Risk factors include: pelvic inflammatory disease, infertility, use of an intrauterine device (IUD), previous exposure to diethylstilbestrol (DES), tubal surgery, intrauterine surgery (e.g. D&C), smoking, previous ectopic pregnancy, endometriosis, and tubal ligation. A previous induced abortion does not appear to increase the risk. The IUD does not increase the risk of ectopic pregnancy, but with an IUD if pregnancy occurs it is more likely to be ectopic than intrauterine. The risk of ectopic pregnancy after chlamydia infection is low. The exact mechanism through which chlamydia increases the risk of ectopic pregnancy is uncertain, though some research suggests that the infection can affect the structure of fallopian tubes. Tube damage
Tubal pregnancy is when the egg is implanted in the fallopian tubes. Hair-like cilia located on the internal surface of the fallopian tubes carry the fertilized egg to the uterus. Fallopian cilia are sometimes seen in reduced numbers subsequent to an ectopic pregnancy, leading to a hypothesis that cilia damage in the fallopian tubes is likely to lead to an ectopic pregnancy. Women who smoke have a higher chance of an ectopic pregnancy in the fallopian tubes. Smoking leads to risk factors of damaging and destroying cilia. As cilia degenerate, the amount of time it takes for the fertilized egg to reach the uterus will increase. The fertilized egg, if it does not reach the uterus in time, will hatch from the non-adhesive zona pellucida and implant itself inside the fallopian tube, thus causing the ectopic pregnancy.
African Americans are found to be at increased risk. Historically, some have hypothesized that CCCA represents an end stage of traction alopecia. However, the veracity of this theory is low as many patients who have CCCA have not employed traction hairstyling. Histopathologic features
Histopathologic features include a perifollicular lymphocytic infiltrate, concentric lamellar fibrosis (layers of fibroblasts in the papillary dermis), sebaceous gland loss and premature disintegration of the internal root sheath. Additionally, granulomatous inflammation secondary to follicular rupture has been noted. Perifollicular erythema and follicular keratosis is usually absent. Treatment
Treatments for CCCA remain investigational. Altering hair care practices has not been proven to assist in hair rejuvenation. High-dose topical steroids, antibiotics, immunomodulators such as tacrolimus (Protopic) and pimecrolimus (Elidel), and anti-androgen/5alpha Reductase inhibitors have been used with unknown efficacy. : 648–9 : 760

Epidemiology
CCCA tends to present itself in the 20s and progresses over 20–30 years. One should consider this diagnosis in African Americans with what appears to be a female-pattern hair loss. Terminology
The terminology of CCCA has been a source of regular confusion. Recent clarifications have been made, with the term "central centrifugal cicatritial alopecia" adopted as a diagnostic category by the North American Hair Research Society. It has also been referred to as:
Hot comb alopecia
Follicular degeneration syndrome
Pseudopelade in African Americans
Central elliptical pseudopelade in CaucasiansAlso in this category is cicatricial pattern hair loss (CPHL). This CCCA pattern is a potential alopecia mimic that can be confused for androgenetic alopecia.