Pemicu 1

Vonny Verania Khuangga

405130005
ANATOMY OF UPPER
GASTROINTESTINAL TRACT
Quadrants of Abdomen
Anatomy of GIT
Mouth and Throat
Human Deciduous and Permanent
Teeth
 Vascular Supply And Lymphatic
Drainage Abdominal Oesophagus
• Arteries
– The abdominal oesophagus is supplied by oesophageal branches of
the left gastric artery and branches of inferior phrenica artery.
• Veins
– Veins drain via plexuses to the left gastric and upper short gastric
veins.
• Lymphatic drainage
– Lymphatic drainage occurs to the left gastric and left and right
paracardial nodes and from the posterior surface directly to the
uppermost para-aortic nodes.
• Innervation
– Parasympathetic system: r.anterior et posterior N.vagus
– Sympathetic system: n. splanchnici
HISTOLOGY OF UPPER
GASTROINTESTINAL TRACT
 Labium oris / Lips
• 3 layers:
– Pars cutanea/outer layer:
1. Stratified keratinizing squamous cell epithelium
2. Hair follicle with sebaceous and sweat glands
3. Orbicularis oris muscle
– Pars Intermedia
– Pars oral mucosa:
1. Stratified nonkeratinizing squamous cell epithelium
2. Tunica propria
a. Labialis glands
3. Orbicularis oris muscle
4. Labialis artery
5. Small chorium
 Pars cutanea
Stratified keratinizing squamous
cell epithelium

Hair follicle with sebaceous and

sweat glands

Orbicularis oris
muscle
Pars intermedia and pars oral mucosa
Stratified nonkeratinizing squamous cell
epithelium
Pars oral mucosa
Pars Intermedia
Tunica propria

Labialis glands
Orbicularis oris muscle
Labialis artery
Labium Oris
 Tongue/Lingua
• There are 3 forms of papillae:
– Circumvalata papillae:
A. Circumvalata papillae:
1. Secondary papillae
2. Taste bud
B. Ebneri glands
– Filiform papillae
– Fungiform papillae
– Foliata papillae
 Circumvalata
papillae

A. Circumvalata
papillae:
1. Secondary
papillae
2. Taste bud
B. Von Ebner glands
 Lingual Glands
• Parotid glands
1. Pars terminalis (serous)
2. Secretory duct
3. Intercalaris duct
4. Intelobular tissue
• Submandibular glands
1. Pars terminalis (mucoserous)
2. Secretory duct
3. Excretory duct
• Sublingual glands
1. Pars terminalis (mucoserous)
2. Secretory duct
 Parotid Glands

1. Pars terminalis (serous)

2. Secretory duct
3. Intercalaris duct
4. Intelobular tissue
Submandibular
glands

1. Pars terminalis
(mucoserous)
2. Secretory duct
3. Excretory duct
Sublingual glands

1. Pars terminalis
(mucoserous)
2. Secretory duct
 Teeth

1. Dental cement
a. Sharpey’s fiber
2. Tomes granular layer
3. Dentine + dentine
canals
Oesophagus
A. Tunica mucosae
1. Stratified nonkeratinizing
squamous cell epithelium
2. T. propria
3. T. muscularis mucosae
B. Tunica submucosae
4. Oesephagus glands
5. Excretory duct
C. Tunica muscularis
6. T. Musc. Circular
7. T.Musc. Longitudinal
D. Tunica adventitia
Fundus

A. T. Mucosae
1. Columnar surface
epithelium
2. Gastric foveolae
3. T.propria+fundus
glands
4. Elastic membran
5. T. M. Mucosae
B. T. Submucosae
 Pyloric

A. T. Mucosae
1. Columnar surface
epithelium
2. Gastric foveolae (wide and
deep)
3. T.propria+pyloric glands
4. Elastic membran
5. T. M. Mucosae
B. T. Submucosae
C. T.muscularis
 Duodenum

A. T. mucosae
1. Vili
2. Columnar surface
epithelium+goblet
cell
3. Crypt/of lieberkuhn
4. T.M. Mucosae
B. T. submucosae
C. T.muscularis
 Jejunum

