Clinical and Epidemiological Evaluation of Actinic Keratosis in Seven Dogs
World Small Animal Veterinary Association World Congress Proceedings, 2009
S.S. Costa; T.D. Munhoz; S.G. Calazans; N.F. Gava; M.R. Hatayde; M. Tinucci-Costa; C.R. Daleck
Jaboticabal, SP, Brazil


Actinic keratosis (AK) is a well-known disease in humans (Ortonne, 2002; Cockerell, 2003; LEBWOHL, 2003) and also affects dogs and cats. It usually occurs in skin with prolonged sun exposed and in short-coated, white-haired skin, such as ventral and lateral abdomen and flank (Gross et al., 2005). Dalmatians, American Staffordshire terriers, Beagles, Basset Hounds and Bull terriers have an increased incidence of AK (Scott et al., 2001). The main risk factor is increased ultraviolet (UV) light exposure (Lebwohl, 2003). UV exposure of skin causes important local and systemic immunologic consequences, changing Langerhans' cell morphologic features and function, and influences cutaneous cytokine production (Scott et al., 2001). Photooxidative stress induced by UV light causes characteristic DNA mutations. In the absence of appropriate repair mechanisms, these DNA changes represent the initiation of keratinocyte mutations that can progress into the development of AK (Stockfleth & Kerl, 2006). Lesions vary from areas of erythema, crusts, scales, and papules to plaques and keratotic nodules. Diagnosis is based on clinical findings and must have histopathological confirmation (Stockfleth & Kerl, 2006). The term "actinic keratosis" refers to a clinical description of a disease that has histopathological confirmation, and is based only on these findings (Röwert-Huber et al., 2007). Epidermal changes are variable and depend on clinical stage. The main findings include epidermal hyperplasia and dysplasia, the basement membrane zone is intact (Gross et al., 2005). Other findings include atypia of the epidermis and superficial hair follicle epithelium, hyperkeratosis, especially parakeratotic (Scott et al., 2001). Dysplasia involving all layers of the epidermis defines carcinoma in situ, also called Bowen's disease (Berman et al., 2006). On the other hand, when dermal invasion occurs means the squamous cell carcinoma (SCC) is already developed (Gross et al., 2005). It is impossible to predict which AK will become thicker or more invasive with a potential for destructive growth, followed by the development into metastatic SCC (Stockfleth & Kerl, 2006). Early lesions regress with avoidance of sunlight and photoprotection. If pruritus or pain is prominent, topical or oral glucocorticoids are beneficial. More advanced lesions require systemic retinoids (isotretinoin, etretinate, acitretin), cryosurgery, or surgical excision (Scott et al., 2001). Many authors state that AK is a pre-neoplastic disease that may develop into SCC (Ortonne, 2002; Cockerell, 2003; Lebwohl, 2003). However, other researches consider AK as SSC in situ (Ortonne, 2004) and some agree that there is no pathobiological difference between AK and SCC and that both represent the sequence of a disease (Lebwohl, 2003; Röwert-Huber et al., 2007). The purpose of this paper is to describe seven AK's cases in dogs attempted at the Veterinary Teaching Hospital "Governador Laudo Natel" at College of Agricultural and Veterinarian Sciences--Sao Paulo State University, Campus of Jaboticabal regarding the clinical findings and follow up, since there are few case reports in dogs on national and international literature.

Material and Methods

This research was based on the evaluation and follow up of seven dogs with actinic keratosis attempted at the Veterinary Hospital "Governador Laudo Natel" at Sao Paulo State University (Jaboticabal, Brazil), all through the year 2008. Anamnesis and physical examination were accomplished. Owners were asked about the time of exposure to the sun. Five samples were collected from affected skin of each dog, by means of incisional biopsy, using a 6mm punch. These samples were carefully dried to remove blood appropriately and the epidermis surface was faced upside in a piece of wood to minimize any artifact induced by shrinking. After this, they were fixed in 10% buffered formalin (formalin: tissue in a 3:1 proportion), about 24 hours. Paraffin block were cut at 10 μm to Hematoxylin-Eosin Staining and histopathological evaluation was based on Gross et al. (2005) to conclude the actinic keratosis diagnosis. By following clinical evaluation, it was possible to analyze the treatment response, recurrence and the evolution to squamous cell carcinoma.


The majority of dogs were American Pit Bull breed, corresponding to six animals. Just one of them was crossbreed. The age varied from 4 to 8 years (5.8 ±1,2). Regarding sex predilection, there were more females (5) than males (2). All dogs were short-coated and white-haired skin. The dogs were originated from Jaboticabal city, Sao Paulo, Brazil. All owners reported that their dogs have had prolonged sun exposure. The skin lesions were located on flank (7), ventral abdomen (6), lateral thorax (6), medial thighs (2) and scrotum (1). The main dermatological lesion included alopecia, erythema, comedones, scales, excoriation, pustules, epidermal collarettes, crusts and scars. Deep and superficial bacterial folliculitis was common. The lesions characterized as actinic keratosis demonstrated histopathological findings on epidermis such as hyperplasia, parakeratosis, orthokeratosis, loss of keratinocyte polarity, moderate cellular pleomorphism, disorganization of epidermal layers, hydropic degeneration of squamous cell and more than one nucleoli evident in each nucleus. On loose connective tissue, located on the dermis, there were collagen fiber degeneration and proliferation of fibroblast. The elastotic fibers were degenerated, showing the solar elastosis. On cutaneous appendices some hair follicle showed infundibular dilatation due to hyperkeratosis. In some samples there were bacterial colonies with proliferation of neutrophils, confirming secondary infection.

