JADA Continuing Education
Gingival Involvement in Crohn Disease
Junu Ojha, BDS,
Donald M. Cohen, DMD, MS, MBA,
Nadim M. Islam, BDS,
Carol M. Stewart, DDS, MS,
Joseph Katz, DMD, MS and
Indraneel Bhattacharyya, DDS, MSD
 |
ABSTRACT
|
|---|
Background. Although the oral manifestations of Crohn disease are well-established, there is little specific documentation of the gingival involvement.
Case Descriptions. The authors describe four patients with significant gingival involvement and identify clinical signs and symptoms of the disease involving the gingivae, along with other oral manifestations. Patients had persistent gingival lesions manifesting as pustular ulcerations, erythema, swelling and cobblestoning. The authors also discuss the differential diagnosis, treatment options and prognostic factors.
Clinical Implications. Patients with gingival and/or other oral lesions with or without other constitutional symptoms should be evaluated for Crohn disease. Dentists can play a critical role in the early diagnosis, and they can help prevent complications and improve the prognosis.
Key Words: Gingiva; Crohn disease; extraintestinal CrohnAbbreviations: CD: Crohn disease • TB: Tuberculosis
Crohn disease (CD) (regional enteritis, granulomatous colitis), first described by Crohn and colleagues in 1932,1 is characterized by a chronic granulomatous, relapsing inflammatory involvement of the gastrointestinal tract, particularly the terminal ileum. About 25 to 35 percent of patients with CD develop at least one extraintestinal manifestation.2
The incidence of oral lesions in patients with CD ranges between 6 and 20 percent.3–6 These lesions are of significance, because they have been reported to precede the intestinal symptoms in up to 60 percent of cases, in some instances by as much as one year or more.1,2,4,5,7 Common oral manifestations of CD include hypertrophy and swelling of lips, gingival soft-tissue swelling resembling epulis fissuratum, cobblestone appearance of the buccal mucosa and palate, and deep ulcers. These ulcers may be yellowish-whitish and appear linear within the vestibule and on the gingiva. Aphthouslike ulcerations also may be present.5,8 Polypoid "taglike" lesions that have been interpreted as pyostomatitis vegetans also are associated with CD. These lesions are soft and friable and are detached easily from the underlying tissue, leaving an erythematous and ulcerated zone.9,10 Some of the smaller lesions may coalesce to form larger ramifying areas of necrosis and are described as "snail-track" lesions.
The cases discussed below focus on the oral manifestations, with special emphasis on the gingival presentation of CD.
|
CASE REPORTS
|
|---|
Case 1.
A 31-year-old woman was referred to the Clinical Oral Pathology Clinic, University of Nebraska, Lincoln, for evaluation of widespread oral lesions. Her medical history included previously diagnosed CD, for which she was receiving treatment with prednisone (30 milligrams) and azathioprine (50 mg) daily. The patient’s chief complaints were bleeding and swelling of her gums.
One of the authors (D.M.C.) performed the extraoral examination, the results of which were unremarkable. The clinician noted no evidence or history of skin, conjunctival or genital lesions. The intraoral examination revealed generalized swollen gingivae on the facial aspects of all four quadrants, with yellow linear pustular ulcerations measuring 1 to 3 mm in size. These lesions were tender and sloughing (Figure 1A
). The clinician also noted multiple whitish-yellowish pustules on the buccal mucosa and ventral surface of the tongue. The lips appeared crusted and hemorrhagic (Figure 1B).
View larger version (249K):
[in this window]
[in a new window]
|
Figure 1. A. Swollen gingiva with yellow pustular ulcerations, mainly on the facial aspects. B. Lips appeared swollen, crusted and hemorrhagic. C. Patient exhibited significant resolution of lesions within two weeks of receiving topical steroid therapy.
| |
The clinician referred the patient to the Oral Surgery Department, University of Nebraska, for a biopsy of the mandibular attached gingival tissue from the molar area. The microscopic examination revealed ulcerated keratinized mucosa with intraepithelial inflammation and edema (Figure 2A). The epithelium was infiltrated by aggregates of numerous neutrophils and lymphocytes. Two of the authors (D.M.C., I.B.) also observed occasional eosinophils and acantholysis of the epithelium. The clinicians noted numerous granulomas with epithelioid histiocytes intermixed with lymphocytes and Langhans giant cells in the subjacent connective tissue (Figure 2B). They considered this to be compatible with the histologic spectrum of CD.
