| FIGURE 9.1 |
The tooth and its supporting tissues. |
| FIGURE 9.2 |
Chronic periodontitis, with redness and swelling of the attached gingiva. |
| FIGURE 9.3 |
Periapical radiolucency, indicating resorption of bone and replacement by either inflammatory soft tissue or a cyst. |
| FIGURE 9.4 |
Periapical cyst, projecting into which are the roots of a molar with a large amalgam restoration. |
| FIGURE 9.5 |
Odontogenic keratocyst lining: a one-cell thick layer of intensely eosinophilic parakeratin on the surface of otherwise unremarkable benign stratified squamous epithelium. |
| FIGURE 9.6 |
Ameloblastoma: slices from this example show a partially cystic tumour with a solid tumour nodule within the cyst wall. |
| FIGURE 9.7 |
Angular cheilitis: inflammation and fissuring at the labial commissure is often a marker of chronic candidal infection. |
| FIGURE 9.8 |
Atrophic tongue: the rough filiform papillae of the dorsum of the tongue are replaced by flat mucosa; causes include chronic candidal infection, acute candidal infection after antibiotic treatment and various vitamin/mineral deficiencies. |
| FIGURE 9.9 |
Chronic erythematous candidosis: the pattern of inflammation on the hard palate mirroring the outline of the upper denture strongly suggests candidal infection. |
| FIGURE 9.10 |
Lichen planus: a lacy network of white striae on the buccal mucosa is usually symmetrical; other lesions of lichen planus include atrophy, erosions and white plaques (the last often on the tongue). |
| FIGURE 9.11 |
Leucoplakia: irregular white patch on the gum due to keratin production by the gingival squamous epithelium. |
| FIGURE 9.12 |
Lip cancer: squamous cell carcinoma presenting as a raised berry-like tumour on the mucosal aspect of the lower lip. |
| FIGURE 9.13 |
‘Early’ cancer of floor of mouth: squamous cell carcinoma presenting as a small non-healing ulcer in the floor of mouth; this is a ‘high-risk area’ for development of oral cancer particularly in smokers who drink alcoholic spirits. |
| FIGURE 9.14 |
Advanced cancer of tongue: squamous cell carcinoma typically presents as an indurated plaque-like mass in the ventral and lateral aspects of the tongue. |
| FIGURE 9.15 |
Mucocoele of lower lip: a bluish-grey cyst immediately below the labial mucosa caused by damage to a minor salivary gland duct and liberation of salivary juice into the loose connective tissues of the lip; traumatic injury to the lip by the teeth after a fall is typical. |
| FIGURE 9.16 |
Pleomorphic adenoma (on the left) separated from normal parotid tissue (on the right) by a thin capsule of collagenous tissue. Pleomorphic adenoma is a benign epithelial neoplasm of ‘mixed patterns’, here represented as fused glands (left) and spindle-celled cartilage-like tissue (centre). |
| FIGURE 9.17 |
In the most common variant of oesophageal atresia the upper oesophagus is a blind-ended tube, while the lower part is in communication with the trachea. |
| FIGURE 9.18 |
Hiatus hernia. (A) In a sliding hiatus hernia the proximal stomach is ‘pulled’ into the mediastinum. (B) In the ‘rolling’ variant, part of the fundus of the stomach protrudes through an abnormally large diaphragmatic orifice. |
| FIGURE 9.19 |
Oesophageal varices. Markedly dilated lower oesophageal veins in a patient dying from the effects of cirrhosis. |
| FIGURE 9.20 |
Biopsy of the squamocolumnar junction in an endoscopically obvious case of Barrett’s oesophagus. There is glandular epithelium in addition to the normal squamous mucosa. Intestinal metaplasia is indicated by the presence of goblet cells (arrow). |
| FIGURE 9.21 |
(A) Macroscopic view of an ulcerated, stenosing carcinoma of the lower oesophagus. (B) Squamous cell carcinoma with islands of neoplastic cells showing central keratin formation. |
| FIGURE 9.21 |
(C) Adenocarcinoma showing obvious gland formation. |
| FIGURE 9.22 |
FIGURE 9.22 Schematic representation of the microscopic structure of a gastric gland. The relative proportion of different cell types varies across the stomach. In the cardia, mucous cells predominate. The body (‘fundic’) glands contain the great bulk of secretory parietal and chief cells. In the antrum, gastrin-producing endocrine cells are prominent. |
| FIGURE 9.23 |
(A) Active chronic gastritis. Chronic inflammatory cell infiltration of the lamina propria with neutrophil movement into crypts (arrows). (B) Helicobacter pylori organisms in the surface mucus are better seen (arrow) in a Giemsa stain. |
| FIGURE 9.24 |
In chemical gastritis there is striking expansion of the proliferative ‘neck’ cell compartment of the pits (arrows). |
| FIGURE 9.25 |
Helicobacter pylori disease associations. The size of the arrow is a rough indication of the clinical magnitude of the association. MALToma = mucosal associated lymphoid tumours. |
| FIGURE 9.26 |
Whole mount histological preparation of a chronic gastric ulcer. There is a mucosal defect (small arrows) extending through the wall of the stomach. The muscle coat is destroyed, and the base of the ulcer is made up of fibrous tissue (large arrow). |