A. T. mucosae
1. Vili
2. Columnar surface
epithelium+goblet cell
3. Crypt/of lieberkuhn
4. T.M. Mucosae
B. T. submucosae
5. Kerckring’s folds
(T/mucosae+T.submucosae)
C. T.muscularis
BIOCHEMISTRY OF UPPER
GASTROINTESTINAL TRACT
 The digestive enzymes
Digestive enzymes are enzymes which help break down food
substances into forms that can be absorbed and assimilated by the
body.
Digestive enzymes are normally secreted :
1) in the mouth (as part of the saliva),
2) by the stomach
3) released into the small intestines from the liver and pancreas.
The major enzymes are:
• Amylase, also called ptyalin, is an enzyme that aids the breakdown
of starches. It is secreted in the saliva and the pancreatic juices.
• Mycozyme is an enzyme that also digests starches.
• Lipase, secreted by the pancreas, refers to any of several enzymes
that increase the breakdown of fats (lipids).
 Digestive Enzymes
ENZYME SOURCE SUBTRATES PRODUCTS
SALIVA
Salivary amylase Salivary glands. Starches. Maltose, maltotriose, α-
dextrins.
Lingual lipase Lingual glands. Triglycerides (fats & oils) Fatty acids &
and other lipids. diglycerides.
GASTRIC JUICE
Pepsin Stomach chief cells. Proteins. Peptides.
Gastric lipase Stomach chief cells. Triglycerides. Fatty acids &
monoglycerides.
PANCREATIC JUICE
Pancreatic amylase Pancreatic acinar cells. Starches. Maltose, maltotriose, α-
dextrins.
Trypsin Pancreatic acinar cells. Proteins. Peptides.
Chymotrypsin Pancreatic acinar cells. Proteins. Peptides.
Elastase Pancreatic acinar cells. Proteins. Peptides.
 ENZYME SOURCE SUBSTRATES PRODUCTS
Carboxypeptidase. Pancreatic acinar cells. Amino acid at carboxyl Amino acids & peptides.
end peptides.
Pancreatic lipase Pancreatic acinar cells. Triglycerides that have Fatty acids &
been emulsified by bile monoglycerides.
salts.
Ribonuclease Pancreatic acinar cells. RNA. Nucleotides.
Deoxyribonuclease Pancreatic acinar cells. DNA. Nucleotides.
BRUSH BORDERS
α-Dextrinase Small intestine. α-Dextrins. Glucose.
Maltase Small intestine. Maltose. Glucose.
Sucrase Small intestine. Sucrose. Glucose & fructose.
Lactase Small intestine. Lactose. Glucose & galactose.
Enterokinase Small intestine. Trypsinogen. Trypsin.
Aminopeptidase Small intestine. Amino acid at amino end Amino acids & peptides.
of peptides.
Dipeptidase Small intestine. Dipeptidases. Amino acids.
Nucleosidases & Small intestine. Nucleotides. Nitrogenous bases,
phosphatases pentoses & phosphates.
 Organ
Hormon Sasaran Fungsi

Motility control, support absorption

Exocrine glands
and digestion process
Stomach Gastrin and smooth
muscle

Sekretin,
Digestive tract, Motility control, support absorption
kolesistokinin,
Duodenum pancreas, liver, and digestion process
gastric inhibitor,
vesica velea
peptide

Bones, Soft
Liver Somatomedin Growth trigger
Tissues

-Insulin (B cell) Almost all cell

Supporting absorption, using and
saving nutrients by cell for maintain
nutrient level after absorption phase
Pancreas; -Glukagon Almost all cell
Inhibit digestion and absorption
langerhans (sel A)
island
-Somastatine Digestive system
Inhibit all pancreatic hormones
(sel D) Pancreatic cell;
secretion
langerhans island
PHYSIOLOGY OF UPPER
GASTROINTESTINAL TRACT
Physiology of Gastrointestinal

Picture : process of swallowing

 Basic Digestive Processes
1. Motility
2. Secretion
3. Digestion
4. Absorption
 *Motility
• MOTILITY The term motility refers to the
muscular contractions that mix and move
forward the contents of the digestive tract.
• maintains a constant low level of contraction
known as tone
• Two basic types of phasic digestive motility are
superimposedn on this ongoing tonic activity:
– propulsive movements
– mixing movements.
• Propulsive movements propel or push the
contents forward through the digestive tract
• Mixing movements serve a twofold function.
– First, by mixing food with the digestive juices, these
movements promote digestion of the food
– Second, they facilitate absorption by exposing all parts of
the intestinal contents to the absorbing surfaces of the
digestive tract
 *Secretion
• Exocrine glands
• On appropriate neural or hormonal
stimulation, the secretions are released into
the digestive tract lumen.
• Normally, the digestive secretions are
reabsorbed in one form or another back into
the blood after their participation in digestion.
 *Digestion
• Humans consume three diff erent biochemical
categories of energy-rich foodstuffs:
carbohydrates, proteins, and fats.
• Th e term digestion refers to the biochemical
breakdown of the structurally complex
foodstuff s of the diet into smaller, absorbable
units by the enzymes produced within the
digestive system as follows:
• The simplest carbohydrates are the simple sugars
or monosaccharides (“one-sugar” molecules),
such as glucose, fructose, and galactose
• Most ingested carbohydrate is in the form of
polysaccharides (“many-sugar” molecules)
• Starch derived from plant sources
• Meat contains glycogen
• Cellulose, another dietary polysaccharide, found
in plant walls, (represents the indigestible fiber or
“bulk” of our diets).
• Proteins consist of various combinations of amino
acids held together by peptide bonds
• Digestion  proteins are degraded primarily into their
constituent amino acids as well as a few small
polypeptides

