Histopathology of Pilonidal Sinus

This is a presentation about the pathology of pilonidal sinus, covering its pathophysiology, histology, and the development of secondary carcinoma.

1. Histopathology of Pilonidal Sinus Dr. Rawa Muhsin Ali MBChB, ABHS- APath The Ninth Fast Track Review

2. Contents Overview Pathogenesis Histology Role of pathology Differentials Malignancy Should we examine?

3. Pilonidal Sinus pilus = hair nidus = nest sinus = pocket

4. Incidence of 26 per 100,000 population Male: female ratio 2-4:1 Mean age 20 Most common site is natal cleft Risk factors include obesity, prolonged sitting, trauma, deep cleft, increased hair density, PCOS Overview

5. Acquired is favored over congenital Gender disparity and onset in adolescence Association with occupation (Jeep drivers and barbers’ hands) Similar lesions in other body sites Lack of skin appendages and lining epithelium in wall of sinus despite presence of hair shafts deeply embedded Lack of success of surgical methods Pathogenesis

6. Bascom showed the midline pits to be enlarged and distorted hair follicles Gravity and motion may create a vacuum pulling on the follicles Inflammation and debris occlude the mouth of the follicle Further expansion and rupture leads to foreign body reaction and micro abscesses Lateral epithelialized tracts develop from the abscesses, creating a sinus Pathogenesis John Bascom (1925-2013)

7. Follicular occlusion tetrad: Hidradenitis suppurativa, acne conglobata , dissecting cellulitis, and pilonidal sinus disease Defect in follicular keratinization leading to obstruction of the follicle Retinoids to reduce size, activity, and inflammation of sebaceous glands

8. Karydakis insisted that hair insertion was the only cause of pilonidal sinus and not an internal etiology Three factors in hair insertion: Invader (loose hair) Force (causing insertion) Skin (vulnerability) Pathogenesis

9. Stretching of natal cleft damages hair follicles and opens a pore Pores collect and embed shed hairs and debris Movement and skin tightening create negative pressure Hairs are drawn deeper and friction creates the main sinus Rupture and secondary infection cause foreign body reaction and abscess with secondary lateral tracts Pathogenesis

10. Macroscopy

11. Hair follicle often not identified Tract filled with hair, debris, and granulation tissue Tract may be epithelialized, but not the cavity (not a true cyst) Inflammation with foreign body giant cell reaction Secondary infection creates abscess which may rupture Histology

12. Confirmation of diagnosis Perianal abscess Anorectal fistula Crohn disease Exclusion of malignancy Role of pathology

13. Perianal abscess

14. Anorectal fistula

15. Crohn disease

16. Same mechanism as Marjolin ulcer Chronic inflammation impairs DNA repair mechanisms through free radicals Long-standing and recurrent cases Average age and duration higher than usual pilonidal disease No carcinoma in 86,333 cases in WWII that were treated early Rate of transformation reported from 0.02% to 0.1% Underreported and under published Malignancy

17. 140 cases in 103 papers from 1900 to 2022 Mean age 54 years, males 91% Squamous cell carcinoma (94.6%), basal cell carcinoma, mixed Disease-specific survival rate of 59.8% (5-year) and 53.2% (10-year) Lower survival with higher stage and higher grade Recurrence in 46.6%, on average within 15 months Worse prognosis than primary squamous cell carcinoma Similar to Marjolin ulcer Surgery is mainstay (no much role for adjuvant chemoradiotherapy) Safadi et al paper

18. Outcome of primary vs secondary carcinoma Primary squamous cell carcinoma Secondary squamous cell carcinoma from pilonidal disease 3-year survival rate 95.3% 61.7% 5-year survival rate 93.6% 59.8% 10-year survival rate 93.6% 53.2% Recurrence rate after curative resection 4.6% 46.6% Regional metastases at diagnosis 3.7% 8.5% Distant metastases at diagnosis 0.2% 5.4%

19. Should we examine?

20. Thank You The Ninth Fast Track Review - Pilonidal Sinus