Solar Elastosis Condition: An Orofacial Perspective

What Is Solar Elastosis?

In solar elastosis, the patient suffers from a degenerative dermal disease of photodamaged skin. This is associated with aging and influenced by hereditary factors such as pigmentation and exposure to sunlight and wind. The disease is also characterized by the accumulation of abnormal elastic tissue in the dermis layer. The appearance of solar elastosis is mainly seen in these patients as patches of thick, coarsely furrowed skin that may have a bumpy or rough hard surface. The solar elastotic syndromes group includes the following disorders: solar elastosis, Favre-Racouchot syndrome (a disorder consisting of multiple open and closed comedones in the presence of actinically damaged skin), elastotic nodules of the ears, collagenous and elastotic plaques of the hands, and colloid milia (a small, white, benign cysts that appear on the skin). The most common solar elastotic syndrome commonly or more often clinically observed remains solar elastosis. The chief etiological factors causing the lesions are chronic exposure to sunlight (ultraviolet, visible, and infrared radiation). Ultraviolet-A radiation causes inflammation and redness of skin or erythema with deep penetration into the dermis (a sign of skin undergoing chronic photodamage).

Can Solar Elastosis Affect the Oral Cavity or the Lips?

Solar elastosis condition can even involve, in some affected individuals, the lips or the labial mucosa region that may be exposed to the sun. This degenerative condition, however, usually does not affect the oral mucous membranes, except in very rare cases recorded in medical literature. Oral elastofibromatous lesions that can be seen routinely in the oral cavity are possibly associated with trauma or pathogenesis due to the irritation caused by solar elastosis-induced actinic cheilitis of the mouth or actinic keratosis.

What Causes Solar Elastosis?

The normal collagen or elastic fibers in the skin undergo a degradation process due to ultraviolet radiation. This is when the fibroblasts respond to photodamage by oversecreting troponelastin. This elastic tissue then subsequently turns hyperplastic and loses its normal appearance with a disordered pathologic arrangement. This is further aggravated by the action of matrix metalloproteinases that destroy the surrounding tissues.

The disruption of either collagen or elastic tissues in the dermis layer of the skin causes the normal cellular structure to be replaced by excessive deposition of residual material, resulting in the skin undergoing a rigorous vasodilatation phenomenon. The normal dermal architecture is disrupted this way in the affected region.

What Is the Relationship Between Photoaging and Solar Elastosis?

Photoaging is a similar mechanism in this pathogenesis used for the elaboration of the clinical, histologic, and functional changes in chronically sun-exposed skin of the population, most commonly in groups of middle-aged or elderly adults. In solar elastosis, the photoaging effect refers to the accumulation of abnormal elastic tissue in the dermal layer, more often attributed to long-term sun exposure. Solar diagnosis is not a degenerative dermatologic disease associated with aging as such but rather a result influenced by hereditary factors like pigmentation and exposure to sunlight and wind. Specifically in individuals suffering from skin damage by prolonged exposure to weather, be it sunlight or wind, it is often colloquially referred to as sailor's skin or farmer's skin.

Severe photoaging not only accentuates prominent or deep ridging and furrowing defects, but the skin specifically shows clinically a leathery appearance, severe atrophy, milia, cobblestone effect as a result of elastosis, actinic purpura, and mostly epidermal and dermal thickening.

Chronologic aging of patients suffering from this condition has always been characterized by either fine lines developing on the skin surface or increased skin laxity tone. This laxity is because of volume loss of soft tissues accompanied by atrophy of fat, soft tissue redistribution, of a reduction in the skeletal support of the face associated with bone resorption.

Can Smoking Also Cause Solar Elatosis?

Solar elastosis may also be a manifestation of premature skin aging that is caused by tobacco smoking. Tobacco smoke mainly interferes with the production and synthesis of collagen, increasing in turn the production of tropoelastin and matrix metalloproteinases (MMP). The tropoelastin and MMPs then degrade the matrix proteins and produce abnormal elastotic material in the dermis. The elastic fiber changes again in smokers' extensions may be quite deep into the reticular dermis compared to the changes seen only with weather or sun damage. In weather conditions causing changes, they tend to be restricted usually only to the superficial papillary dermis, whereas in smokers, to the contrary, it might be deeper because of the interference in collagen synthesis and pathogenesis induced by tobacco-specific nitrosamines (TSNAS). TSNAS are commonly the cause of solar elastosis-induced oral conditions or lesions and are also implicated in the development of oral cancers in regular smokers.

How Is Solar Elastosis Diagnosed?

On physical examination by the dermatologist or physician, the skin texture may appear rough, thickened, and wrinkled. Additionally, the presence of yellowish papules or plaques or overall yellow discoloration may be common in most cases of solar elastosis. The diagnosis is, however, mainly confirmed through light microscopy only. The histologic presence of subepidermal grenz, fragmented collagen fibers, or groups of “elastotic” deposits of fragmented elastic fibers is confirmative of this condition. Solar elastosis is diagnosed clinically by its appearance histologically or microscopically on performing a skin biopsy.

What Does Histology Reveal?

The histologic examination may show loss of eosin staining on hematoxylin and eosin (H and E) sections; it reveals a bluish color of the upper dermis with an accumulation of irregularly arranged or thickened elastic fibers. These elastic fibers may further be observed as a degraded form of disorganized tropoelastin or fibrillin-tangled structures.

The differential diagnosis of solar elastosis in the hand region is what the physician may observe or look out for which includes keratoelastoidalis marginalis (a pearly papules on the sides of thumbs and index fingers due to sunexposure), an acquired form of marginal keratoderma (a pearly papules on sides of hands), affecting the index fingers and thumb.

What Is the Management of Solar Elastosis?

The most effective strategy for managing solar elastosis is prevention, as there are no effective curative or surgical treatment methods available. Prevention of actinic-related damage to the skin is achieved by avoiding sunlight and wearing tightly woven clothing. Treatment can also be recommended by the physician through regular intake of antioxidants (Vitamin E or beta-carotene supplements), tretinoin creams (0.1 percent), and alpha-hydroxy acid sunscreens, which can be topically applied to reduce the severity of photodamage to the cutaneous tissues. A dose-dependent improvement can be seen in mild to moderate cases of photodamage after topical retinoid therapy. These therapies are suggested based on the extent of the condition and the affected areas involved. They can last around 12 months to show an increase in the number of fibroblasts in the dermis. Skin resurfacing procedures are a recent advancement in the dermatologist field, such as ablative Er:YAG (Erbium Yttrium-Aluminum-Garnet) laser resurfacing or a combination of fractionated CO2 (carbon dioxide) laser with platelet-rich plasma resurfacing. Also, newer techniques like laser radiofrequency and neurotoxin injections with botulinum toxin have been implemented for cosmetic improvement and as therapeutic measures to combat solar elastosis.

Conclusion:

Solar elastosis patients can hence have aesthetic complaints and need psychosocial support as well as physician and dermatologic guidance. This condition can occur mainly over the sun-exposed areas of the face, lips, hands, and forearms, ears, or neck. In the oral cavity, the oral mucous membranes are seldom affected, but the lips or labial mucosa would still be possibly exposed to the sun, degenerating these perioral tissues.