• Most dietary fats are in the form of triglycerides,

which are neutral fats, each consisting of a glycerol
with three fatty acid molecules attached (tri means
“three”)
• Triglycerides  monoglycerides + free fatty acids
 *Absorption
• Through the process of absorption, the small
absorbable units that result from digestion,
along with water, vitamins, and electrolytes,
are transferred from the digestive tract lumen
into the blood or lymph
• Four factors are involved in regulating
digestive system function
1. Autonomous smooth muscle function
2. Intrinsic nerve plexuses
3. Extrinsic nerves
4. Gastrointestinal hormones
 Mouth
• Motility
Food enters the digestive system through the mouth,
where it’s chewed and mixed with saliva to facilitate
swallowing
• Secretion
Enzyme amylase begins the digestion of carbohydrates
• Digestion
polysaccharides ---------amylase salivary----------->
disaccharides maltose
• Absorption  NO Absorption
 A. Despopoulos et al - Color Atlas of Physiology 5th Ed Thieme 2003

Reflex stimulation of saliva secretion occurs in the larger salivary glands. Salivant
stimuli: smell, taste, tactile stimulation of the buccal mucosa, etc.
Conditioned reflexes: ie. thinking about food.
Sleep and dehydration inhibit saliva secretion.
Stimulated via the sympathetic and parasympathetic nervous systems
 Digestive Activities in the Mouth
STRUCTURE ACTIVITY RESULT
Cheeks & lips Keeps food between teeth. Food uniformly chewed during mastication
Salivary glands Secrete saliva Lining of mouth and pharynx moistened &
lubricated. Saliva softens, moistens, and
dissolves food & cleanses mouth & teeth.
Salivary amylase splits starch into smaller
fragments.
Tongue
Taste buds Serve as receptors for Secretion of saliva stimulated by nerve
gustation and presence impulses from taste buds to salivary nuclei in
food in the mouth. the brain stem to salivary glands.
Lingual glands Secrete lingual lipase Triglycerides broken down into fatty acids
and diglycerides.
Teeth Cut, tear, and pulverize Solid foods reduced to smaller particles for
food. swallowing.
 Pharynx and Esophagus
• Motility
Following chewing, the tongue propels the bolus
of foods to the rear of the throat, which initiates
the swallowing reflex
• Secretion
The esophageal secretion, mucus is the
protective
• Digestion  NO Digestion
• Absorption  NO Absorption
 A. Despopoulos et al - Color Atlas of Physiology 5th Ed Thieme 2003

Physiology - Deglutition

1. The tongue pushes a bolus of food into the throat

2. The nasopharynx is reflexively blocked
3. Respiration is inhibited, the vocal chords close and the epiglottis seals off the trachea
4. The upper esophageal sphincter opens
5. A peristaltic wave forces the bolus into the stomach

If the bolus gets stuck, stretching of the affected area triggers a secondary peristaltic wave
 Digestive Activities in the Pharynx &
Esophagus
STRUCTURE ACTIVITY RESULT
Pharynx Pharyngeal stage of Moves bolus from oropharynx to
deglutition. laryngopharynx and into esophagus;
closes air passageways.
Esophagus Relaxation of UES. Permits entry of bolus from
laryngopharynx into esophagus.
Esophageal stage of Pushes bolus down esophagus.
deglutition (peristalsis).
Relaxation of LES. Permits entry bolus into stomach.
Secretion of mucus. Lubricate esophagus for smooth
passage of bolus.
DYSPHAGIA
 Definiton
• Sensation of “sticking” or obstruction of the
passage of food through the mouth, pharynx, or
esophagus ~ swallowing difficulty
– Aphagia  complete esophageal obstruction
– Odynophagia  painful swallowing
– Globus pharyngeus  sensation of a lump lodged in
the throat
– Misdirection of food  nasal regurgitation and
laryngeal and pulmonary aspiration during
swallowing (oropharyngeal dysphagia)
– Phagophobia  fear of swallowing, and refusal to
swallow may occur in hysteria, rabies, tetanus, and
pharyngeal paralysis due to fear of aspiration
 Etiology
• Central nervous system disorders
– GBS, brain tumors, alzheimer, stroke, parkinson, multiple sclerosis
• Muscular disorders
– muscular dystrophies, spinal muscular atrophy, polymyositis, dermatomyositis
• Neuropathic disorders
• Endocrine disorders
– Hyperthyroidism, hypothyroidism, vitamin B12 deficiency
• Pharmacologic causes
– Corticosteroids, aminoglycosides, anticholinergic drugs, NSAID, antibiotics
(doxycycline, tetracycline, clindamycin, trimethoprim-sulfamethoxazole),
antihistamines, ACEI
• Surgical causes
– Laryngectomy, pharyngectomy, esophagectomy reconstructed by gastric pull-
up, head and neck surgery (oral cavity cancer)
• Tracheostomy
 Epidemiology
• Prevalence of dysphagia is around 16-22%
• 2nd most indication for endoscope in USA
• 5-8% in more than 50 years old people
• 16% in elderly
• 60% oropharynx dysphagia in householder/
nursing care
 Pathophysiology
• Based on anatomic site of involvement  oral,
pharyngeal, and esophageal dysphagia