View larger version (70K):
[in this window]
[in a new window]
|
Figure 2. A. Histomicrograph showing ulcerated keratinized mucosa with intraepithelial inflammation and edema (hematoxylin-eosin stain, original magnification x10). B. Histomicrograph exhibiting a true granuloma with epitheloid histiocytes intermixed with lymphocytes and Langhans giant cells (hematoxylin-eosin stain, original magnification x20).
| |
The clinicians treated the patient with a topical steroid ointment (clobetasol propionate 0.05 percent mixed with benzocaine). Significant resolution of most of the oral lesions occurred within two weeks (Figure 1C
). Very few pustular ulcers remained. The improvement in the lip lesions began within about one day of applying the topical steroid. The patient continued to have severe gastrointestinal problems, including diarrhea, cramping and pain. One of the authors (D.M.C.) advised her to resume the topical steroid application if the oral lesions recurred. To date, she continues to receive care from her primary care physician and gastroenterologist for treatment of the gastrointestinal disease.
Case 2.
A 42-year-old woman was referred to the Clinical Oral Pathology Clinic, University of Nebraska, for evaluation of yellow pustules on the facial and palatal aspects of the attached gingiva involving both the left and right sides of the maxilla. The lesions were painful and had been present for a few months. Her medical history was noncontributory, with the exception of gastrointestinal symptoms including occasional cramping and loose stools for the previous two years. One of the authors (D.M.C.) noted no extraoral abnormalities. The intraoral examination revealed diffuse pustular eruptions on an erythematous background involving most of the facial gingiva, especially in the maxillary right first molar area. The lesions extended to the anterior region and involved facial and lingual surfaces (Figure 3). A clinical differential diagnosis included pyostomatitis vegetans, recurrent herpes and Wegener granulomatosis.
View larger version (104K):
[in this window]
[in a new window]
|
Figure 3. Diffuse pustular eruptions on an erythematous background involving the entire facial aspect of the gingiva.
| |
The clinician obtained a biopsy specimen from the attached gingival tissue from the left maxillary premolar area. The microscopic examination revealed keratinized mucosa exhibiting large areas of ulceration. Two of the authors (D.M.C., I.B.) noted multiple intraepithelial eosinophilic abscesses. They also observed areas of coagulation necrosis, superficial and deep vasculitis consisting of numerous eosinophils and occasional neutrophils, and edema of the superficial lamina propria. The clinicians made a provisional diagnosis of pyostomatitis vegetans with a possible association with CD. They referred the patient to a gastroenterologist for further evaluation. The gastroenterologist made a diagnosis of CD on endoscopic examination and biopsy. The clinicians treated the oral lesions with a topical steroid (0.05 percent fluocinonide gel) applied two to three times daily for two weeks. They noted significant resolution of the oral lesions and improvement of clinical symptoms, and they advised the patient to resume using topical steroids as directed only if the lesions recurred or symptoms returned. The patient was lost to follow-up.
Case 3.
A 62-year-old woman was referred to one of the authors (D.M.C.) at the Clinical Oral Pathology Clinic, University of Nebraska, with a chief complaint of swollen gums and white spots on the gingivae. Her medical history was significant for thyroid cancer and a thyroidectomy several years previously, as well as intermittent crampy abdominal pain for the previous 10 to 20 years. Her physician had referred her recently to a gastroenterologist for evaluation; she was diagnosed as having CD via an endoscopic biopsy.
The extraoral examination was unremarkable. During the intraoral examination, two clinicians (D.M.C., I.B.) observed multiple yellowish pustular linear ulcerations involving the left mandibular facial attached gingiva extending into the mucobuccal fold (Figure 4A). In addition, they noted multiple whitish-yellowish linear ulcerations and fissures with an erythematous background on the left posterior buccal mucosa near the left mandibular first molar (Figure 4B). Also noticeable were cobblestonelike raised pustules and ulcerations on the anterior mandibular facial attached gingiva and mandibular vestibule (Figure 4C). One of the clinicians (I.B.) obtained biopsy specimens from the posterior left mandibular facial gingiva. The histologic features were similar to those noted in cases 1 and 2 and were highly suggestive of pyostomatitis vegetans, an oral manifestation of CD. The clinicians treated the oral lesions with a topical steroid (0.05 percent clobetasol propionate ointment) applied two times a day for two weeks. This led to marked improvement of the oral lesions. To date, the patient continues to receive treatment from a gastroenterologist for the gastrointestinal disease.
