Type-B PDL

Type-B PDLs are particularly common in pregnant women among various forms of PDLs classified since Matzumoto first described PDL in 1913 (3). Initially, PDL was classified into four types A to D by Miura (7) and twenty-four years later another class E was added by Selmanowitz et al. (4) Facial PDL has also been well documented and were classified into F, G, and H among the Indian population (8,9). Type-B PDL can coexist with type-A in a few number of patients (10).
It can also occur in the absence of pregnant (2,4). In this cross-sectional study of 220 primigravidae and 220 controls, the age group ranges between 18 to 40 years for both cases and controls. The mean age of the cases and controls were respectively 27.61 ± 3.928 (SD) and 26.83 ± 4.069 (SD). The highest proportion of participants, more than 75%, recruited for the study belong to the age less than 30 years.
The pattern of age distribution in this study is similar to that reported by Kumar et al (11) and Rathore et al (12) in their study of cutaneous changes in pregnancy. This may reflect higher pregnancy rate among the younger age population possibly due to higher fertility rate in this age group. Pigmentary changes in pregnancy is the commonest physiological cutaneous changes witness by pregnant women (13). As many as over 90% in some studies developed one form of pigmentary changes or the other with lots of cosmetic concerns to the patients (13).

However, the prevalence of pigmentary demarcation lines (PDL) are low in this studies (11,13)The prevalence of pigmentary demarcation lines in this study varies with increasing gestational age. Type-A PDL was not observed among the pregnant women studied but was noticed in 0.5 percent of the controls group. The proportion of patients with type-B PDL in second trimester was 1.8%, this figure was however doubled 3.6% by third trimesters suggesting the fact that PDL tend to occur more as pregnancy advances attributable to neurogenic inflammation from compression of peripheral nerves S1 and S2 by enlarging uterus (14).
This result is similar to 2% earlier reported by Kumar et al (11). However, other researchers have documented lower prevalence than our study. Rathore et al (12) reported 0.25%, Kumari et al (13) 0.3% and Singh et al (6) 0.32% among pregnant population. The higher prevalence observed in this study compare to these previous studies may be due to the fact that our patients were followed up to the third trimester, some of which could have been missed in earlier trimesters without follow up.
Besides, type-b PDL are observed to develop more in later part of pregnancy probably as a result of increasing pregnancy hormones. Other possible reasons for discrepancies is the skin phototypes and racial differences of the studied populations as it has been observed to be commoner among Negroes (4). Type-B can also co-exist with type-A PDL although this is an infrequent phenomenon (15). This pattern was evident in this study as one patient had type A and B PDL together for the first time throughout her pregnancy and another one only develop type B co-existing with type-A only in third trimester.
This pattern is similar to the findings by Nakama et al (16) and Arunachalam et al (17). The pathogenesis of type B pigmentary demarcation lines is largely unknown (18). The influence of pregnancy hormones such as beta-melanocyte-stimulating hormone, eostrogen and progesterone has been suggested as one of the possible explanations for the development of pigmentary demarcation lines (19,20). The hormonal theory appeared plausible when the cases in our study are compare with the controls, this was however challenge by the fact that type-B PDL has been reported in amenorrhiec Chinese woman with low estradiol (2)
This should further prompt more research to unravel the pathogenesis of PDL.Other types of pigmentary demarcation lines C, D, E and facial PDL F, G, H were not observed in this study. This may probably be due to the fact that skin of negroid pregnant woman present with darker generalized hyperpigmentation that make this types of PDL difficult to discern. Other possible explanations is the close resemblance of facial PDL to melasma, exogenous onchronosis, periorbital hyperpigmentation and post inflammatory hyperpigmentation, naevus of Ota or Ito (9,21,22).
The pathogenesis of PDL remains controversial with many theories been propounded to explain the enigma. Even though PDL is well classified and accepted, there is no consensus yet on the pathogenesis, possibly multiple mechanism are interacting together to explain the aetiology of PDL. Among these theories are:Familiar clustering – genetic and racial predisposition play a role in the development of PDL as it has been reported to occur among family members and relatives in up to 22.2% of cases (23). Although PDL occurs in all races and skin types it is however commoner among the blacks than Caucasians (24).
It is postulated that PDL is dominantly inherited (9). However, none of our patients could give family history of PDL.Atavistic remnant phenomenon- this is an evolutionary throwback in which there is reappearance of a primitive characteristic. This characteristic is an adaptive mechanism in which the more pigmented dorsal surface protects against the effect of ultraviolet radiations and for temperature regulation (9,25).Pigmentary mosaicism- mosaicism occurs when two or more genetically distinct population of cells occur side by side in an individual (26). This is a consequence of structural or functional genetic mutation (27).
A classic pattern of cutaneous mosaicism is depicted by lines of Blaschko which has been described in many pigmentary disorders. Krivo proposed cutaneous mosaicism as the possible aetiology of type-b PDL (28). Mosaicism has also been ascribed to familiar clustering and preponderance in females with facial PDL (9).Axial-neural theory- Maleville et al (29) in an attempt to explain this enigma opined that the pathogenesis of PDL is better explained by virtual axial lines of Sherrington described by Miura (7) other than the clonal-Blaschko theory proposed by Krivo (28).
Blaschko lines correspond to distribution of linear nevoid conditions, or dermatomal lines.(30,31) The axial lines of Sherrington coincide with subsets of Voigt’s line and cutaneous nerve distributions that divide dermatomes when noncontiguous dorsal root give rise to two contiguous dermatome (7,29). Additionally, melanogenesis are under neural control, and nerve endings may be different in their sensitivity to neural stimulation resulting in dual population of melanocyte with subtle variation in pigmentation in-between dermatomes given rise to PDL (6).

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