INTRODUCTION
The incidence of skin cancer appears to be increasing around the world.1 Basal cell carcinoma (BCC) accounts for the majority of non-melanoma skin cancers (NMSC) and is the most common cancer in humans. The actual incidence of BCC is likely underestimated, as many lesions are treated non-surgically. These cases are also difficult to quantify due to lack of reporting.2 Because of its high frequency and potential morbidity, this cancer can be traumatic for patients and their families and causes a significant financial impact on the health care system.3
The head and neck are common sites for the occurrence of BCC accounting for 80 to 85 percent of all BCC.4 BBCs are slow growing with local invasion and low potential to metastasize.5 However, due to their location and proclivity to invade important anatomical areas, they can be locally destructive and disfiguring.6 Dentists are in a unique position to identify these lesions and give appropriate recommendations that expedite referral and treatment for these patients.
The cause of BCC is multifactorial. Exposure to ultraviolet radiation has been identified as a risk factor for most NMSC.3,6,7 Sunburns in childhood have also been implicated in leading to increased incidence of skin cancer.8 The role of sunscreen in reducing and preventing skin cancer is important.9 However, repeated applications of sunscreen with a high sun protection factor is necessary.6 The use of sunscreen alone is controversial, as there is some indication that it can lead people to believe they are fully protected.10 Sun avoidance is now being promoted, particularly avoiding sun exposure between 10 a.m. and 4 p.m. Use of tanning beds are another avoidable risk factor for both melanoma and NMSC such as BCC.11 Other indentifiable risk factors that are important for BCC are fair skin types, freckling, genetic predisposition, red or blonde hair, and light eye colour.6,12
BCC is a cancer of non-keratinizing basaloid cells in the epidermis. Basal cell carcinomas are most commonly classified into four groups.13 The most common subtype is the nodular or nodulo-ulcerative type. This is the most common presentation usually occurring with central ulceration and a peripheral rolled border —the classic “rodent ulcer.” The pigmented form can mimic the appearance of melanoma. The less distinct forms include the superficial subtype and the morpheaform subtype. The morpheaform BCC can spread beyond the apparent lesion and requires wider excision margins. The superficial subtype appears as a scaly or erythematous plaque and may be mistaken for other lesions.
Biopsies of potential lesions are useful to confirm the diagnosis prior to initiating treatment.14 Excisional biopsies may be used for small lesions. Shave biopsies can be used for superficial lesions in the epidermis and upper dermis but have the potential to miss deeper lesions. Punch biopsies are completed using a dermal punch held perpendicular to the tissue and harvest a core of tissue to be sent as a specimen. Incisional biopsies are used to sample deeper lesions or lesions suspicious for melanoma or squamous cell carcinoma.
TREATMENT
BCCs have several different treatment options depending on the location, size, and subtype of the lesion.15 The gold standard for treatment is surgical excision.16,17 The classic form of surgery is excision with a wide margin. The specimen is then sent for pathological analysis. The specimen is embedded in a paraffin block and then sectioned or sliced in a bread loaf fashion prior to staining and microscopic inspection. The disadvantage of this technique is that the margins are not known until the specimen has been assessed histologically.
Mohs’ micrographic surgery is preferred for recurrent basal cell carcinoma or in high risk cases with increased size.18 The Mohs’ technique involves an initial resection with a narrow margin and then immediate frozen sections and possible re-resection to ensure clean margins. This surgical technique allows for the smallest possible defect with a low recurrence rate.19 This is the preferred technique if the resources are available, however this may not be the case in smaller peripheral hospitals.
Other techniques that are utilized are curettage with cautery or electrodessication, photodynamic therapy, cryotherapy, laser ablation, topical fluorouracil, and topical imiquimod.17,20 Regardless of the treatment modality, there is no doubt that patients with BCC benefit from early diagnosis and prompt treatment to improve the esthetic and functional outcome.21
CASE 1
SUPERFICIAL BCC RIGHT NECK
This 78-year-old male presented with a biopsy confirmed superficial BCC in the right infra-auricular area (Fig. 1). In this area, the redundancy in the skin tissue allows for excision and primary closure. The BCC was identified and the planned excision site was marked (Fig. 2). The specimen was removed and tagged using two short sutures at the superior margin and two long sutures at the lateral margin (Fig. 3). Meticulous cauterization of bleeding vessels was completed in the resection site prior to closure (Fig. 4). The incision was closed in a layered fashion using 4-0 chromic gut sutures in the skin in a continuous interlocking fashion (Fig. 5). A pressure dressing was placed using non-stretch tape dressings for additional wound support and a breathable dressing overtop (Fig. 6).
