First, etiology
There are many classification methods for colorectal polyps, which can be divided into solitary and multiple according to the number of polyps. However, the most widely used method in China and abroad is based on Morson's histological classification, which divides colorectal polyps into tumorous, hamartomatous, inflammatory, and hyperplastic (Table 1). The greatest advantage of this classification method is that it unifies colorectal polyps as adenomas, while other non-tumor polyps are collectively referred to as polyps. This classification can clearly distinguish the pathological nature of colorectal polyps and has greater guiding significance for treatment.
In China, adenomatous polyps are the most common, while some foreign reports indicate that proliferative polyps are the most common, with an incidence rate as high as 25% to 80%; the incidence rate of proliferative polyps in adults is at least 10 times higher than that of adenomas, but some scholars have found that the incidence rate of adenomas is 3 times higher than that of proliferative polyps during colonoscopy. According to research data, the occurrence of polyps may initially mainly occur in the distal colon, which can be verified from the fact that the left-sided polyps are often more than the right-sided ones in post-mortem examination materials. With the increase of age, polyps gradually develop from the left side to the right side.
2. Pathogenesis
The origin of adenomas is not yet fully understood. Initial studies have shown that deep crypt cells gradually develop into atypical hyperplasia as they migrate towards the surface. The normal crypt epithelium in the deep part is mainly expressed in sulfuric acid mucin, while the sulfuric acid mucin of adenomatous epithelium is more than that of sialic acid mucin. Recent studies have shown that blood group Ley antigen is diffusedly stained in many adenomas, while it is only seen in the deep crypts of normal mucosa with a positive reaction. The consistency of histochemical reactions between the adenoma epithelium and the deep crypt epithelium strongly supports the possibility that adenomas originate from the deep crypts. Another hypothesis for the origin of adenomas is eosinophilic epithelium, which is often located near the adenoma epithelium and shows a transitory phenomenon. Based on the sequential theory of colorectal adenoma → colorectal cancer, there is a sequential phenomenon from normal colorectal mucosa → tubular adenoma → tubular-villous adenoma → villous adenoma → colorectal cancer. It is believed that the occurrence of adenomas is initially mostly tubular adenomas, which gradually transform into tubular-villous adenomas and villous adenomas, and finally evolve into colorectal cancer. Canceration can also occur at the stages of tubular adenoma and tubular-villous adenoma.
Regardless of the location of the adenoma in the crypt, the proliferation of adenoma tissue is mainly towards the lumen to form an outward protruding mass. Although all adenomas start with a broad-based growth, as the adenoma grows larger, some adenomas become pedunculated or subpedunculated. In the descending colon and sigmoid colon, due to strong peristalsis and well-formed feces, it is easier to form pedunculated polyps at this site than at other parts of the intestine.
1. The histological characteristics of adenomatous polyps are not only the histological basis for the classification of adenomatous polyps, but also the basis for the diagnosis of adenomatous polyps. Adenomatous polyps are divided into tubular adenomas, villous adenomas, and mixed adenomas (i.e., tubular-villous adenomas). The histological sections of adenomatous polyps often show villous components, which are many delicate branches extending from the base of the lesion, with abundant mucus secretion visible. The core is composed of loose fibrous connective tissue, and the surface is covered with a single or multiple layered columnar epithelial cells. The amount of villous components is positively correlated with the malignancy of adenomas, so correctly evaluating the amount of villous components in adenomas is helpful for judging their potential for malignancy. It should be understood that the distribution of villous components in the same adenoma at different sites is not uniform, and the pathological diagnosis of the tissue obtained by biopsy at different sites can be different.
