The effect of wood modification on wood-water interactions in modified wood is poorly understood, even though water is a critical factor in fungal wood degradation. A previous review suggested that decay resistance in modified wood is caused by a reduced wood moisture content (MC) that inhibits the diffusion of oxidative fungal metabolites. It has been reported that a MC below 23%–25% will protect wood from decay, which correlates with the weight percent gain (WPG) level seen to inhibit decay in modified wood for several different kinds of wood modifications. In this review, the focus is on the role of water in brown rot decay of chemically and thermally modified wood. The study synthesizes recent advances in the inhibition of decay and the effects of wood modification on the MC and moisture relationships in modified wood. We discuss three potential mechanisms for diffusion inhibition in modified wood: (i) nanopore blocking; (ii) capillary condensation in nanopores; and (iii) plasticization of hemicelluloses. The nanopore blocking theory works well with cell wall bulking and crosslinking modifications, but it seems less applicable to thermal modification, which may increase nanoporosity. Preventing the formation of capillary water in nanopores also explains cell wall bulking modification well. However, the possibility of increased nanoporosity in thermally modified wood and increased wood-water surface tension for 1.3-dimethylol-4.5-dihydroxyethyleneurea (DMDHEU) modification complicate the interpretation of this theory for these modifications. Inhibition of hemicellulose plasticization fits well with diffusion prevention in acetylated, DMDHEU and thermally modified wood, but plasticity in furfurylated wood may be increased. We also point out that the different mechanisms are not mutually exclusive, and it may be the case that they all play some role to varying degrees for each modification. Furthermore, we highlight recent work which shows that brown rot fungi will eventually degrade modified wood materials, even at high treatment levels. The herein reviewed literature suggests that the modification itself may initially be degraded, followed by an increase in wood cell wall MC to a level where chemical transport is possible.

Acetylation has been shown to delay fungal decay, but the underlying mechanisms are poorly understood. Brown-rot fungi, such as Rhodonia placenta (Fr.) Niemelä, K.H. Larss. & Schigel, degrade wood in two steps, i.e., oxidative depolymerization followed by secretion of hydrolytic enzymes. Since separating the two degradation steps has been proven challenging, a new sample design was applied to the task. The aim of this study was to compare the expression of 10 genes during the initial decay phase in wood and wood acetylated to three different weight percentage gains (WPG). The results showed that not all genes thought to play a role in initiating brown-rot decay are upregulated. Furthermore, the results indicate that R. placenta upregulates an increasing number of genes involved in the oxidative degradation phase with increasing WPG.

The aim of this study was to investigate Rhodonia placenta expression patterns of genes involved in the depolymerisation during the non-enzymatic phase in acetylated (W_Ac) and furfurylated wood (W_FA). During the 98-day-long exposure, W_Ac [22.6% weight per cent gain (WPG) on average] and W_FA (69% WPG on average) lost no more than 3% mass while the untreated wood (W_Un) reached 41% mass loss (ML) in 55 days. Expression of six genes putatively involved in the non-enzymatic degradation process were investigated. In conclusion, expression levels of alcohol oxidase Ppl118723 (AlOx1) and laccase Ppl111314 (Lac) were significantly higher in the modified wood materials (W_Mod) than in W_Un, which is in accordance with previous results and may be explained by the absence of the degradation products that have been proposed to down-regulate the non-enzymatic degradation process. However, copper radical oxidase Ppl156703 (CRO1) and a putative quinate transporter Ppl44553 (PQT) were expressed at significantly lower levels in W_Mod than in W_Un while quinone reductase Ppl124517 (QRD) and glucose oxidase Ppl108489 (GOx) were expressed at similar levels as in W_Un. These results suggest that gene regulation in W_Mod is more complex than a general up-regulation of genes involved in the non-enzymatic degradation phase.