Discussion and Conclusions

Dalmatians, American Staffordshire terriers, Beagles, Basset Hounds and Bull terriers have an increased incidence of AK (Scott et al. 2001). However, in the present study, American Pit Bull was the breed mainly observed. Reports regarding sex influence on the development of AK were not found. There was higher frequency of females (5) than males (2). According to Gross et al (2005), lesions occur primarily in older dogs, however, in this study, the findings were not similar, since the disease was diagnosed in 4 year-old dogs. The authors believe this early age of disease onset occurs due to early sun exposure of short-coated and white-haired skin dogs. The dermatological findings were similar to those stated by Scott et al (2001) and Gross et al (2005). The early lesions affected ventral abdomen and flank, probably due to the position that dogs lay down and also from light reflection in abdomen. The skin lesions varied from areas of erythema from crusts and scales. Also, all dogs were short-coated, white-haired skin. These cases were diagnosed in Jaboticabal, a tropical city (latitude 21°, 25'S), in Sao Paulo State, Brazil, with a high sun incidence. Lebwohl (2003) states that AK is more common in countries with low latitude, where UVB light exposure may reach twice than that in higher latitudes. Some studies about actinic keratosis in humans are concerned about risk factors such as high-fat diet (Lebwohl, 2003), chronic immunosuppression, arsenic exposure and chronic cutaneous inflammation (Ulrich et al., 2007). However, the main risk factor noticed in this study was the owners report about the high sun exposure. The authors concluded this was the etiological factor in agreement to Scott et al (2001), who asserts that sun radiation is involved on pathogenesis of many skin diseases in dogs. Also, on histopathological evaluation, all sample revealed on loose connective tissue, located on the dermis, collagen fiber degeneration and proliferation of fibroblast. The elastotic fibers were degenerated, showing the solar elastosis. According to Kligman & Sayre (1991), the elastotic changes are the main signal of cumulative solar exposure in the dermis. The treatment was based on prednisone, isotretinoin, 5-fluorouracil cream, ,-caroteno, C and E vitamin, shampoo, sunscreen and sun avoidance, demonstrating the severity of the disease and the difficulty in controlling the disease. Dogs with deep and superficial folliculitis were treated with cephalexin, 30mg/kg, with food, twice daily, 30 to 45 days, depending on the case severity, and they showed no recurrence until now. All dogs had keratosis recurrence after some months of treatment. One dog developed to AK from SCC 3 months after the initial diagnosis. It was a five-year old female American Pit Bull presenting skin disease on lateral thorax and ventral portion. Histopathological evaluation showed epidermal changes such as regular hyperplasia and lamellar and compact orthokeratosis. There was degeneration of collagen fibers. Many hair follicles exhibited infundibular dilatation. Chemotherapy treatment was performed using carboplatin. Nevertheless, the owner gave up. Until now, the bitch has not shown metastases occurrence. This research confirms that AK is a disease with high recurrence rate; hard preventive measures in dogs due to the living habits, complex treatment protocol and that may develop into SCC. The authors reinforce the necessity of researches related to this topic, so that new preventive option arises and more effective therapeutically protocols may be developed.


1.  Ortonne J-P. From actinic keratosis to squamous cell carcinoma. British Journal of Dermatology. 146: 20-23. 2002.

2.  Cockerell CJ. Pathology and pathobiology of the actinic (solar) keratosis. British Journal of Dermatology. 149: 34-36. 2003.

3.  Lebwohl M. Actinic keratosis: Epidemiology and progression to squamous cell carcinoma. British Journal of Dermatology. 149: 31-33. 2003.

4.  Gross LT, Ihrke PJ, Walder EJ, Affolter VK. 2005. Skin diseases of the dog and cat: clinical and histopathologic diagnosis. Blackwell, Oxford, 932p.

5.  Scott D, Miller WH, Griffin CE. 2001. Small Animal Dermatology. 6 ed. Saunders, Philadelphia, 1528p.

6.  Stockfleth E, Kerl H. Guidelines for the management of actinic keratoses. European Journal of Dermatology.16: 599-606. 2006.

7.  Röwert-Huber J, Patel MJ, Forschner T, Ulrich C, Eberle J, Kerl H, Sterry W, Stockfleth E. Actinic keratosis is an early in situ squamous cell carcinoma: a proposal for reclassification. British Journal of Dermatology. 156: 8-12. 2007.

8.  Berman B, Bienstock L, Kuritzky L, Mayeaux EJ, Tyring SK. Actinic keratoses: sequelae and treatments. Supplement to the Journal of Family Practice. 1:1-8. 2006.

9.  Ortonne J-P. Anti-inflammatory vs. inflammatory treatments for actinic keratoses. Journal of Cosmetic Dermatology. 2: 135-140. 2004.

10. Ulrich M, Maltusch A, Röwert-Huber J, González, S, Sterry W, Stockfleth E, Astner S. Actinic keratoses: non-invasive diagnosis for field cancerization. British Journal of Dermatology. 156: 13-17. 2007.

11. Kligman LH, Sayre RM. An action spectrum for ultraviolet induced elastosis in hairless mice: quantification of elastosis by image analysis. Photochemistry and Photobiology. 53: 237-242. 1991.


Speaker Information
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S.S. Costa
Jaboticabal, SP, Brazil

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