The susceptibility of surface-modified wood, surface-modified acetylated wood and acetylated wood to mold and blue stain fungi was investigated. The surface modifications were based on fluorinated and non-fluorinated silicone nanofilaments for increased hydrophobicity. Results showed an increased mold resistance of the surface-modified superhydrophobic wood with mold appearing later or with less intensity on the modified surfaces than on the untreated wood in accelerated mold chamber tests due to the increased water resistance of the samples. All acetylated wood samples exhibited good mold resistance as the available water in acetylated wood was reduced. The surface modifications on acetylated wood had a slightly negative effect on mold resistance due to side effects from the modification. The surface-modified wood showed high blue stain fungi coverage, whereas almost no blue stain fungi were observed on the acetylated wood and surface-modified acetylated wood. The surface-modified superhydrophobic wood showed high mold coverage after conditioning in a high-humidity environment or after exposure to UV irradiation. Meanwhile, the acetylated wood and surface-modified superhydrophobic acetylated wood showed a small amount of mold coverage in these conditions. © 2023 The Authors

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 (WAc) and furfurylated wood (WFA). During the 98-day-long exposure, WAc [22.6% weight per cent gain (WPG) on average] and WFA (69% WPG on average) lost no more than 3% mass while the untreated wood (WUn) 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 (WMod) than in WUn, 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 WMod than in WUn while quinone reductase Ppl124517 (QRD) and glucose oxidase Ppl108489 (GOx) were expressed at similar levels as in WUn. These results suggest that gene regulation in WMod is more complex than a general up-regulation of genes involved in the non-enzymatic degradation phase.

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.

The study of degradation and growth patterns of fungi in modified wood may increase the understanding of their mode of action and may lead to more accurate service-life predictions. The aim of this paper was to study the degradation and growth patterns of brown rot fungi in modified wood and to measure moisture content (MC), structural integrity and the acetyl content by frequent monitoring over 300 days. Mass loss (ML) in the modified wood materials increased slowly up to 3% for 50–100 days after which it flattened out and remained constant during the remainder of the test. Structural integrity and acetyl content were maintained in the modified wood materials and MC was lower compared to untreated wood throughout the decay test. ML results of untreated wood indicate that fungi in solid wood go through distinct phases; the degradation patterns in the modified wood materials were more difficult to interpret.

The mechanism by which modified wood resists decay has long been discussed, but is still not fully understood. A better understanding of decay resistance mechanisms could improve wood protection processes and product properties. In this study, the dynamics of brown rot decay in thermally modified wood was examined through measurements of mass loss, strength loss and gene expression. Close monitoring of mass loss over 120 days in thermally modified wood exposed to Postia placenta showed a delay in the onset of degradation compared to untreated wood, and once the degradation had started, the rate was lower. Thermally modified wood did not inhibit expression of wood degradation-related genes before mass loss and was similar to that in untreated wood once mass loss could be detected. Comparing gene expression as well as strength loss at the same stage of decay rather than at the same time after exposure showed smaller differences in decay patterns between thermally modified and untreated wood than previous results indicate. It is concluded that the key to understanding degradation resistance in thermally modified wood is to compare the decay patterns in thermally modified wood and untreated wood before mass loss occurs.

Modified wood shows resistance against wood deteriorating fungi, but the mechanisms are still not fully understood. The aim of this paper was to summarise the molecular studies performed on modified wood with regard to brown rot decay fungi. The DNA data showed that fungi are present inside the laboratory wood test samples already after two weeks of inoculation. Generally the fungal DNA content reflects mass loss and wood moisture content. The oxidative gene expression seems to be higher in modified wood than in untreated wood and it tend to increase during incubation. Based on the gene expression data we suggest that the hypothesis of lack of substrate recognition by the fungus should be rejected. In the reviewed studies, total wood moisture content in the samples was generally not low enough to inhibit fungal colonisation. Hence, moisture distribution within the wood should be studied more closely.

The mode of action of nontoxic wood modifications and the fungal response to modified wood are not fully elucidated. The aim of this study was to investigate the reaction of Postia placenta in terms of gene expression of selected genes upon the encounter of acetylated, DMDHEU-treated and thermally modified wood. Quantitative PCR (qPCR) showed that the investigated P.placentagenes involved in oxidative degradation were expressed at higher levels in modified wood than in untreated wood, while expression levels in modified wood for the investigated genes involved in enzymatic degradation were slightly lower than those in untreated wood. The results indicate that the response of P.placenta upon the encounter of modified wood is to up-regulate the expressionof the oxidative degradation machinery. In addition, our results support the theory that the decay resistance of the herein studied modified woods is due to inhibition of fungal molecules, needed for oxidative degradation of wood polymers, to penetrate the wood cell wall.

Fungal cellulases have been shown to be less efficient in modified wood than in untreated wood (Lekounogou et al. 2008; Vena°s 2008). However, Verma and Mai (2010) showed that cellulase efficacy is partly restored in 1,3-dimethylol-4,5-dihydroxyethyleneurea (DMDHEU) treated wood by pre-treatment with Fenton's reagent, simulating the oxidative degradation phase in initial brown rot decay. In this study, we examined whether Fenton derived hydroxyl radicals (OH) and cellulases are able to cleave polysaccharides in furfurylated and acetylated wood and to what extent enzyme efficacy is increased by oxidative pre-treatment of these materials. The results show that fungal cellulases were able to degrade acetylated wood and that the cellulase efficacy was increased by oxidative pre-treatment by 20%, which is half of the increase in untreated wood. Furthermore, the results indicate that poly(furfuryl alcohol) is degraded by Fenton derived OH. This indicates a possible route for the eventual degradation of modified wood.