According to Riddell et al.  dysplasia is strictly a histopathological diagnosis and is characterised microscopically by the following histological features:
1. architectural changes often resembling colonic adenoma.
2. Cellular atypia as characterised by nuclear stratification, loss of polarity, hyperchromasia and an increase in mitotic figures. High-grade epithelial dysplasia commonly shows a greater degree of glandular architectural abnormality (complex budding and branching), with enlarged hyper-chromatic nuclei with prominent nucleoli and stratification (Fig. 1).
3. The above changes are sometimes associated with the so-called 'incomplete crypt maturation'. This is characterised by a marked reduction in the number of goblet cells (or their focal absence) rendering some of the crypts containing absorptive cells only and dystrophic goblet cells (upside down rotation of goblet cells/signet ring formation).
In practice, however, the distinction between reac-
Research Committee on IBD of the Ministry of Health and Welfare of Japan
Table 3. Classification of gastrointestinal neoplasia (Vienna classification) 
1. Negative for dysplasia/neoplasia
2. Indefinite for dysplasia/neoplasia
3. Non-invasive low-grade neoplasia (low-grade adeno-ma/dysplasia)
4. Non-invasive high-grade neoplasia (high-grade adeno-ma/dysplasia, non-invasive carcinoma, suspicious for invasion)
5. Invasive neoplasia (intramucosal carcinoma, submu-cosal carcinoma or beyond)a a In the modified Vienna classification [11, 12], intramucosal carcinoma moved to category 4.
tive and dysplastic epithelium is not always straight forward. While the dysplastic epithelium shows certain histological changes that distinguish it from normal epithelium, it is not always easy to differentiate dysplasia from the reactive type morphology seen in cases of inflammation or repair. In a reactive process, there are usually enlarged nuclei, nuclear pseudostratification but no loss of polarity and no nuclear coarse chromatin formation. They may both, however, show some degree of mucin loss together with increased density of the cytoplasm and high mitotic figures.
Macroscopically, dysplasia can be categorised as either flat or raised. The former is usually detected during random biopsies taken by conventional colonoscopy . In contrast, the raised dysplastic areas are usually visible endoscopically and have been referred to as a dysplasia associated lesion or mass (DALM) . Raised lesions can take many forms including plaques, polyps, velvety patches, clusters of polyps or nodular areas .
As mentioned earlier, the first problem encountered by the pathologist is the histologic recognition of dysplasia, and its distinction from that of a repar-ative process. As noted in several studies, there is a significant degree of intra- and interobserver variability in recognising dysplasia, particularly in the distinction between indefinite probably positive for dysplasia vs. low-grade dysplasia [15,16]. This necessitates a well-accepted policy of diagnosing dysplasia by two different pathologists with one of them having a special interest in gastrointestinal pathology and dysplasia . The distinction between high-grade dysplasia is less of an issue because the degree of concordance is better than with low-grade dysplasia . The distinction between high and low-grade dyspla-sia bears significant consequences to the patient in some colorectal surgical units because the detection of high-grade dysplasia requires immediate intervention, which is usually colectomy, since it is associated with 40-70% of invasive carcinomas , while in some centres, low-grade dysplasia requires a less radical approach.
In contrast to high-grade dysplasia, some studies have shown that low-grade dysplastic change has a positive predictive value of 7-24% for development of cancer and 16-54% for progression to high-grade dysplasia in 5 years, and this has been demonstrated by the increase frequency of p53 mutation in low-grade dysplasia [19, 20]. However, there are no strict criteria for distinguishing between low and highgrade dysplasia, and the distinction between them depends on the subjective interpretation of the reporting pathologist. An active chronic colitis that shows marked reparative changes can be difficult if not impossible to differentiate from genuine dyspla-
sia and, under such circumstances, a diagnosis of indefinite for dysplasia is warranted.
Mapping studies by Levine et al.  and Rute-gard et al.  have shown that dysplasia may be localised to a small area within the colon, and may require extensive sampling beyond what is clinically or economically feasible, thus creating another hurdle in detecting the small foci of epithelial changes that may require surgical intervention.
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