Causes
Sometimes there is no obvious explanation for the cause of PGP but usually there is a combination of factors such as:

The pelvic joints moving unevenly. A change in the activity of the muscles in the pelvis, hip, abdomen, back and pelvic floor. A history of pelvic trauma. The position of the baby altering the loading stresses on the pelvic ligaments and joints. Strenuous work. Previous lower back pain. Previous pelvic girdle pain during pregnancy. Hypermobility, genetical ability to stretch joints beyond normal range. An event during the pregnancy or birth that caused injury or strain to the pelvic joints or rupture of the fibrocartilage. The occurrence of PGP is associated with twin pregnancy, first pregnancy and a higher age at first pregnancy. Mechanism
Pregnancy related Pelvic Girdle Pain (PGP) can be either specific (trauma or injury to pelvic joints or genetical i.e. connective tissue disease) and non-specific. PGP disorder is complex and multi-factorial and likely to be also represented by a series of sub-groups driven by pain varying from peripheral or central nervous system,
altered laxity/stiffness of muscles, laxity to injury of tendinous/ligamentous structures to mal-adaptive body mechanics.Pregnancy begins the physiological changes through a pattern of hormonal secretion and signal transduction thus initiating the remodelling of soft tissues, cartilage and ligaments. Over time, the ligaments could be stretched either by injury or excess strain and in turn may cause PGP. Anatomy
The pelvis is the largest bony part of the skeleton and contains three joints: the pubic symphysis, and two sacroiliac joints.
Pathophysiology
The bullae are formed by an immune reaction, initiated by the formation of IgG autoantibodies targeting dystonin, also called bullous pemphigoid antigen 1, and/or type XVII collagen, also called bullous pemphigoid antigen 2, which is a component of hemidesmosomes. A different form of dystonin is associated with neuropathy. Following antibody targeting, a cascade of immunomodulators results in a variable surge of immune cells, including neutrophils, lymphocytes and eosinophils coming to the affected area. Unclear events subsequently result in a separation along the dermoepidermal junction and eventually stretch bullae. Diagnosis
Diagnosis consist of at least 2 positive results out of 3 criteria (2-out-of-3 rule): (1) pruritus and/or predominant cutaneous blisters, (2) linear IgG and/or C3c deposits (in an n- serrated pattern) by direct immunofluorescence microscopy (DIF) on a skin biopsy specimen, and (3) positive epidermal side staining by indirect immunofluorescence microscopy on human salt-split skin (IIF SSS) on a serum sample. Routine H&E staining or ELISA tests do not add value to initial diagnosis. Treatment
Treatments include topical steroids such as clobetasol, and halobetasol which in some studies have proven to be equally effective as systemic, or pill, therapy and somewhat safer. However, in difficult-to-manage or widespread cases, systemic prednisone and powerful steroid-free immunosuppressant medications, such as methotrexate, azathioprine or mycophenolate mofetil, may be appropriate. Some of these medications have the potential for severe adverse effects such as kidney and liver damage, increased susceptibility to infections, and bone marrow suppression. Antibiotics such as tetracycline or erythromycin may also control the disease, particularly in patients who cannot use corticosteroids.