View larger version (40K):
[in this window]
[in a new window]
|
Figure 4. A. Multiple yellowish pustular linear ulcerations involving the mandibular facial aspect of the attached gingiva extending into the mucobuccal fold. B. Multiple whitish-yellowish linear ulcerations and fissures on the left posterior buccal mucosa near the left mandibular first molar. C. Cobblestonelike raised pustules and ulcerations on the anterior mandibular facial aspect of the attached gingiva and mandibular vestibule.
| |
Case 4.
A 37-year-old man was referred by his general dentist to the Clinical Oral Pathology Clinic, University of Nebraska, with a diagnosis of nonhealing gingivostomatitis of approximately three months’ duration. His medical history was significant for an oozing and boggy lesion on the posterior scalp. Shortly after the scalp lesion developed, the patient developed ulcers in his mouth. The patient’s dermatologist prescribed cephalexin and griseofulvin therapy, which was ineffective in reducing the size of the scalp lesion. Two of the authors (D.M.C., I.B.) then initiated treatment with systemic steroids (that is, prednisone, beginning with 40 milligrams for three days, followed by a 10-mg reduction every fourth day until the patient received a final dosage of 10 mg for three days); this resulted in complete resolution of the oral lesions. However, the skin lesions appeared to worsen with a decrease in steroid use. The clinical examination revealed multiple yellowish ulcerative lesions over an erythematous base that were distributed throughout the gingivae but concentrated mainly on the facial aspect (Figure 5). The buccal mucosae were hyperplastic, with an irregular pebbly surface and multiple mucosal folds.
View larger version (100K):
[in this window]
[in a new window]
|
Figure 5. Multiple yellowish ulcerative lesions over an erythematous base distributed throughout the gingivae, but concentrated mainly on the facial aspect (photograph courtesy of Timothy McVaney, DDS, Creighton University School of Dentistry, Omaha, Neb.).
| |
One of the clinicians (I.B.) performed an incisional biopsy from the left mandibular facial aspect of the gingiva. On the basis of the histologic findings, which were similar to those seen in cases 1 and 2, and of the clinical findings, the clinicians (D.M.C., I.B.) rendered a diagnosis of pyostomatitis vegetans. They added a comment that the patient should be evaluated for possible CD. The clinicians referred him to a gastroenterologist for further evaluation when the diagnosis of CD was confirmed, even though no gastrointestinal symptoms were present at the time.
|
DISCUSSION
|
|---|
In 1969, Dudeney8 published the first report of CD involving the mouth. Oral lesions may precede or develop concomitantly with intestinal symptoms and can involve all regions of the oral cavity, including lips, gingivae, vestibular sulci and buccal mucosae.5,7,8 Evaluating a patient with a complaint of oral ulcerations along with a history of gastrointestinal symptoms, fatigue and/or weight loss requires a biopsy of the oral lesions and prompts a referral to a gastroenterologist for a diagnostic workup for CD.
Recognizing the oral lesions early and establishing an association with CD are essential to rendering a timely diagnosis. Oral lesions may be present for months before the patient seeks professional attention, and dentists may find the lesions on routine examination.4,5,11 Sigusch12 reported that the main oral manifestation of CD involves only the gingival tissues and appears as cobblestonelike alterations along with pronounced tissue thickening. Therefore, dentists should be familiar with this entity and refer patients promptly to a gastroenterologist or primary care physician for an early diagnosis.
Three of the four patients in our series were female and their mean age was 43 years. Three patients had gastrointestinal symptoms before their first visit, which included abdominal cramping and loose stools. One had scalp lesions. All patients exhibited significant gingival involvement, which was present at the initial visit. All patients had a chief complaint of gingival disease that included swollen, bleeding and erythematous gingivae; diffuse pustular eruptions on an erythematous background involving the facial aspect of the gingivae; cobblestonelike raised lesions; and multiple yellowish pustular ulcerations. Other oral lesions included multiple whitish-yellowish pustules and irregular mucosal folds with a pebbly surface located on the buccal mucosa, mucobuccal fold and ventral surface of the tongue.
Literature review.
