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Thermal modification (TM) of wood has occupied a relatively narrow but stable niche as an alternative for chemical wood protection. There are different technological solutions for TM and not all details of their effects on wood tissue have been understood. The one-stage hydrothermal modification (HTM) at elevated vapour pressure essentially changes the wood’s composition and structure. In the present paper, the changes in three hardwood lignins (alder, aspen, and birch) were observed within the cell wall by means of cellular UV microspectrophotometry. The lignin absorbances in the compound middle lamella (CML) of unmodified wood are 1.7- to 2.0-fold higher than those in the fibre S2 layer. The woods were modified in the temperature range from 140 to 180°C, while in the lower temperature range (140°C/1 h), the UV absorbances are little affected. Essential changes occur in the range of 160–180°C and the UV data reflect these by absorbtion changes, while the absorbances at 278 nm rise with factors around 2 more in the S2 layer than in the CML. The absorbance increments are interpreted as polycondensation reactions with furfural and other degradation products of hemicelluloses with the lignin moiety of the cell wall.

Brown rotted Scots pine (Pinus sylvestris) sapwood was studied using scanning UV microspectrophotometry. Wood blocks were exposed to the fungus Coniophora puteana (Schum.: Fr.) Karst. (BAM Ebw.15) for 6, 8, 10, 30, and 50 days. No wood weight loss was detected in the initial decay periods. On the other hand, point analyses of lignin distribution in wood cells revealed higher absorbance after 6–10 days of decay, which we interpret as an increase in the absorption coefficient of lignin due to its oxidative modification by the fungus. Uneven wood degradation occurred in the later periods (30 and 50 days), with both significantly decayed and visually sound cells observed. The decayed cells showed a higher absorbance at 280 nm, although the apparently sound cells were also degraded to a lower extent. Degradation of lignin-rich compounds in middle lamellae and cell corners was not observed during fungal attack.