al: The pathology of head and neck tumors, part 15. Verrucous carcinoma. Head Neck Surg 5:29, 1982 7. Eisenberg E, Rosenberg B, Krutchkoff D: Verrucous carcinoma: A possible viral pathogenesis. Oral Surg Oral Med Oral Pathol 59:52, 1985 8. Ackerman LV, McGavran MH: Proliferating benign and malignant epithelial lesions of the oral cavity. J Oral Surg 16:400. 1958 9. Shear M, Pindborg JJ: Verrucous hyperplasia of the oral mucosa. Cancer 46:1855, 1980 10. Nair MK, Sankaranarayanan R, Padmanabhan TK, et al: Oral verrucous carcinoma. Treatment with radiotherapy. Cancer 61:458, 1988