Our literature review indicates that patients with gingival manifestations of CD have a wide variety of symptoms that are similar to those in our series of patients (Table3,7,9,11–30). We observed gingival involvement in CD most commonly on the facial aspects of both the maxillary and mandibular gingivae. In the majority of reports of CD with oral involvement, the primary complaint of patients did not include gingival lesions. Thirty-five of the subjects were male, 28 female. Reported ages ranged from 3 to 67 years. The prevalence of gingival lesions in CD is poorly documented in the literature, and, therefore, we could not determine it.
The gingival presentation of CD may clinically resemble numerous entities, including generalized papillomatosis of the oral mucosa, vesicular eruptions such as pemphigus vegetans, viral and fungal infections, drug-induced gingival hyperplasia, systemic drug reactions and allergic reactions such as erythema multiforme. In addition, the clinical and microscopic differential diagnosis also includes orofacial granulomatosis, tuberculosis (TB), deep fungal infections, sarcoidosis, Wegener granulomatosis, cat-scratch disease and foreign body reaction.25
We should point out that oral manifestations may precede gastrointestinal symptoms in a high proportion of patients, with some studies reporting rates as high as 60 percent of patients.1,2,4,5,7 Therefore, a biopsy specimen exhibiting chronic granulomatous inflammation should be followed by a prompt referral of the patient to a gastroenterologist or primary care physician for a thorough evaluation. Orofacial granulomatosis encompasses a spectrum of clinical presentations that share common histopathologic findings of noncaseating giant cell granulomas.27 These conditions include TB, sarcoidosis and cheilitis granulomatosa, as well as CD.27
The lips are the most frequent site of involvement in orofacial granulomatosis; the labial tissues demonstrate a nontender, persistent swelling that may involve one or both lips. When these signs are combined with facial paralysis and a fissured tongue, the clinical presentation is Melkersson-Rosenthal syndrome.27,31 Involvement of the lips alone is cheilitis granulomatosa.
Diagnosis.
A clinician usually makes the diagnosis after excluding other diseases and conditions that cause granulomatous inflammation, such as TB, sarcoidosis and cat-scratch disease.27,31,32 To rule out TB, clinicians can use special stains, such as acid-fast bacillus or Ziehl-Neelsen stain, along with a purified protein derivative skin test, a sputum culture and a chest radiograph. To exclude possible fungal infections, clinicians can use Grocott-Gomori methenamine–silver nitrate or periodic acid–Schiff stains of the tissue. Wegener granulomatosis, a systemic autoimmune condition, is characterized by a triad of lesions that include necrotizing granulomatous lesions in the upper or lower respiratory tracts, granulomatous lesions in the kidneys and systemic vasculitis of small arteries and veins, including those in the oral cavity.
Oral lesions usually present as hyperplastic, erythematous gingivitis. Clinicians may confirm the diagnosis with serologic tests, including assays for antineutrophil cytoplasmic antibody (c-ANCA and p-ANCA). They also may perform lung and kidney biopsies.33
Treatment.
There is no specific cure for CD, and symptomatic relief is the goal of therapy. Oral lesions have been treated effectively with medium- and high-potency topical steroids. We observed significant resolution of the oral lesions in all four of our patients. However, the oral lesions in one of our patients recurred when the gastrointestinal disease flared up. Researchers have advocated various treatment modalities, with variable rates of success, including immuno-suppressive therapy with systemic or local steroids.30,34–36 In addition, drugs such as cyclosporine and thalidomide,24 as well as steroid-sparing agents such as azathioprine, methotrexate and hydroxychloroquine35 have been used effectively. The fully human immunoglobulin G1 antitumor necrosis factor agents (such as infliximab and adalimumab) and the humanized anti-alpha4-integrin IgG4 antibody (natalizumab) have yielded the most promising results in controlled trials for the treatment of patients with CD.36 Agents inhibiting the crucial interleukin 12/interferon gamma feedback loop also suggest therapeutic potential.36 Surgery is reserved for severe cases in which patients exhibit bowel obstruction, fistulae or perforations.36
|
CONCLUSION
|
|---|
Patients with persistent gingival and/or other oral lesions and symptoms, including gingival ulcerations, edema, burning, erythema, swelling and pustules, as well as other constitutional symptoms, such as abdominal pain, diarrhea, arthralgia and skin lesions, should be evaluated with CD in mind. This may prevent complications and progression of early CD to a more advanced disease. Gingival manifestations should alert the general dentist and specialist (such as a periodontist) to probe further regarding gastrointestinal symptoms, fever and weight loss, as well as generate a prompt referral to a physician.
|
FOOTNOTES
|
|---|
At the time this study was conducted, Dr. Ojha was a graduate student at the University of Nebraska, Lincoln. She now is an assistant professor, Department of Diagnostic Sciences, School of Dentistry, University of Detroit Mercy.
