Cheilitis Glandularis Workup

  • Author: Ellen Eisenberg, DMD; Chief Editor: William D James, MD   more...
 
Updated: Feb 28, 2012
 

Laboratory Studies

  • To rule out systemic granulomatous diseases (eg, sarcoidosis, Crohn disease) - ACE levels, erythrocyte sedimentation rate, CBC count and differential
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Other Tests

  • Microbial culture and sensitivity testing: In cases with acute or chronic suppuration, bacterial culture and sensitivity testing is indicated for selection of appropriate antibiotic therapy.
  • Fungal culture or smear: Chronic angular cheilitis or erosive surface changes may be indicative of chronic candidal infection. Confirmation is an indication for appropriate antifungal therapy.
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Procedures

  • Lip biopsy is indicated to rule out specific granulomatous diseases that predispose to lip enlargement and to aid in establishing a definitive diagnosis. A representative incisional biopsy specimen should consist of a wedge (or punch) of lip tissue that includes surface epithelium and is of adequate depth to ensure inclusion of several submucosal salivary glands.
  • Labial minor salivary gland biopsy (ie, sampling 8-10 labial minor salivary glands obtained through an incision into the mucosa of the lower lip) should be performed if Sjögren syndrome is suspected.
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Histologic Findings

The term cheilitis glandularis is a provisional clinically descriptive designation rather than a definitive diagnosis. It refers to a constellation of clinical findings that can reflect a broad scope of possible histologic changes; therefore, no consistent or pathognomonic features of this disorder are seen at the microscopic level. Instead, a diverse array of possible alterations can be seen in both the surface epithelium and the submucosal tissues. These findings best enable the clinician to presumptively determine the etiology and the nature of an individual case.

The maturational profile of the epithelium can be essentially normal or show evidence of disturbance that ranges from varying degrees of atypia or dysplasia to frank carcinoma. Epithelial alterations attended by basophilic collagen degeneration (solar elastosis) constitute a diagnosis of actinic cheilitis. The presence of epithelial maturational disturbance indicates risk for progression to carcinoma.

The minor salivary glands may appear normal under the microscope, or they may exhibit various changes indicative of nonspecific sialadenitis. These changes can include atrophy or distention of acini, ductal ectasia with or without squamous metaplasia, chronic inflammatory infiltration and replacement of glandular parenchyma, and interstitial fibrosis. Suppuration and sinus tracts may be present in cases that involve bacterial infection.

Other possible histologic findings include stromal edema, hyperemia, surface hyperkeratosis, erosion, or ulceration.

Note the images below.

Medium-power photomicrograph. Note mildly atypicalMedium-power photomicrograph. Note mildly atypical epithelial maturation, modest lymphocytic infiltrate within the lamina propria region, and the striking basophilic collagen degeneration within the superficial stroma plus telangiectasias. The composite features are consistent with a diagnosis of actinic cheilitis (hematoxylin and eosin, original magnification, X100). Low-power photomicrograph. Deep submucosa of the lLow-power photomicrograph. Deep submucosa of the lip. Several minor salivary glands demonstrate ductal ectasia, interstitial inflammation, atrophy, and fibrosis. No evidence of salivary gland hypertrophy is seen (hematoxylin and eosin, original magnification X40). Lip biopsy specimen. Low-power photomicrograph revLip biopsy specimen. Low-power photomicrograph reveals focal surface hyperkeratosis accompanied by vascular congestion and fibrosis of the underlying stroma (hematoxylin and eosin, original magnification X40). High-power photomicrograph of the minor salivary gHigh-power photomicrograph of the minor salivary glands. Note ductal ectasia, acinar atrophy, interstitial fibrosis, and inflammation (hematoxylin and eosin, original magnification X100).
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Contributor Information and Disclosures
Author

Ellen Eisenberg, DMD  Professor, Section Chair and Director, Oral and Maxillofacial Pathology, Oral Pathology Biopsy Service, Department of Oral Health and Diagnostic Sciences; Associate Professor, Division of Anatomic Pathology, Department of Pathology and Laboratory Medicine, University of Connecticut Health Center

Ellen Eisenberg, DMD is a member of the following medical societies: American Academy of Oral and Maxillofacial Pathology

Disclosure: Nothing to disclose.

Specialty Editor Board

Mark W Cobb, MD  Consulting Staff, WNC Dermatological Associates

Mark W Cobb, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and American Society of Dermatopathology

Disclosure: Nothing to disclose.

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS  Consulting Staff, Department of Dermatology, Dermatology Research Associates of Cincinnati

Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, and American Dental Association

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD  Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Elsevier Royalty Other

References

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A 56-year-old woman with an 18-month history of chronic swelling and a dry, burning sensation in her lower lip. She reports intermittent increases and decreases in size of the lip with painful episodes of erosion, crusting, and rare instances of drainage. History reveals medication-induced xerostomia plus a tendency to compulsively lick the lip to maintain hydration. Note eversion of the mucosal surface, which appears erythematous and dry, and narrowing of the vermilion border. The lower labial mucosa appears nodular; however, on palpation, it is diffusely soft. The composite features are consistent with a clinical impression of cheilitis glandularis. A lip biopsy sample was obtained.
Medium-power photomicrograph. Note mildly atypical epithelial maturation, modest lymphocytic infiltrate within the lamina propria region, and the striking basophilic collagen degeneration within the superficial stroma plus telangiectasias. The composite features are consistent with a diagnosis of actinic cheilitis (hematoxylin and eosin, original magnification, X100).
Low-power photomicrograph. Deep submucosa of the lip. Several minor salivary glands demonstrate ductal ectasia, interstitial inflammation, atrophy, and fibrosis. No evidence of salivary gland hypertrophy is seen (hematoxylin and eosin, original magnification X40).
Note the fullness of the lower portion of the lip and the indistinct junction between the vermilion border and the skin.
Lip biopsy specimen. Low-power photomicrograph reveals focal surface hyperkeratosis accompanied by vascular congestion and fibrosis of the underlying stroma (hematoxylin and eosin, original magnification X40).
High-power photomicrograph of the minor salivary glands. Note ductal ectasia, acinar atrophy, interstitial fibrosis, and inflammation (hematoxylin and eosin, original magnification X100).
 
 
 
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