## 4 Discussion  
The body reacts to the silicone implant by forming a capsule around it, but is yet unknown why some of them contract [18; 19; 20]. [PERSON] et al. demonstrated in vivo study that the implant triggered a foreign body reaction, which led to a cascade of inflammatory cell recruitment, fibroblast proliferation and collagen synthesis which eventually led to capsule formation. At the same time, they showed that a stronger reaction of the foreign body leads to the formation of a denser capsule with a higher density of collagen, reason why they considered that the collagen is a decisive factor in capsular formation. They also correlated the impact of the capsular thickness in the appearance of the capsular contracture as being directly proportional [21; 22]. Capsular Contratures typically form in the early postoperative period, but they also may appear many years later with an increasing incidence over time [23; 24]. Two commonly accepted hypotheses exist: an infectious process theory describing a chronic subclinical infection located immediately adjacent to the implant sheath in a microscopic biofilm that is relatively inaccessible to cells and immune humoral function; this apparent process is determined by contamination and a hypertrophic scar theory in which the mechanism involved is to stimulate the activity of myofibstats that are present in the capsule, which determines the subsequent formation of hypertrophic scars that contracts due to a series of phenomena similar to those of an inflammatory reaction [25; 26; 27; 28; 29]. The type of cells that predominate in the capsule are macrophages, lymphocytes and fibroblasts. More recent studies have shown the role of mast cells present in significant numbers in the capsule. Apparently mast cells play an important role in the formation of capsular contract through their contribution in the formation of fibrotic tissue; mast cells have profibrotic mediators renin-_angiotensin II_, histamine and _transforming growth factor beta \begin{table}
\begin{tabular}{c c c c c c c c} \hline \hline  & & **V1** & **PMN** & **Ly-PL** & **EOZ** & **Macrophage** & **Gigantocellular Reaction** & **Mastocyte** \\ \hline \multirow{5}{*}{V1} & Pearson Correlation & 1 & 102 & \(-35\) & \(-77\) & \(357\)\({}^{*}\) & \(-354\)\({}^{*}\) & \(417\)\({}^{**}\) \\ \cline{2-8}  & Sig. (2-tailed) & & 492 & 816 & 601 & 13 & 14 & 3 \\ \cline{2-8}  & Sum of Squares and & \multirow{2}{*}{49,917} & \multirow{2}{*}{87,917} & \multirow{2}{*}{\(-42\),042} & \multirow{2}{*}{\(-542\)} & \multirow{2}{*}{133,917} & \multirow{2}{*}{\(-243\),792} & \multirow{2}{*}{81,500} \\  & Cross-products & & & & & & \\ \cline{2-8}  & Covariance & 1062 & 1871 & \(-895\) & \(-12\) & \(2849\) & \(-5187\) & \(1734\) \\ \cline{2-8}  & N & 48 & 48 & 48 & 48 & 48 & 48 \\ \hline \hline \end{tabular}  
\begin{tabular}{c c c c c} \hline \hline  & & **V1** & **Acute Inflammation** & **Chronic Inflammation** & **Chronic Active Inflammation** \\ \hline \multirow{5}{*}{V1} & Pearson Correlation & 1 & \(-186\) & \(-364\)\({}^{*}\) & \(-94\) \\ \cline{2-5}  & Sig. (2-tailed) & & 206 & 11 & 526 \\ \cline{2-5}  & Sum of Squares and & \multirow{2}{*}{49,917} & \multirow{2}{*}{\(-4542\)} & \multirow{2}{*}{\(-8708\)} & \multirow{2}{*}{\(-2042\)} \\  & Cross-products & & & & \\ \cline{2-5}  & Covariance & 1062 & \(-97\) & \(-185\) & \(-43\) \\ \cline{2-5}  & N & 48 & 48 & 48 & 48 \\ \hline \hline \end{tabular}  
* V1: capsular contracture.
* Correlation is significant at the 0.05 level (2-tailed).  
\end{table} 
Table 2: Correlations of inflammatory type cells. (TGF-\(\beta\)) on their cell surface that activate angiotensin _receptors_ (ATiR) and TGF-\(\beta\) receptors on the surface of the fibroblasts also present in the capsular tissue. It appears that these cells are responsible for the initial production and storage of collagen, which subsequently causes the formation of fibrotic tissue [4].