Among various states that need total hip arthroplasty, about 90% of cases are osteoarthrosis, and others are: avascular necrosis of the femoral head, femoral neck fracture or traumatic joint injury, inflammatory arthropathy . Year after year, implants are inhanced, among other means, with the use of new biomaterials. In general, biomaterials are widely applied in orthopedics and traumatology. These are frames and carbon materials, bioactive glass, natural and synthetic polymers and composites developed on their basis [2-5]. Among biomaterials, we can mention metal materials and their alloys, titanium with different coatings, of which implants and devices for intramedullary and external fixation are made.
The normal ranges of the maternal thyroid hormones (THs) during the gestation are required to get a regular development during the prenatal and postnatal periods [1-65]. On the other hand, postpartum thyroiditis represents as a transient thyroid disorders (inflammation in the thyroid gland) due to thyroid autoantibodies (positive thyroid peroxidase (TPO), thyroid-stimulating hormone-receptor (TSH-R) and thyroglobulin (Tg)) and lymphocytic infiltration of the thyroid that happens during the postpartum period [66-71]. The release of stored thyroxine (T4) and 3,5,3’-triodothyronine (T3) can cause a destructive thyroiditis and transient thyrotoxicosis. Postpartum thyroiditis can be classified into De Quervain’s (painful subacute, granulomatous thyroiditis), Hashimoto’s (chronic lymphocytic/autoimmune), painless sporadic, painless postpartum, and Riedel’sthyroiditis (invasive fibrous thyroiditis)[68-70].
Postpartum thyroiditis can alter the cellular immunity as the following :
1. Elevationthe thyroidal β cells 
2. Elevationthe peripheral large granular lymphocytes 
3. Increase the peripheral lymphocyte CD4+/CD8+ratio [73,74]
4. Elevationthe thyroidal lymphocyte helper (CD4+)/suppressor (CD8+) ratio . Moreover, postpartum thyroiditis can change the humoral immunity as the following
a. elevation the complement activation 
b. Thyroid microsomal antibodies rebound , and
c. Increased IgG1 TPO antibody subclass . In addition, amiodarone, lithium or therapy using interferon-α and
interleukin-2 are a common causes of postpartum thyroiditis [68,69,71]. On the other hand, there are several symptoms of postpartum thyroiditis such as fatigue, palpitations, muscle stiffness, irritable, tachycardia, depression, psychoneurosis, anxiety, hair loss, weight loss, dry hair, coldness, careless, and impaired concentration/memory .
From the previous data, it can be concluded that postpartum thyroiditis may interrupt the actions of THs and cause several complications during the neonatal and adulthood periods. However, the mechanisms underlying postpartum thyroiditis remain indefinite. The present view highlights the necessity to measure thyroid autoantibodies, a marker for early detection of postpartum thyroiditis, in the first trimester of pregnancy. Also, following the thyroid function should be acquired in antibody-positive dam at the initial and final postpartum stages (at 3 and 6 months after delivery). Thus, adjustment of thyroid functions is warranted to avoid postpartum thyroiditis and to improve the adulthood consequence. Further experiments are needed to determine the association between pregnancy, postpartum thyroiditis and neonatal and adulthood consequences, and to discover new diagnostic assays or treatments [77-85].