CASE 2
NODULAR BCC RIGHT LATERAL NOSE
A 74-year-old male presented with a biopsy confirmed nodular BCC on the right lateral nose (Fig. 7). Primary closure with an elliptical incision is often difficult in these cases. Other options include rhomboid flaps, transpositional flaps, bilobed flaps, and skin grafting.
In this case, a bilobed flap was utilized. The excision site was marked with adequate margins around the lesion (Fig. 8). The bilobed flap was then marked with the pedicled donor tissue sites outlined superiorly (Fig 8). The lesion was then excised at the deep margin being careful to stay above the perichondrium to ensure adequate cartilaginous blood supply and to prevent cartilage collapse or deformity (Fig. 9).
The lesion was then tagged in the standard fashion and sent to the pathology department in formalin (Fig. 10). The bilobed flap was then created superior to the surgical defect (Figs. 11, 12). The flap was undermined, allowing for sufficient thickness to facilitate blood supply and to match the native tissue thickness at the donor site (Fig. 13). The bilobed tissue flap was then rotated and advanced allowing for passive closure using 5-0 vicryl sutures in the subcutaneous plane (Fig. 14). The skin was closed using interrupted 6-0 prolene sutures (Fig. 15) followed by a pressure dressing using a layered tape dressing (Fig 16) and protective splint (Fig. 17). The flap edema slowly settles over a three month period (Fig. 18) and a good esthetic outcome was achieved after nine months (Fig. 19).
CASE 3
NODULAR BCC ANTERIOR SCALP
An 85-year-old female presented with a biopsy confirmed nodular BCC on the anterior scalp (Fig. 20). These lesions are difficult to identify and can present at advanced stages, as it is tricky for the patient and the physician to evaluate and monitor this area. Often these scalp BCCs can become quite large prior to being identified and diagnosed.
Depending on the s
ize, primary closure may or may not be possible. In cases when primary closure is not achievable, balloon expansion with secondary reconstruction using rotation and/or advancement flaps may be necessary to complete closure of the surgical defect.22
In this elderly female, the lesion was located in the hair bearing area of the anterior scalp (Fig. 20). The hair was shaved pre-operatively to accurately identify the lesion and to expose any other peripheral lesions in this area (Fig. 21). This patient was treated with local anaesthesia and intravenous sedation with oxygenation via nasal prongs (Fig. 21). In this case, the defect was small enough to allow primary closure, so an elliptical excision site was outlined in the scalp with adequate margins around the BCC (Fig. 22).
An incision was made through the skin, subcutaneous tissue, and the aponeurosis to gain access to the loose areolar tissue plane (Fig. 23). Dissection was easily carried out in this plane underneath the lesion (Fig. 24). The specimen was removed and tagged (Figs. 25 & 26) before being placed in formalin for immediate fixation, prior to being sent to the pathology department. Supraperiosteal dissection was then carried out anterior, posterior, and lateral to the surgical defect to allow for passive tension free closure. The scalp is extremely vascular, so bleeding vessels were cauterized carefully to prevent hematoma formation which can result in infection or necrosis and loss of scalp tissue (Fig. 27).
The aponeurosis was re-approximated using 2-0 prolene sutures to provide adequate support for the frontalis and occipitalis muscle function and to decrease the potential for dead space (Figs. 27, 28, & 29). Once passive closure had been achieved (Fig. 30), the skin was closed with buried subcuticular 5-0 vicryl sutures (Fig. 31) and running interlocking 4-0 chromic sutures (Fig. 32). A cranial head dressing was then applied to provide pressure to aid in comfort and to prevent hematoma formation. One week post-operatively, the dressings were removed and the partially dissolved sutures can be easily removed from the scalp (Fig. 33).