| FIGURE 9.27 |
Base of an ulcer in small bowel showing complete replacement of the muscle coat by fibrous tissue. The surface of the ulcer is arrowed. |
| FIGURE 9.28 |
(A) Duodenal biopsy pretreatment. Note shortened, slightly swollen villi, but no other abnormalities. (B) Jejunal biopsy following treatment; note the normal mucosa. |
| FIGURE 9.29 |
(A) Large ulcerated gastric carcinoma. (B) Infiltrative carcinoma showing marked thickening of the wall in the region of the antrum and pylorus (arrow). |
| FIGURE 9.30 |
(A) Intestinal-type gastric adenocarcinoma with well-formed glands. (B) Diffuse carcinoma made up of dissociated mucin-producing, signet-ring cells (arrow). |
| FIGURE 9.31 |
Gastric B-cell lymphoma of MALT origin (marginal zone lymphoma). (A) The characteristic lymphoepithelial lesion shows atypical lymphoid cells invading a gastric gland. The extent of this process is emphasized in (B), where the glands are highlighted by an immunohistochemical demonstration of cytokeratin. |
| FIGURE 9.32 |
Stromal tumour of the small intestine manifested as a well-demarcated nodule in the muscularis. |
| FIGURE 9.33 |
(A) A normal duodenal biopsy, showing well-formed villi. (B) In this case of coeliac disease the villous architecture is lost (‘subtotal villous atrophy’). (C) There is an increased complement of intraepithelial lymphocytes (arrows). |
| FIGURE 9.34 |
Haematoxylin and eosin staining of lymph node, showing fat and large numbers of pink swollen macrophages (arrows). |
| FIGURES 9.35 |
(TOP) AND 9.36 Low-power and higher-power views of duodenal biopsy, showing features described in the text. Arrows indicate dilated lymphatics in Figure 9.35, and macrophages in Figure 9.36. |
| FIGURE 9.37 |
Duodenal biopsy following broad-spectrum antibiotic therapy. Note the normal villus architecture, no dilated lymphatics, and normal inflammatory cell component in the lamina propria. |
| FIGURE 9.38 |
Pseudomembranous colitis. The colonic mucosal surface shows an erupting fibrinous ‘pseudomembrane’. |
| FIGURE 9.39 |
In this case of Crohn’s disease, a segment (arrow) in which the wall is thickened by inflammation and fibrosis obstructs the small intestine. |
| FIGURE 9.40 |
Low-power histology of Crohn’s disease. Fissures (small arrow) disrupt the mucosa, and lymphoid chronic inflammation extends through the wall to the subserosal fat (large arrows). |
| FIGURE 9.41 |
Inflammatory infiltration of the lamina propria and a granuloma (arrow) in a colonic biopsy from a patient with Crohn’s disease. |
| FIGURE 9.42 |
Specimen from a total colectomy performed for refractory ulcerative colitis. The mucosa is diffusely red and inflamed. Many inflammatory pseudopolyps are present. |
| FIGURE 9.43 |
(A) Diffuse mucosal inflammation and crypt shortening in ulcerative colitis. (B) A higher-power view of a crypt abscess (arrow). |
| FIGURE 9.44 |
Dark discoloration of ischaemic small intestine removed from an inguinal hernia. |
| FIGURE 9.45 |
(A) Sigmoid colon resected for diverticular disease. Multiple mucosal outpouchings are visible, some with impacted hard faeces (faecoliths; arrows). (B) A full-mount histological preparation showing a mucosal diverticulum extending through the muscle wall of the colon. |
| FIGURE 9.46 |
(A) Longitudinal section through resected bowel, showing two distinct adenomas. The lesion on the left shows the frond-like architecture of a villous adenoma, while that on the right shows the smoother lobulated outline of a tubular adenoma. (B) Low-power photomicrograph of a tubular adenoma, showing that the lesion is made up of distorted, elongated crypts. Even at this power the dark (‘hyperchromatic’) nuclei are visible. Note the raised stalk. This must be examined carefully for signs of early invasion. |
| FIGURE 9.47 |
(A) Rectum opened up to give a view of a stenosing cancer (arrow) at the rectosigmoid junction. Note the enlarged white nodes in the adjacent fat. Microscopy showed these to be largely replaced by metastatic carcinoma. (B) Transverse section through a total mesorectal excision for rectal carcinoma. The tumour presents as a raised plaque (large arrow). There is extension through the wall into perirectal fat. Margin involvement was confirmed microscopically in the region indicated by the small arrow. The patient was therefore referred for radiotherapy. |
| FIGURE 9.48 |
Invasive, moderately differentiated adenocarcinoma arising in large bowel mucosa. |
| FIGURE 9.49 |
Dukes’ staging system for large bowel carcinoma. Stage A tumours are confined to the bowel muscle wall. Stage B cancers show invasion completely through the muscle wall. Dukes’ stage C is defined by the presence of lymph node metastases, irrespective of the depth of invasion of the primary tumour. |
| FIGURE 9.50 |
Appendicectomy specimen. The tip of the appendix is swollen, haemorrhagic, and partly covered by a purulent white exudate, typical of acute appendicitis. |
