Specific conditions which can produce a similar appearance include Dariers disease, discoid lupus erythematosus, oral candidiasis, and oral lichen planus.If a biopsy is taken, the histopathologic appearance is one of hyperkeratosis and acanthosis. There may be squamous metaplasia of excretory ducts, which results in the visible papules if the ducts become hyperplastic. Neutrophils may fill some ducts. It is characterized as a "fissured" or "dried mud" appearance from excess keratin production by cells. Dysplasia is rarely seen. Treatment
When the appearance is caused by heat, the lesion is usually completely reversible within a few weeks if the smoking habit is stopped. This is the case even if the condition has been present for decades. Without stopping smoking, spontaneous remission of the lesion is unlikely. If the lesion persists despite stopping smoking, this is usually then considered to be a true leukoplakia rather than a reactionary keratitis, and may trigger the decision to carry out a biopsy to confirm the diagnosis. Since this condition almost always develops in the setting of long term heavy smoking, it usually indicates the need for regular observation for cancers associated with smoking, e.g. lung cancer. Epidemiology
The condition is uncommon. It occurs usually in elderly males who have a history of heavy pipe smoking, but it also can occur in cigar or cigarette smokers. The condition was once common, but has become more rare as habits such as pipe and cigar smoking have decreased in popularity. See also
Smokers melanosis
Smokeless tobacco keratosis

References

Kahn, Michael A. Basic Oral and Maxillofacial Pathology. Volume 1. 2001.
Sensenbrenner syndrome (OMIM #218330) is a rare (less than 20 cases reported by 2010) multisystem disease first described by Judith A. Sensenbrenner in 1975. It is inherited in an autosomal recessive fashion, and a number of genes appear to be responsible. Three genes responsible have been identified: intraflagellar transport (IFT)122 (WDR10), IFT43—a subunit of the IFT complex A machinery of primary cilia, and WDR35 (IFT121: TULP4)It is also known as Sensenbrenner–Dorst–Owens syndrome, Levin syndrome I and cranioectodermal dysplasia (CED)

Presentation
These are pleomorphic and include
dolichocephaly (with or without sagittal suture synostosis)
microcephaly
pre- and postnatal growth retardation
brachydactyly
narrow thorax
rhizomelic dwarfism
epicanthal folds
hypodontia and/or microdontia
sparse, slow-growing, hyperpigmented, fine hair
nail dysplasia
hypohydrosis
chronic kidney failure
heart defects
liver fibrosis
visual deficits
photophobia
hypoplasia of the posterior corpus callosum
aberrant calcium homeostasisElectroretinography shows gross abnormalities. Two fetuses of 19 and 23 weeks gestation have also been reported. They showed acromesomelic shortening, craniofacial characteristics with absence of craniosynostosis, small kidneys with tubular and glomerular microscopic cysts, persistent ductal plate with portal fibrosis in the liver, small adrenals, an enlarged cisterna magna and a posterior fossa cyst. Cause
The gene IFT122 is located on the long arm of chromosome 3 (3q21-3q24). The gene lies on the Watson (plus) strand and is 80,047 bases in length. The encoded protein has 1241 amino acids and a predicted weight of 141.825 kiloDaltons (kDa). It is a member of the WD repeat protein family.WDR35 is also a member of the WD repeat protein family.