CONCLUSION
BCC, a type of non-melanoma skin cancer and the most common cancer in humans, is increasing in frequency due to sun exposure and our aging population. BCC occurs frequently in the head and neck region and dentists are often involved the initial diagnosis and counselling of patients. BCC is slow growing and has a low potential to metastasize, however it is locally invasive and destructive. Early diagnosis is important as it improves the functional and esthetic outcome for the patient. OH
Dr. Hogg is an Oral and Maxillofacial Surgeon in private practice in London, Ontario. Email: drhogg@drnicholashogg.com
Oral Health welcomes this original article.
REFERENCES
1. Kenneaster, DG. Introduction to skin cancer. Oral Maxillofacial Surg Clin N Amer 2005; 17: 133-42.
2. Rubin AI, Chen EH, Ratner D. Basal-cell carcinoma. N Engl J Med 2005; 353: 2262-69.
3. Wong CSM, Strange RC, Lear JT. Basal cell carcinoma. BMJ 2003: 327: 794-98
4. McCormak, CJ, Kelly, JW, Dorevitch AP. Differences in age and body site distribution of the histogical subtypes of basal cell carcinoma: a possible indicator of differing causes. Arch Dermatol 1997; 133: 593-96.
5. Lo J,Snow S, Reizner G. Metastatic basal cell carcinoma: a report of twelve cases with a review of the literature. J Am Acad Dermatol 1991; 24: 715-19.
6. Chinem VP, Miot HA. Epidemiology of basal cell carcinoma. An Bras Dermatol 2011; 86(2): 292-305.
7. Zaynoun S, Ali L, Shaib J. The relationship of sun exposure and solar elastosis to basal cell carcinoma. J Am Acad Dermatol 1985; 12: 522-25.
8. Corona R, Dogliotti E, D’Errico M, Sera F, Iavarone I, Baliva G, et al. Risk factors for basal cell carcinoma in a Mediterranean population. Arch Dermatol 2002; 137: 1162-68.
9. Stern RS, Weinstein MC, Bake SG. Risk of non-melanoma skin cancer with childhood sunscreen use. Arch Dermatol 1986; 122: 537-45.
10. Autier P. Sunscreen abuse for intentional sun exposure. Br J Dermatol 2009; 161 Suppl 3: 40-45.
11. Schulman JM, Fisher DE. Indoor ultraviolet tanning and skin cancer: health risks and opportunities. Curr Opin Oncol 2009; 21: 144-49.
12. Lear JT, Harvey I, de Berker D, Strange RC, Fryer AA. Basal cell carcinoma. J R Soc Med 1196; 91: 585-88
13. Baxter JM, Patel AN, Varma S. Facial basal cell carcinoma. BMJ. 2012; 345: e5342.
14. Dixon AJ, Hall RS. Managing skin cancer. Austral Fam Physic 2005; 34(8): 669-671
15. Telfer NR, Colver GB, Morton CA. Guidelines for the management of basal cell carcinoma. Br J Dermatol 2008; 159: 35-48.
16. Incomplete excision of squamous cell carcinoma of the skin: a prospective observational study. Plast Reconstr Surg 2007; 120: 910-16.
17. Bath-Hextall F, Bong J, Perkins W, Williams H. Interventions for basal cell carcinoma of the skin: a systematic review. BMJ 2004; doi: 10.1136/bmj.38219.515266.AE
18. Perkins, W. Who should have Mohs micrographic surgery? Curr Opin Otolaryngol Head Neck Surg 2010; 18: 283-89.
19. Malhotra R, Huilgol SC, Huynh NT, Selva D. The Australian Mohs database, part I: periocular basal cell carcinoma experience over 7 years. Opthalmology 2004; 111: 624-30.
20. Weinstein MC, Brodell RT, Bordeaux J, Honda K. The art and science of surgical margins for the dermatopathologist. Am J Dermatopathol. 2012; 34(7): 737-45.
21. Gulleth Y, Goldberg N, Silverman RP, Gastman BR. What is the best surgical margin for a basal cell carcinoma: a meta-analysis of the literature. Plast Reconstr Surg 2010; 126: 1222-31.
22. Hogg, NJV. Primary and secondary management of pediatric soft tissue injuries. Oral Maxillofacial Surg Clin N Amer 2012; 24: 365-75.
