Other causes include:

Immunological diseases
Extreme climatic conditions
Prolonged deficiency to iron and vitamins in the diet

Pathogenesis
"Exposure to areca nut (Areca catechu) containing products with or without tobacco (ANCP/T) is currently believed to lead to OSF in individuals with genetic immunologic or nutritional predisposition to the disease. "This hypersensitivity reaction results in a juxta-epithelial inflammation that leads to increased fibroblastic activity and decreased breakdown of fibers. The fibroblasts are phenotypically modified, and the fibers they form are more stable, produce thicker bundles that progressively become less elastic. once the original loosely arranged fibrous tissue is replaced by the ongoing fibrosis, the movability of the oral tissues is reduced, there is loss of flexibility and reduced opening of the mouth. These collagen fibers are non degradable and the phagocytic activity is minimized. According to a  recent cross sectional study the time taken for return  of salivary pH to baseline levels after chewing areca nut containing mixtures is significantly longer in habitual users with  OSF when compared to unaffected users. Prolonged Alkaline pH induces death fetal fibroblast type and replacement by a profibrotic fibroblast. The patterns of intraoral fibrotic bands produced by alkaline chemical injury mimic those produced by areca nut chewing. Sharma et al., have equated the pathogenesis of OSF to an over-healing  wound, to explain its evolution as well as malignant transformation. Increased mechanical stiffness through YAP/TAZ pathway accelerates the malignant transformation of OSF.
(2001) with arsenite-exposed human lung A549, kidney UOK123, UOK109 and UOK121 cells isolated eight different DNA fragments by methylation-sensitive arbitrarily primed polymerase chain reactions. It turned out that six of the fragments were hyper- and two of them were hypomethylated. Higher levels of DNA methyltransferase mRNA and enzyme activity were found.Kitchin (2001) proposed a model of altered growth factors which lead to cell proliferation and thus to carcinogenesis. From observations, it is known that chronic low-dose arsenic poisoning can lead to increased tolerance to its acute toxicity. MRP1-overexpressing lung tumor GLC4/Sb30 cells poorly accumulate arsenite and arsenate. This is mediated through MRP-1 dependent efflux. The efflux requires glutathione, but no arsenic-glutathione complex formation.Although many mechanisms have been proposed, no definite model can be given for the mechanisms of chronic arsenic poisoning. The prevailing events of toxicity and carcinogenicity might be quite tissue-specific. Current consensus on the mode of carcinogenesis is that it acts primarily as a tumor promoter. Its co-carcinogenicity has been demonstrated in several models. However, the finding of several studies that chronically arsenic-exposed Andean populations (as most extremely exposed to UV-light) do not develop skin cancer with chronic arsenic exposure, is puzzling. Causes
Organic arsenic is less harmful than inorganic arsenic. Seafood is a common source of the less toxic organic arsenic in the form of arsenobetaine. The arsenic reported in 2012 in fruit juice and rice by Consumer Reports was primarily inorganic arsenic.