IADR Abstract Archives
Central Giant Cell Granuloma: Macrophage Maturation-related Markers and Therapeutic Options
Objectives: Central giant cell granuloma (CGCG) constitutes ~10% of benign jawbone lesions, 75% being diagnosed in patients younger than 30 years. While about 70% CGCG are asymptomatic, slow-growing, non-aggressive (nA-CGCG), 30% show an aggressive, progressively destructive behavior (A-CGCG). Consequently, management ranges from conservative surgery for nA-CGCGs to en-bloc resection for A-CGCGs. Histopathologically, both subtypes are identical with no reliable markers to distinguish between them. We aimed to investigate expression of macrophage maturation-related markers in a large series of CGCGs and define relations to biological behavior.
Methods: Formalin-fixed, paraffin-embedded sections of 36 A-CGCGs and 31 nA-CGCGs were immunohistochemically stained for CD68, CD163, CD115 and NF-kB. Staining score was assessed by multiplying the percentage of stained cells by staining intensity (1 – weak staining, 2 – moderate, 3 – strong), separately for the mononuclear and multinuclear cells. Mean score of each type of cell for each marker was compared between A-CGCG and nA-CGCG. T-test was used for statistical analysis.
Results: In A-CGCG, the expression of CD163 in the multi-nuclear cells was significantly lower compared to nA-CGCG (p<0.05); no differences found for the other markers. In both A-CGCGs and nA-CGCGs the expression of CD163, CD68 and NF-kB in the multi-nuclear cells was higher compared to mono-nuclear cells, whereas that of CD115 was higher in mono-nuclear than in multi-nuclear cells. The finding was more pronounced in A-CGCG than in nA-CGCG, although the difference was statistically insignificant.
Conclusions: The examined molecular markers cannot distinguish between A-CGCG and nA-CGCG. Nevertheless, the expression of CD115 in CGCGs can open a new therapeutic platform with pharmacologic, immunobiological agents that are already under advanced stages of development for CD115-positive multinuclear cell-containing lesions. This may have an important impact on the treatment approach for A-CGCGs in young patients that can be offered other treatment than extensive and mutilating surgical procedures.
Methods: Formalin-fixed, paraffin-embedded sections of 36 A-CGCGs and 31 nA-CGCGs were immunohistochemically stained for CD68, CD163, CD115 and NF-kB. Staining score was assessed by multiplying the percentage of stained cells by staining intensity (1 – weak staining, 2 – moderate, 3 – strong), separately for the mononuclear and multinuclear cells. Mean score of each type of cell for each marker was compared between A-CGCG and nA-CGCG. T-test was used for statistical analysis.
Results: In A-CGCG, the expression of CD163 in the multi-nuclear cells was significantly lower compared to nA-CGCG (p<0.05); no differences found for the other markers. In both A-CGCGs and nA-CGCGs the expression of CD163, CD68 and NF-kB in the multi-nuclear cells was higher compared to mono-nuclear cells, whereas that of CD115 was higher in mono-nuclear than in multi-nuclear cells. The finding was more pronounced in A-CGCG than in nA-CGCG, although the difference was statistically insignificant.
Conclusions: The examined molecular markers cannot distinguish between A-CGCG and nA-CGCG. Nevertheless, the expression of CD115 in CGCGs can open a new therapeutic platform with pharmacologic, immunobiological agents that are already under advanced stages of development for CD115-positive multinuclear cell-containing lesions. This may have an important impact on the treatment approach for A-CGCGs in young patients that can be offered other treatment than extensive and mutilating surgical procedures.