Striae Distensae are a form of pathological scarring

Striae indicate a pathological condition of the connective tissue.1 The pathogenesis of Striae Distensae describes definitive changes in the extracellular matrix, especially changes in collagen, elastin and fibrillin.2–5

Histologically Striae are form of atrophic scarring, in which the dermal collagen ruptures and separates; the intervening gap is filled with newly synthesized collagen, which then becomes aligned in response to local stress forces.6

Although they are not detrimental to health, they can cause physical symptoms such as itchiness, tenderness and pain.7 Because of their visual appearance, they can also significantly affect a woman’s self-esteem and image.7

The development of Striae has been likened to wound healing or scar formation.8

Studies found no correlation between:

The strength of the skin’s strain is not the primary cause of Striae.

Clinical publications confirm that hormonal change is one of the main risk factors for the development of Striae.

Three-dimensional representation of skin replicas.

Distribution of gestational ages when Striae first appeared3

Histological comparison of normal skin, Striae Rubrae and Striae Albae9

Normal skin: haphazardly arranged small collagen fibres and thin elastin fibres in the papillary dermis, surrounded by ground substance; coarse elastic fibres and thick bundles of collagen parallel to the direction on the skin in the reticular dermis.

Striae Rubrae: fine elastic fibres predominate in the dermis with thicker tortuous fibres in the periphery; there is a reduction and reorganization of elastin and fibrillin fibres and structural changes in collagen are seen.

Striae Albae: histology demonstrates epidermal atrophy and loss of the rete ridges; densely packed, thin eosinophilic collagen bundles are arranged horizontally, parallel to the surface of the skin in a similar way to a scar.

1. Viennet C et al. Arch Dermatol Res. 2005 Jul; 297(1):10–7
2. Rotsztejn H et al. Advances in Medical Sciences 2010; 55
3. Chang AL et al. Acad Dermatol 2004; 51:881–885
4. Lee KS et al. Clin Exp Dermatol 1994; 19(4):285–288
5. Klehr N. Acta Derm Venereol Suppl 1979; 59(85):105–108
6. Tsuji T et al. J Cutan Pathol 1988; 15:215–222
7. Osman H et al. BJOG 2008; 115:1138–1142
8. Atwal GS et al. Br J Dermatol 2006; 155:965–969
9. Al-Himdani S et al. Br J Dermatol 2014; 170:527–547