At the time this study was conducted, Dr. Cohen was a professor at the University of Nebraska, Lincoln. He now is a professor, Department of Oral and Maxillofacial Surgery and Dental Diagnostic Sciences, University of Florida College of Dentistry, Gainesville.
At the time this study was conducted, Dr. Islam was a research fellow at the University of Florida College of Dentistry, Gainesville. He now is an assistant professor, Department of Oral Pathology, Medicine and Radiology, School of Dentistry, Indiana University, Indianapolis.
Dr. Stewart is a professor, Department of Oral and Maxillofacial Surgery and Dental Diagnostic Sciences, University of Florida College of Dentistry, Gainesville.
Dr. Katz is a professor, Department of Oral and Maxillofacial Surgery and Dental Diagnostic Sciences, University of Florida College of Dentistry, Gainesville.
At the time this study was conducted, Dr. Bhattacharyya was an assistant professor at the University of Nebraska, Lincoln. He now is an assistant professor, Department of Oral and Maxillofacial Surgery and Dental Diagnostic Sciences, University of Florida College of Dentistry, 1600 Archer Road, Gainesville, Fla. 32610, e-mail "ibhattacharyya{at}dental.ufl.edu". Address reprint requests to Dr. Bhattacharyya.
|
REFERENCES
|
|---|
- Crohn BB, Ginzburg L, Oppenheimer GD. Regional ileitis: a pathologic and clinical entity, 1932. Mt Sinai J Med 2000;67(3):263–8.[Medline]
- Mottet NK. Histopathologic spectrum of regional enteritis and ulcerative colitis. Major Probl Pathol 1971;2:1–249.[Medline]
- Basu MK. Oral manifestations of Crohn’s disease: studies in the pathogenesis. Proc R Soc Med 1976;69(10):765–6.[Medline]
- Greenstein AJ, Janowitz HD, Sachar DB. The extra-intestinal complications of Crohn’s disease and ulcerative colitis: a study of 700 patients. Medicine (Baltimore) 1976;55(5):401–12.[Medline]
- Plauth M, Jenss H, Meyle J. Oral manifestations of Crohn’s disease: an analysis of 79 cases. J Clin Gastroenterol 1991;13(1):29–37.[Medline]
- Rankin GB. Extraintestinal and systemic manifestations of inflammatory bowel disease. Med Clin North Am 1990;74(1):39–50.[Medline]
- Tyldesley WR. Oral Crohn’s disease and related conditions. Br J Oral Surg 1979;17(1):1–9.[Medline]
- Dudeney TP. Crohn’s disease of the mouth. Proc R Soc Med 1969;62(12):1237.[Medline]
- Cataldo E, Covino MC, Tesone PE. Pyostomatitis vegetans. Oral Surg Oral Med Oral Pathol 1981;52(2):172–7.[Medline]
- Hansen LS, Silverman S Jr, Daniels TE. The differential diagnosis of pyostomatitis vegetans and its relation to bowel disease. Oral Surg Oral Med Oral Pathol 1983;55(4):363–73.[Medline]
- Pittock S, Drumm B, Fleming P, et al. The oral cavity in Crohn’s disease. J Pediatr 2001;138(5):767–71.[Medline]
- Sigusch BW. Periodontitis as manifestation of Crohn’s disease in primary dentition: a case report. J Dent Child (Chic) 2004;71(3):193–6.[Medline]
- Ayangco L, Rogers RS 3rd, Sheridan PJ. Pyostomatitis vegetans as an early sign of reactivation of Crohn’s disease: a case report. J Periodontol 2002;73(12):1512–6.[Medline]
- Bens G, Laharie D, Beylot-Barry M, Vergier B, Noblesse I, Beylot C. Successful treatment with infliximab and methotrexate of pyostomatitis vegetans associated with Crohn’s disease. Br J Dermatol 2003;149(1):181–4.[Medline]
- Bernstein ML, McDonald JS. Oral lesions in Crohn’s disease: report of two cases and update of the literature. Oral Surg Oral Med Oral Pathol 1978;46(2):234–45.[Medline]
- Borradori L, Saada V, Rybojad M, et al. Oral intraepidermal IgA pustulosis and Crohn’s disease. Br J Dermatol 1992;126(4):383–6.[Medline]
- Field EA, Tyldesley WR. Oral Crohn’s disease revisited: a 10-year-review. Br J Oral Maxillofac Surg 1989;27(2):114–23.[Medline]
- Frankel DH, Mostofi RS, Lorincz AL. Oral Crohn’s disease: report of two cases in brothers with metallic dysgeusia and a review of the literature. J Am Acad Dermatol 1985;12(2 part 1):260–8.[Medline]
- Frost SS, Elstein MP, Latour F, Roth JL. Crohn’s disease of the mouth and ovary. Dig Dis Sci 1981;26(6):568–71.[Medline]
- Galbraith SS, Drolet BA, Kugathasan S, Paller AS, Esterly NB. Asymptomatic inflammatory bowel disease presenting with mucocutaneous findings. Pediatrics 2005;116(3):439–44.
