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利用Ｘ射线衍射法测得ＰＦ预聚物处理材的晶区大小和相对结晶度，结果表明，ＰＦ预聚物的引入没有改变纤维素的结构。解析ＦＴＩＲ光谱图得知．经ＰＦ预聚物处理后的压密材酯化羰基 （１７３６ ｃｍ－１）峰强度增加、半纤维素异头碳（８９７ｃｍ－１）峰强度增加，纤维素、半纤维素醚键（１０５６ ｃｍ－１）峰强度减少、说明半纤维素聚木糖经ＰＦ预聚物处理后发生改变木材细胞壁物质中的纤维素、半纤维素、木质素分子中的某些基团发生交联．形成了新的基团。从ＥＳＲ和ＥＳＣＡ测试结果可知．由于ＰＦ预聚物处理木材的机械自由基（Ｍｅｃｈａｎｏｒａｉｄｃａｌ）的浓度明显降低，可以推断出木材自由基与ＰＦ预聚物之间发生了化学作用，导致ＥＳＲ信号绝大部分丧失、ＥＳＣＡ能谱分析表明ＰＦ预聚物处理后的压密材，随着ＰＦ预聚物浓度的增加。ＣＩ态含量逐渐减少．而ＣⅡ态、 ＣⅢ态却逐渐增加、 ＣⅣ态变化不大。结果表明， ＰＦ预聚物处理能够稳定木材尺寸、固定木材横纹压缩变形的主要原因是由于ＰＦ预聚物填充于木材细胞壁空隙中和细胞腔的内表面。活性很高的羟甲基等基团与木材细胞壁物质发生反应，形成共价键和其它键型，部分取代了羟基（－ＯＨ）以及其它基因形成交联化作用。
The crystal size and relative crystallinity of PF prepolymer were measured by X-ray diffraction. The results showed that the introduction of PF prepolymer did not change the structure of cellulose. Analyze the FTIR spectra. The peak intensity of esterified carbonyl group (1736 cm-1) increased with the PF prepolymer treatment, and the peak intensity of hemicellulose anomeric carbon (897cm-1) increased. The cellulose and hemicellulose ether bond (1056 cm- -1), indicating that the hemicellulose-xylan changed after PF prepolymer treatment. Some of the cellulose, hemicellulose and lignin molecules in the wood cell wall material were cross-linked. Formed a new group. From ESR and ESCA test results we can see. Due to the significantly lower concentration of Mechanoraidcal in the PF prepolymer treated wood, it can be inferred that a chemical interaction between the wood free radical and the PF prepolymer occurred, resulting in the vast majority of ESR signal loss. ESCA spectrum analysis revealed PF prepolymer treated compacted wood, with PF prepolymer concentration increases. CI state content gradually reduced. The C Ⅱ state, C Ⅲ state but gradually increased, C Ⅳ state little change. The results show that the PF prepolymer treatment can stabilize the wood size. The main reason for fixing the compression deformation of the wood is that the PF prepolymer is filled in the space of the wood cell wall and the inner surface of the cell cavity. Highly reactive groups such as methylol react with the wood cell wall material to form covalent and other bond types, partially replacing the hydroxyl group (-OH) and other genes to form cross-linkages.