Histologically, tubular adenomas show early changes with dense arrangement of columnar cells in the crypts, with deep nuclear staining, a decrease or disappearance of goblet cells. As the lesion progresses, there is marked hyperplasia, elongation, branching, and expansion of the glands, with varying sizes of glandular cavities and hyperplasia of epithelial cells. They tend to protrude into the lumen, forming papillary structures; nuclear staining is intense, with a few nuclear mitoses, all located at the base, with a small amount of connective tissue stroma, small blood vessels, and inflammatory cell infiltration. Unlike tubular adenomas, villous adenomas usually originate from the surface epithelium of the large intestine, grow into the intestinal lumen, and form papillary protruding masses. Histologically, they show typical delicate villous structures, with villi often directly connecting to the mucosal surface, with a single or multilayered columnar epithelial cell layer on the surface, cells of unequal size and regular arrangement, nuclear staining intense at the base, with frequent nuclear mitoses, and the core of the villi is composed of fibrous connective tissue, containing an unequal amount of small blood vessels and inflammatory cell infiltration. Mixed adenomas show a tubular adenoma basis, mixed with villous adenoma components.
2, Canceration of colonic adenomas The canceration of adenomas is characterized by nuclear atypia, loss of polarity, increased nuclear-cytoplasmic ratio, and the appearance of a large number of nuclear mitotic figures. According to the depth of invasion, they can be divided into in situ cancer and invasive cancer, with the mucosal muscular layer as the boundary. The reason why in situ cancer does not metastasize is that there are no lymphatic vessels in the固有层 of the intestinal mucosa, so what is often referred to as adenoma canceration in clinical practice is usually for invasive cancer. The vast majority of colorectal cancers come from the canceration of colonic adenomas. The factors affecting adenoma canceration are mainly the degree of atypical hyperplasia, the size of adenomas, and the degree of villous component hyperplasia. Both the increase in adenoma size and the increase in villous components can exacerbate the degree of atypical hyperplasia. Adenomas with a diameter less than 1 cm rarely develop canceration. The canceration rate of tubular adenomas is relatively low, while the canceration rate of villous adenomas is about 5 times higher than that of tubular adenomas.
3, Familial multiple adenomatosis is a dominant autosomal hereditary disease. Under endoscopic examination, it is characterized by a large number of small adenomas, most of which are only a few millimeters in size, and a few are more than 1 cm. Morphologically, they are sessile half-circular, nodular elevations, with a smooth or lobulated surface, red in color and soft in texture, with or without pedicles, and dense ones showing a carpet-like structure. Histologically, they are basically the same as adenomas, with rare hyperplastic polyps, but a high incidence of cancer. Canceration will occur within 5 to 20 years, with an average age of 39 years, and multiple centers are more common.
4, Turcot syndrome is a syndrome characterized by multiple adenomas of the large intestine and malignant tumors of the central nervous system, which is an autosomal recessive inheritance, different from familial adenomatosis. The adenomas in this syndrome also show a distribution throughout the entire large intestine, but the number is less and scattered. There are rarely more than 100 before the age of 10, and more than 100 after the age of 10. The age of cancer development is early, generally below 20 years old, and it is more common in women.
5, Gardner syndrome consists of 4 lesions:
(1) Multiple adenomas in the large intestine.
(2) Osteomas (commonly found in the mandible, skull, and long bones).
(3) Desmoid tumors (commonly found in the mesentery after surgery).
(4) Dermatofibroma (including sebaceous cysts and epithelioid cysts, which are commonly found on the head, back, face, and limbs, and some may have dental malformations).
Some refer to the occurrence of all the above lesions as the complete type, while if two of the latter three lesions occur, it is considered an incomplete type, and if only one occurs, it is a simple type. It is generally believed that the heredity, age of onset, number, type, distribution, and cancer risk of colonic adenomas are the same as those in general familial adenomatous polyposis patients. Clinically, compared with familial adenomatous polyposis, the onset age of colonic adenomas is later, and they can appear after extraintestinal symptoms, with fewer adenomas.
6, Peutz-Jeghers syndrome, also known as hamartomatous polyposis, is an autosomal dominant genetic disorder, but only half of the cases have a family history in clinical practice. Its characteristics are: multiple gastrointestinal polyps; hereditary; the skin and mucous membranes of specific sites appear melanotic spots, which are often found around the lips and buccal mucosa, with clear edges and a diameter of about 1-2mm. The histological features are an increase in the number of melanocytes in the dermal basement membrane and melanin deposition. Most polyps exceed 100, and they are most common in the small intestine (64%-96%), followed by the large intestine (30%-50%). This disease can also lead to cancerous changes.