Until the late 1990s colorectal polyps were generally divided into two major subtypes: hyperplastic polyps and adenomatous polyps. Although a continuum between the two was proposed as early as 1970, it was generally held that these two subtypes were unique and had separate outcomes [1
]. Despite scattered objections over the next 30 years, the consensus opinion was that adenomatous polyps were the precursor of colorectal cancer while hyperplastic polyps were considered to be non-neoplastic hyperproliferations with little clinical significance [3
]. The historical highlights of this paradigm shift are of interest for this review.
Goldman initially proposed a morphological continuum between hyperplastic polyps and adenomatous polyps in 1970 and suggested that hyperplastic polyps may represent the precursor of some neoplastic adenomas [1
]. Throughout the following decades recurring suggestions of some sort of a relationship between hyperplastic polyps and colorectal cancer appeared [4
]. These included isolated reports of foci of cancers occurring within HPs and the association of a high risk of CRC in individuals with multiple HPs. Observational epidemiologic studies also reported substantial overlap in the risk factors for hyperplastic polyps, adenomas and colorectal cancer; smoking, alcohol, obesity, and low folate intake were associated with both HPs and adenomas whereas calcium intake, non-steroidal anti-inflammatory drugs and hormone replacement therapy were associated with protection for both [5
]. The presence of distal hyperplastic polyps at sigmoidoscopy was reported to be a modest risk factor for colorectal cancer and some putative biomarkers of colorectal cancer were strongly expressed in hyperplastic polyps [6
]. Despite these suggestions the prevailing view held that HPs were innocuous hyperproliferations until detailed histologic studies began to suggest otherwise.
In 1984, Urbanski described a polyp with mixed morphology, having features of both a hyperplastic polyp and adenomatous polyp that was adjacent to and appeared to give rise to a colonic adenocarcinoma [8
]. Around the same time, Jass and colleagues termed a similar lesion an “atypical metaplastic polyp.” In 1990, Longacre and Fenoglio- Preiser first used the term “serrated adenoma” to describe a serrated polyp that had rather uniform dysplastic cytology [9
]. The term “serrated” came from the observation of the saw tooth-shaped infoldings of the surface and crypt epithelium of these polyps that was similar to that of HPs. In this landmark report, the authors identified 110 serrated adenomas by retrospectively reviewing 18,000 polyps [9
]. In 2003, Torlakovic et al. suggested that serrated polyps be further divided into two groups, traditional serrated adenomas (TSA) for those initially described by Longacre et al [8
] and a new category termed the sessile serrated adenoma (SSA) for lesions that had serrated histology but did not have uniform cytologic dysplasia [10
]. In retrospect, it appears that SSAs had been previously grouped with HPs by most pathologists. SSAs could have subtle cytologic areas of atypia but if they had features of SSA with distinct foci of unequivocal dysplasia they were termed mixed polyps (MPs). In this review, we will use the terms HP, TSA, SSA and MP whenever the data allows and will use the term serrated polyp or serrated neoplasia to refer to the entire group.