Pilonidal disease is described back as far as 1833, when Mayo described a hair-containing cyst located just below the coccyx (see the image below). Hodge coined the term "pilonidal" from its Latin origins in 1880, and, today, pilonidal disease describes a spectrum of clinical presentations, ranging from asymptomatic hair-containing cysts and sinuses to large symptomatic abscesses of the sacrococcygeal region that have some tendency to recur. [1, 2]
In the 19th and early 20th centuries, pilonidal disease was studied on an embryologic basis by many authors who considered it to be of congenital origin. Excision of the lesion was thought to be fundamental to removing all embryologic remnants. This was the prevailing thought process well into the 20th century, when pilonidal disease gained prominence and practical importance amongst World War II soldiers with a high incidence of the disease, so much so it came to be known as Jeep disease. According to US Army publications, nearly 80,000 US soldiers were admitted and treated at US Army Hospitals between the years 1941-1945. Prompt return of soldiers to the field was important, and, during that time, several articles proposed a variety of surgical treatments aimed at this goal.
After the war, Patey and Scarf hypothesized the origin of pilonidal disease was acquired by penetration of hair into the subcutaneous tissue with consequent granulomatous reaction, basing this theory on the high incidence of recurrence, as well as occurrence of disease in other areas of the body, such as the hands of a barber or sheep shearer. Other authors have followed this emphasis of hair as disease origin, and, in fact, an acquired etiology of the disease is now the prevailing theory in the medical world. 
Incidence of pilonidal disease is about 26 per 100,000 population. Pilonidal disease occurs predominantly in males, at a ratio of about 3-4:1. It occurs predominantly in white patients, typically in the late teens to early twenties, decreasing after age 25 and rarely occurs after age 45. [1, 3] One publication listed local irritation to the SC site, positive family history of pilonidal disease (PD), sedentary life style, and obesity as occurring in notable percentages of patients with PD (all factors between 34-50% occurrence in PD). 
It has been postulated that hair penetrates into the subcutaneous tissues through dilated hair follicles, which is thought to occur particularly in late adolescence, though follicles are not found in the walls of cysts. Upon sitting or bending, hair follicles can break and open a pit. Debris may collect in this pit, followed by development of a sinus with a short tract, with a not clearly understood suction mechanism involving local anatomy, eventually leading to further penetration of the hair into the subcutaneous tissue. [5, 3] This sinus tends to extend cephalad, likely owing to mechanical forces involved in sitting or bending.  A foreign body-type reaction may then lead to formation of an abscess. If given the opportunity to drain spontaneously, this may act as a portal of further invasion and eventually formation of a foreign body granuloma. Infection may result in abscess formation.
Microscopically, the sinus where the hair enters is lined with stratified squamous epithelium with slight cornification. Additional sinuses are frequent. Cyst cavities are lined with chronic granulation tissue and may contain hair, epithelial debris, and young granulation tissue. Cutaneous appendages are not seen in the wall of cysts, meaning the cysts lack epithelial lining, unlike the sinus.  Cellular infiltration consists of PMNs, lymphocytes, and plasma cells in varying proportions. Foreign body giant cells in association with dead hairs are a frequent finding.
In summary, 3 pieces are instrumental in this process: (1) the invader, hair; (2) the force, causing hair penetration; and (3) the vulnerability of the skin. [1, 3, 6] This process has been well characterized by Patey and Scarff as well as a number of other authors from the second half of the 20th century through today.
Pilonidal disease affects approximately 26 per 100,000 people.
In England in 2000-2001, a total of 11,534 admissions were recorded for pilonidal disease. The mean hospital stay was 4.3 days.
Pilonidal disease in the general population has a male preponderance. It occurs in the ratio of 3 or 4:1. In children, however, the ratio is the opposite occurring in 4 females for each male it afflicts.
Pilonidal disease commonly affects adults in the second to third decade of life. Pilonidal cysts are extremely uncommon after age 40 years, and the incidence usually decreases by age 25 years. The average age of presentation is 21 years for men and 19 years for women.