- Gargiulo AV, Ladone JA, Toto PD, Logiudice J. Crohn’s disease: early detection by gingival biopsy. Periodontal Case Rep 1989;11(1):20–2.[Medline]
- Ghandour K, Issa M. Oral Crohn’s disease with late intestinal manifestations. Oral Surg Oral Med Oral Pathol 1991;72(5):565–7.[Medline]
- Giller JP, Vinciguerra M, Heller A, Kunken FR, Kahn E. Treatment of gingival Crohn’s disease with laser therapy. N Y State Dent J 1997;63(5):32–5.[Medline]
- Hegarty A, Hodgson T, Porter S. Thalidomide for the treatment of recalcitrant oral Crohn’s disease and orofacial granulomatosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003;95(5):576–85.[Medline]
- Mergulhao P, Magro F, Pereira P, et al. Gingival hyperplasia as a first manifestation of Crohn’s disease. Dig Dis Sci 2005;50(10):1946–9.[Medline]
- Neville BW, Smith SE, Maize JC, Laden SA, Denton WT. Pyostomatitis vegetans. Am J Dermatopathol 1985;7(1):69–77.[Medline]
- Sciubba JJ, Said-Al-Naief N. Orofacial granulomatosis: presentation, pathology and management of 13 cases. J Oral Pathol Med 2003;32(10):576–85.[Medline]
- Stricker T, Braegger CP. Images in clinical medicine: oral manifestations of Crohn’s disease. N Engl J Med 2000;342(22):1644.[Free Full Text]
- Ward CS, Dunphy EP, Jagoe WS, Sheahan DG. Crohn’s disease limited to the mouth and anus. J Clinic Gastroenterol 1985;7(6):516–21.
- Wiesenfeld D, Ferguson MM, Mitchell DN, et al. Oro-facial granulomatosis: a clinical and pathological analysis. Q J Med 1985;54(213):101–13.[Medline]
- Williams PM, Greenberg MS. Management of cheilitis granulomatosa. Oral Surg Oral Med Oral Pathol 1991;72(4):436–9.[Medline]
- Lloyd DA, Payton KB, Guenther L, Frydman W. Melkerson-Rosenthal syndrome and Crohn’s disease: one disease or two? Report of a case and discussion of the literature. J Clin Gastroenterol 1994;18(3):213–7.[Medline]
- Lourenco SV, Nico MM. Strawberry gingivitis: an isolated manifestation of Wegener’s granulomatosis? Acta Derm Venereol 2006;86(1):90–1.[Medline]
- Mignogna MD, Fedele S, Lo Russo L, Lo Muzio L. The multiform and variable patterns of onset of orofacial granulomatosis. J Oral Pathol Med 2003;32(4):200–5.[Medline]
- van der Waal RI, Schulten EA, van der Meij EH, van de Scheur MR, Starink TM, van der Waal I. Cheilitis granulomatosa: overview of 13 patients with long-term follow-up—results of management. Int J Dermatol 2002;41(4):225–9.[Medline]
- Van Assche G, Vermeire S, Rutgeerts P. Emerging biological treatments in inflammatory bowel diseases. Dig Dis 2006;24(1–2):131–6.[Medline]
This article has been cited by other articles:
|
|
|
|
 
A. Tanchyk and A. Tanchyk
Multisystem Diseases
J Am Dent Assoc,
March 1, 2008;
139(3):
245 - 246.
[Full Text]
[PDF]
|
|
|
TOP
ABSTRACT
CASE REPORTS
