LCPD represents a worldwide health problem, so its study and understanding are crucial. It is a complex disease; the lack of knowledge regarding its etiology is considered the main obstacle to its study. Different etiological factors have been described as the causative agents and some of them are present in our population, like elevated load stress and tobacco smoke exposure. Because the mechanical properties of the hip are affected by osteonecrosis of the femoral head, studies have suggested that elevated load stress acting on the cartilage is one of the major reasons for development in various anomalies of the hip, as well as LCPD (12).
Blood supply alterations due to extrinsic compression of the blood vessels or intravascular occlusion have been suggested as a cause of LCPD, therefore, hemostatic disorders have been studied as probable etiological factors of LCPD, the presence of FVL and prothrombin C20210A mutations, deficiencies in protein c and s, elevated levels of lipoprotein (a) or fibrinogen, as well as FV and FVIII hyperactivity have been reported in populations with LCPD (2–6).
PT is a routine study in the clinical laboratory, PT has been reported as a good diagnostic marker for LCPD, a lower PT is related to greater hemostatic activity, since less time will be required for thrombus formation (13, 14).
Coagulation factor V is an essential cofactor of coagulation factor X in the common pathway of coagulation, FV is a large single-chain glycoprotein of ≈ 330 kDa. Its plasma concentration is ≈ 20 nmol/L, besides circulating in free form in plasma, FV is also present in the α-granules of platelets; this form accounts for ≈ 25% of the total FV content in human blood. However, FV high activity has been related to thrombosis as well as the FV Leiden has been reported as an etiological factor of the LCDP, it by multiples authors (4–6, 14).
Factor IX is a factor of the blood coagulation system, the main function of the activated factor IXa in complex with factor VIIIa and phospholipids in presence of Ca2 + consists of the activation of factor X. Factor IX is synthesized in the liver and is subject to several posttranslational modifications including gamma-carboxylation, beta-hydroxylation, and glycosylation. The majority of FIX resides extravascular, in the subendothelial basement membrane, where it is central for hemostasis. As a matter of fact, High levels of factor XI are a risk factor for deep venous thrombosis, Venous thrombosis of the upper extremity, and LCPD (14–18).
Homocysteine (Hcy) is derived from methionine and is a homologue of cysteine, high Hcy levels are associated with an increased risk for cardiovascular disease, besides elevated Hcy levels are associated with an increased risk for blood clots in the veins. Clots can occur in the extremities, mostly legs, on the other hand, higher Hcy levels have been observed in deep vein thrombosis, coronary artery disease, atherosclerosis, osteoporosis and LCPD (19–23).
On the other hand, cigarette smoke exposure seems to alter the hemostatic process via multiple mechanisms, which include alteration of the function of endothelial cells, platelets, fibrinogen, and coagulation factors, consequently exacerbating clotting (24).
Not only mechanical and metabolic disorders, but also genetic alterations have been linked to LCPD. Polymorphisms and mutations as FVL, COL2A1, G-455-A polymorphism of the β fibrinogen, MTHFR, eNOS Polymorphisms, IL-6 polymorphism, and others, related to LCPD have been reported in recent decades, showing genetics as a central etiological factor in LCPD (25–39).
IL-23 is a member of the IL-6 family of cytokines, the gene location´s 12q13.3, This gene encodes a subunit of the heterodimeric cytokine interleukin 23 (IL23). IL23 is composed of this protein P19 and the p40 subunit of interleukin 12.
The functional receptor for IL-23 (the IL-23 receptor) consists of a heterodimer between IL-12Rβ1 and IL-23R, Upon IL-23 binding to its receptor the Janus kinases JAK2 and Tyk2 become activated followed by activation and nuclear translocation of the transcription factors signal transducer and activator of transcription 3 (STAT3) and 4 (STAT4). IL-23R is produced by antigen-presenting cells, however inflammatory macrophages express IL-23R and are activated by IL-23 to produce interleukin-1, tumor necrosis factor-alpha (TNF-α), and IL-23 itself, IL-23 stimulates a pro-inflammatory condition, these proinflammatory ambient lead to damage in various structures involving joint, bone, and cartilage. On the other hand, IL-23 is also involved in osteoclast genesis and bone destruction, independently from IL-17, via induction of receptor activator of kappa B ligand (RANKL) expression in T cells and tartrate-resistant acid phosphatase (TRAP) activity of osteoclasts (40–46).
Since inflammation is showing as an etiologic factor in LCPD, studying the clinical significance of the SII in LCDP seemed to be relevant. SII is based on peripheral lymphocyte, neutrophil, and platelet counts and has been considered a good index reflecting the local immune response and systemic inflammation. Furthermore, SII has been showed as a risk of osteopenia/osteoporosis, and other diseases (47–50).
Our results show higher levels in the SII index and R N/L, which could even be the result of the genetic variant in IL-23R, we suggest studying this matter deeper by different methods, however, a greater proinflammatory state is showed by the patients.