Dental caries disease

385,940views

Dental caries disease

ETP Gastrointestinal

ETP Gastrointestinal

Anatomy of the gastrointestinal organs of the pelvis and perineum
Anatomy of the oral cavity (dentistry)
Anatomy of the pharynx and esophagus
Anatomy of the anterolateral abdominal wall
Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
Anatomy of the abdominal viscera: Esophagus and stomach
Anatomy of the abdominal viscera: Small intestine
Anatomy of the abdominal viscera: Large intestine
Anatomy of the abdominal viscera: Pancreas and spleen
Anatomy clinical correlates: Anterior and posterior abdominal wall
Abdominal quadrants, regions and planes
Development of the digestive system and body cavities
Development of the gastrointestinal system
Development of the teeth
Development of the tongue
Gallbladder histology
Esophagus histology
Stomach histology
Small intestine histology
Colon histology
Liver histology
Pancreas histology
Gastrointestinal system anatomy and physiology
Anatomy and physiology of the teeth
Liver anatomy and physiology
Escherichia coli
Salmonella (non-typhoidal)
Yersinia enterocolitica
Clostridium difficile (Pseudomembranous colitis)
Enterobacter
Salmonella typhi (typhoid fever)
Clostridium perfringens
Vibrio cholerae (Cholera)
Shigella
Norovirus
Bacillus cereus (Food poisoning)
Campylobacter jejuni
Bacteroides fragilis
Rotavirus
Enteric nervous system
Esophageal motility
Gastric motility
Gastrointestinal hormones
Chewing and swallowing
Carbohydrates and sugars
Fats and lipids
Proteins
Vitamins and minerals
Intestinal fluid balance
Pancreatic secretion
Bile secretion and enterohepatic circulation
Prebiotics and probiotics
Cleft lip and palate
Sialadenitis
Parotitis
Oral candidiasis
Aphthous ulcers
Ludwig angina
Warthin tumor
Oral cancer
Dental caries disease
Dental abscess
Gingivitis and periodontitis
Temporomandibular joint dysfunction
Nasal, oral and pharyngeal diseases: Pathology review
Esophageal disorders: Pathology review
Esophageal web
Esophagitis: Clinical
Barrett esophagus
Achalasia
Zenker diverticulum
Diffuse esophageal spasm
Esophageal cancer
Esophageal disorders: Clinical
Boerhaave syndrome
Plummer-Vinson syndrome
Tracheoesophageal fistula
Mallory-Weiss syndrome
GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review
Gastroesophageal reflux disease (GERD)
Peptic ulcer
Helicobacter pylori
Gastritis
Peptic ulcers and stomach cancer: Clinical
Pyloric stenosis
Zollinger-Ellison syndrome
Gastric dumping syndrome
Gastroparesis
Gastric cancer
Gastroenteritis
Small bowel bacterial overgrowth syndrome
Irritable bowel syndrome
Celiac disease
Small bowel ischemia and infarction
Tropical sprue
Short bowel syndrome (NORD)
Malabsorption syndromes: Pathology review
Malabsorption: Clinical
Zinc deficiency and protein-energy malnutrition: Pathology review
Whipple's disease
Appendicitis: Pathology review
Appendicitis
Appendicitis: Clinical
Lactose intolerance
Protein losing enteropathy
Microscopic colitis
Inflammatory bowel disease: Pathology review
Crohn disease
Ulcerative colitis
Inflammatory bowel disease: Clinical
Bowel obstruction
Bowel obstruction: Clinical
Volvulus
Familial adenomatous polyposis
Juvenile polyposis syndrome
Gardner syndrome
Colorectal polyps and cancer: Pathology review
Colorectal polyps
Colorectal cancer
Colorectal cancer: Clinical
Peutz-Jeghers syndrome
Diverticulosis and diverticulitis
Diverticular disease: Pathology review
Diverticular disease: Clinical
Intestinal adhesions
Ischemic colitis
Peritonitis
Pneumoperitoneum
Cyclic vomiting syndrome
Abdominal hernias
Femoral hernia
Inguinal hernia
Hernias: Clinical
Congenital gastrointestinal disorders: Pathology review
Congenital diaphragmatic hernia
Imperforate anus
Gastroschisis
Omphalocele
Meckel diverticulum
Intestinal atresia
Hirschsprung disease
Intestinal malrotation
Necrotizing enterocolitis
Intussusception
Anal conditions: Clinical
Anal fissure
Anal fistula
Hemorrhoid
Rectal prolapse
Carcinoid syndrome
Crigler-Najjar syndrome
Biliary atresia
Gilbert's syndrome
Dubin-Johnson syndrome
Rotor syndrome
Jaundice: Pathology review
Jaundice
Cirrhosis
Cirrhosis: Pathology review
Cirrhosis: Clinical
Portal hypertension
Hepatic encephalopathy
Hemochromatosis
Wilson disease
Budd-Chiari syndrome
Non-alcoholic fatty liver disease
Cholestatic liver disease
Hepatocellular adenoma
Alcohol-associated liver disease
Alpha 1-antitrypsin deficiency
Primary biliary cholangitis
Viral hepatitis
Hepatitis A and Hepatitis E virus
Hepatitis B and Hepatitis D virus
Viral hepatitis: Pathology review
Viral hepatitis: Clinical
Autoimmune hepatitis
Primary sclerosing cholangitis
Neonatal hepatitis
Reye syndrome
Benign liver tumors
Hepatocellular carcinoma
Gallbladder disorders: Pathology review
Gallstones
Gallstone ileus
Biliary colic
Acute cholecystitis
Ascending cholangitis
Chronic cholecystitis
Gallbladder carcinoma
Gallbladder disorders: Clinical
Cholangiocarcinoma
Pancreatic pseudocyst
Acute pancreatitis
Chronic pancreatitis
Pancreatitis: Clinical
Pancreatic cancer
Pancreatic neuroendocrine neoplasms
Pancreatitis: Pathology review
Abdominal trauma: Clinical
Gastrointestinal bleeding: Pathology review
Gastrointestinal bleeding: Clinical
Pediatric gastrointestinal bleeding: Clinical
Abdominal pain: Clinical
Disorders of carbohydrate metabolism: Pathology review
Glycogen storage disorders: Pathology review
Glycogen storage disease type I
Glycogen storage disease type II (NORD)
Environmental and chemical toxicities: Pathology review
Medication overdoses and toxicities: Pathology review
Laxatives and cathartics
Antidiarrheals
Acid reducing medications
Kwashiorkor
Galactosemia

