Oral cancer pathophysiology

Revision as of 12:49, 11 April 2019 by Natalie Harpenau (talk | contribs)
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to navigation Jump to search

Oral cancer Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Oral cancer from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Staging

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Oral cancer pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Oral cancer pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Oral cancer pathophysiology

CDC on Oral cancer pathophysiology

Oral cancer pathophysiology in the news

Blogs on Oral cancer pathophysiology

Directions to Hospitals Treating Oral cancer

Risk calculators and risk factors for Oral cancer pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2], Simrat Sarai, M.D. [3]; Grammar Reviewer: Natalie Harpenau, B.S.[4]

Overview

It is understood that oral cancers occur as a the result of carcinogen-metabolizing enzymes, alcohol, tobacco and genetic factors. Cytotoxic enzymes such as alcohol dehydrogenase result in the production of free radicals and hydroxylation of DNA base units. Alcohol dehydrogenase oxidizes ethanol to acetaldehyde which is cytotoxic in nature. Cigarette smoke has various carcinogens, which can lead to oral cancers. Low-reactive free radicals in cigarette smoke interact with redox-active metals in saliva.The development of oral cancer is the result of multiple genetic mutations. These mutations occur in tumor suppressor genes (TSGs) and oncogenes. Squamous cell carcinoma is the most common malignancy of the oral cavity. It typically has three gross morphological growth patterns, which are exophytic, ulcerative, and infiltrative. Microscopically, oral cancers are broadly based and invasive through papillary fronds. Oral cancer consists of highly differentiated squamous cells lacking frank cytologic criteria of malignancy with rare mitoses.The surface of the lesion is covered with compressed invaginating folds of keratin layers. A stroma-like inflammatory reaction and a blunt pushing margin may be seen.

Pathophysiology

It is understood that oral cancer occurs as a the result of carcinogen-metabolizing enzymes, alcohol, tobacco and genetic factors.

Carcinogen-metabolizing enzymes

Alcohol

Tobacco

Pathology of classical or conventional squamous cell carcinoma

Pathology of squamous cell carcinoma variants

  • Verrucous carcinoma
    • These tumors make up less than 5% of all oral cavity tumors.
    • They have a wart-like appearance and develop most often on the gums (gingiva), lining of the cheeks (buccal mucosa) and larynx.
    • Verrucous carcinomas are low grade, slow-growing and rarely spread.
    • They are associated with the chronic use of snuff or chewing tobacco.
  • Basaloid SCC
    • This is a rare but aggressive sub-type of squamous cell carcinoma.
    • It is more common in men older than 60 years old.
  • Papillary SCC
    • This is a rare sub-type of squamous cell carcinoma that grows outward from the surface of the epithelium (exophytic).
    • HPV infections may have a role in the development of this type of cancer.
  • Spindle cell carcinoma (SpCC)
    • This is an aggressive, rare variant of squamous cell carcinoma.
    • These tumors contain a mixture of conventional squamous cell carcinoma and spindle cells that resemble a sarcoma.
    • It is also known as sarcomatoid carcinoma, pseudosarcoma, carcinosarcoma, pleomorphic carcinoma, metaplastic carcinoma, collision tumor and Lane tumor.
  • Acantholytic SCC
  • Adenosquamous carcinoma
    • This is a very rare, aggressive type of squamous cell carcinoma.
    • It looks like classical squamous cell carcinoma but also has mucus-producing gland cells.
  • Lymphoepithelial carcinoma

Genetics

Tumor suppressor genes (TSGs)

Oncogenes

Gross Pathology

  • Squamous cell carcinoma is the most common malignancy of the oral cavity.
  • It typically has three gross morphological growth patterns, which are exophytic, ulcerative, and infiltrative.
  • The infiltrative and ulcerative are the growth patterns most commonly observed in the oral cavity.
  • The macroscopic appearance of oral cancer depends on the following:
    • Duration of the lesion
    • The amount of keratinization
    • The changes in the adjoining mucosa
    • A fully developed oral cavity lesion appears as an exophytic bulky lesion that is gray to grayish-red and has a rough, shaggy, or papillomatous surface
Gross pathology of oral SCC, source: By Luca Pastore, Maria Luisa Fiorella, Raffaele Fiorella, Lorenzo Lo Muzio - http://www.plosmedicine.org/article/showImageLarge.action?uri=info%3Adoi%2F10.1371%2Fjournal.pmed.0050212.g001, CC BY 2.5, https://commons.wikimedia.org/w/index.php?curid=15252632

Microscopic Pathology

  • Microscopically, oral cancers are broadly based and invasive through papillary fronds.
  • Oral cancer constitutes of highly-differentiated squamous cells lacking frank cytologic criteria of malignancy with rare mitoses.
  • The surface of the lesion is covered with compressed invaginating folds of keratin layers.
  • A stroma-like inflammatory reaction and a blunt pushing margin may be seen.
Microscopic picture of oral SCC, source: By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=486166

References

  1. Nagler R, Dayan D (2006). "The dual role of saliva in oral carcinogenesis". Oncology. 71 (1–2): 10–7. doi:10.1159/000100445. PMID 17344667.
  2. Peterson BR, Nelson BL (2013). "Nonkeratinizing undifferentiated nasopharyngeal carcinoma". Head Neck Pathol. 7 (1): 73–5. doi:10.1007/s12105-012-0401-4. PMC 3597164. PMID 23015393.
  3. Pathmanathan R, Prasad U, Chandrika G, Sadler R, Flynn K, Raab-Traub N (1995). "Undifferentiated, nonkeratinizing, and squamous cell carcinoma of the nasopharynx. Variants of Epstein-Barr virus-infected neoplasia". Am J Pathol. 146 (6): 1355–67. PMC 1870892. PMID 7778675.


Template:WH Template:WS