Chest
Clinical InvestigationsSquamous Metaplasia of the Bronchial Mucosa and its Relationship to Smoking
Section snippets
METHODS
One hundred six subjects were enrolled into the study under a protocol approved by the committee for protocol research at M.D. Anderson Cancer Center, Houston. All subjects were recruited on the basis of having a history of smoking more than 15 pack-years. One pack-year was defined as the equivalent of smoking one pack per day for one year (eg, one pack per day for 30 years was equivalent to smoking two packs per day for 15 years). Subjects were volunteers from a variety of backgrounds, but
RESULTS
One hundred six patients underwent a bronchoscopy and no significant morbidity related to the procedure occurred. Seven subjects were excluded from the analysis for the following reasons: four had inadequate specimens at four or more biopsy sites, two subjects' biopsy specimens were not available for review when the analysis was done, and one subject smoked only cigars. Sixty-two men and 37 women enrolled in the study. The median age was 44 years (range, 19 to 70 years). The group smoked
DISCUSSION
While squamous metaplasia of the bronchial mucosa has been recognized for many years as a common sequela of tobacco use,1, 2, 5 we performed our study to examine this relationship more closely. Tobacco smoke is not the only condition associated with squamous metaplasia. Various activities such as uranium mining, marijuana smoking, and a variety of chronic pulmonary diseases will also produce squamous metaplasia of the bronchial mucosa,3, 7, 8 but tobacco use is probably the most studied.
REFERENCES (10)
- et al.
Histiologic changes in bronchial tubes of cigarette-smoking dogs
Cancer
(1967) - et al.
Changes in bronchial epithelium in relation to cigarette smoking, 1955–1960 vs 1970–1977
N Engl J Med
(1979) - et al.
Cancer of the lung: the cytology of sputum prior to the development of carcinoma
Acta Cytol
(1965) - et al.
Smoking and lung cancer: an overview
Cancer Res
(1984) - et al.
Changes in bronchial epithelium in relation to cigarette smoking and in relation to lung cancer
N Engl J Med
(1961)
Cited by (85)
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2022, Cell ReportsCitation Excerpt :Chronic diseases that lack the ability to restore injured organs to their normal structure and function, such as chronic obstructive pulmonary disease (COPD), asthma, and idiopathic pulmonary fibrosis (IPF), may have defects in stem/progenitor cell or niche function. For example, the first histological change to the airway epithelium associated with smoking is basal cell hyperplasia (squamous metaplasia), followed by loss of ciliated cells, shorter cilia, goblet cell hyperplasia, and loss of cell-cell junctions (with concomitant loss of barrier function).5,6,7,8,9,10,11,12 An increase in basal cells has also been reported in individuals with asthma,13,14 and there is overwhelming evidence for goblet cell metaplasia (GCM) in asthmatic conducting airways.15,16,17
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2017, Developmental CellCitation Excerpt :This suggests that chronic activation of the ASMC niche in COPD may drive BSC amplification or drive the differentiation of LNEPs present in the conducting airways along the BSC lineage, possibly preventing them from contributing to alveolar epithelial homeostasis and regeneration. This may explain why airway BSC metaplasia precedes emphysema in COPD (Auerbach et al., 1961; Dye and Adler, 1994; Kennedy et al., 1984; Leopold et al., 2009; Lumsden et al., 1984; Peters et al., 1993; Shaykhiev and Crystal, 2013; Shaykhiev et al., 2011). Thus, while transient Fgf10 expression by ASMCs is critical for proper airway epithelial regeneration in response to injury (Volckaert et al., 2011, 2013a), sustained Fgf10 secretion by the stem cell niche, in response to chronic Ilk/Hippo inactivation (i.e., chronic nuclear Yap), results in pathological airway remodeling.
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Supported in part by grant CA-48369 from The National Cancer Institute.
Presented in part at the 57th Annual Meeting, American College of Chest Physicians, San Francisco, November 4-8, 1991.
Manuscript received May 19; revision accepted September 22.