Flashcards

Dental caries disease

0 of 4 complete

Transcript

Watch video only

Dental caries disease, also called tooth decay, refers to demineralization or weakening of the teeth, and the end result of caries disease is a caries lesion.

An advanced caries lesion can progress to a point where the tooth surface forms a cavitation or a hole, which is the physical evidence of tooth breakdown.

Let's start by building a model of a tooth and its surrounding structures.

In the mouth, the bone beneath the bottom row of teeth is the mandible, and the bone above the top row of teeth is the maxilla.

Both bones have an alveolus, or socket, for each tooth.

The socket is lined on the inside by a periodontal ligament.

Protecting the alveolus on the outside, is a layer of soft, supportive tissue called the gingiva, or gums, that sits on top of the bone and covers the root surface from the bone to the cementoenamel junction - where the cementum and enamel come together.

The tooth itself can be roughly divided into a few parts.

The first part is the root, and it sits within the alveolus.

The root is covered by cementum, which is a bonelike substance that the periodontal ligament’s fibers attach to.

Next, there’s the neck, which is the transition between the root portion covered by bone and the crown.

The crown is the visible part of the tooth that protrudes from the gingiva, and it’s covered in enamel, which has such a high mineral content that it’s the hardest substance in the human body.

When the teeth are developing, enamel is made before the tooth erupts into the mouth by a group of cells called the ameloblasts that die once the tooth erupts - meaning that the teeth lose the ability to make more enamel forever.

Now, let’s fill the tooth in from the inside out.

Blood vessels and nerves come from the jaw bones, and enter the center of the root through a narrow passage, called the apical foramen.

From there, they enter the soft center of the tooth, called the pulp, where they provide nutrition and sensation.

The outer wall of the pulp, contains odontoblasts which are cells that secrete a bonelike substance called dentin, which is filled with protein and minerals.

The odontoblasts have long processes, or arms, that lay within tiny tubules in the dentin - like an octopus sticking it’s arms through a block of cement.

These tubules are important for sensory nerves as well, which use them to travel through the dentin from the pulp to the dentin-enamel junction.

Finally, there’s saliva, which is secreted from several glands in the mouth.

Saliva contains bicarbonate ions, which helps to neutralize acid in the mouth, and glycoproteins like mucin which thickens the saliva.

Saliva also contains calcium and phosphate, which serve as replacement minerals, to help remineralization of the tooth surface.

So, when it comes to dental caries, there’s a tug-of-war between the pathogenic factors that promote demineralization of the tooth and protective factors that promote remineralization of the tooth.

Normally, there's a layer called the pellicle that covers the tooth, and bacteria in the mouth, like viridans group streptococci, settle on that pellicle layer.

These bacteria are called early colonizers, and they attach to the surfaces using bacterial surface proteins called adhesins.

Because they’re on the pellicle of the teeth, these bacteria come into contact with sucrose, a sugar found in various foods and drinks including table sugar.

Sucrose contains a glucose molecule bound to a fructose molecule.

So the bacteria use an enzyme called glucosyltransferase to cut the bond between them, use the fructose for energy, and add the glucose to a growing chain of glucose molecules called a glucan.

Glucans allow the bacteria to attach firmly to the surface of the tooth, and form dental plaque, which is a sticky collection of bacteria, proteins from saliva, and dead cells from the lining of the mouth.

Individual bacteria multiply and form many small microcolonies that coalesce, creating a layer of dental plaque - which is a type of biofilm.

Compared to a microcolony, the bacteria in a biofilm communicate with each other via chemical signaling and together they create a complex system where some bacteria work on tunneling between the microcolonies and to the surface in order to bring in a steady supply of food.

As an analogy, if bacteria were ants, then a microcolony would be a tiny group of ants, each doing it’s own thing, whereas a biofilm would be an ant farm with complex tunnels and rooms, and each ant carrying out a specialized task.

So typically, dental plaque can form on the surface of teeth, but if the pH of the local environment around the tooth surface remains above about 5.5, enamel will not demineralize.

One factor that tips the balance towards caries progression is having less bicarbonate-rich saliva, which can result from conditions like Sjogren syndrome, radiation treatment for cancer, gastric reflux, or as a side effect of a medication or recreational drugs.

A key factor that contributes to tooth demineralization is sugar.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "Managing Carious Lesions: Consensus Recommendations on Terminology" Advances in Dental Research (2016)
  5. "Comprehensive Mutational Analysis of Sucrose-Metabolizing Pathways in Streptococcus mutans Reveals Novel Roles for the Sucrose Phosphotransferase System Permease" Journal of Bacteriology (2012)
  6. "Dentin structure composition and mineralization" Frontiers in Bioscience (2011)