• Normal transport of an ingested bolus depends on the

size of the ingested bolus & size of the lumen, force of
peristaltic contraction, deglutitive inhibition
– Dysphagia caused by a large bolus or narrow lumen 
mechanical dysphagia
– Dysphagia caused by weakness of peristaltic contractions
or to impaired deglutitive inhibition causing non
peristaltic contraction and impaired spincter relaxation 
motor dysphagia
 Klasifikasi
Dysphagia may be divided into:
1. Oral Pharyngeal Dysphagia
Associated with poor bolus formation and control.
Pharyngeal stasis leads to nasal regurgitation and laryngeal
aspiration during the process of swallowing.

2. Esophageal Dysphagia
In an adult, the esophageal lumen can distend up to 4 cm in
diameter. When the esophagus cannot dilate beyond 2.5 cm in
diameter, dysphagia to normal solid food can occur. Dysphagia is
always present when the esophagus cannot distend beyond 1.3 cm.
Results abnormalites in peristaltis and deglutitive inhibition due to
diseases of the esophageal striated or smooth muscles.
 Signs and Symptoms
Signs and symptoms of oral or
pharyngeal dysphagia include the
following:
• Coughing or choking with
swallowing
• Difficulty initiating swallowing
• Food sticking in the throat
• Sialorrhea
• Unexplained weight loss
• Change in dietary habits
• Recurrent pneumonia
• Change in voice or speech
(wet voice)
• Nasal regurgitation
Signs and symptoms of esophageal
dysphagia include the following:
• Sensation of food sticking in
the chest or throat
• Change in dietary habits
• Recurrent pneumonia
• Symptoms of
gastroesophageal reflux
disease (GERD), including
heartburn, belching, sour
regurgitation, and water
brash
 Diagnosis
• X-ray with a contrast material (barium X-ray).You drink a barium solution that coats your
esophagus, allowing it to show up better on X-rays. Your doctor can then see changes in the
shape of your esophagus and can assess the muscular activity. Your doctor may also have
you swallow solid food or a pill coated with barium to watch the muscles in your throat as
you swallow or to look for blockages in your esophagus that the liquid barium solution may
not identify.
• Dynamic swallowing study. You swallow barium-coated foods of different consistencies. This
test provides an image of these foods as they travel through your mouth and down your
throat. The images may show problems in the coordination of your mouth and throat
muscles when you swallow and determine whether food is going into your breathing tube.
• A visual examination of your esophagus (endoscopy). A thin, flexible lighted instrument
(endoscope) is passed down your throat so your doctor can see your esophagus.
• Fiber-optic endoscopic swallowing evaluation (FEES).Your may examine your throat with
special camera (endoscope) and lighted tube as you try to swallow.
• Esophageal muscle test (manometry). In manometry, a small tube is inserted into your
esophagus and connected to a pressure recorder to measure the muscle contractions of your
esophagus as you swallow.
• Imaging scans. These may include a CT scan, which combines a series of X-ray views and
computer processing to create cross-sectional images of your body's bones and soft tissues;
an MRI scan, which uses a magnetic field and radio waves to create detailed images of organs
and tissues; or a positron emission tomography (PET) scan, which uses a radioactive drug
(tracer) to show how your tissues and organs are functioning.
 Treatments
• Medications used in the treatment of dysphagia include the
following:
• Botulinum toxin type A (BoNT-A): Injected endoscopically into the
gastroesophageal sphincter and upper esophagus to decrease tone;
this can be very useful in cricopharyngeal spasms causing dysphagia
• Diltiazem: Can aid in esophageal contractions and motility,
especially in the disorder known as the nutcracker esophagus
• Glucagon: Used in disimpacting esophageal bodies; diazepam also is
sometimes used; no major study has proved the effectiveness of
either drug
• Cystine-depleting therapy with cysteamine: Treatment of choice for
patients with dysphagia due to pretransplantation or
posttransplantation cystinosis
• Nitrates: Including isosorbide dinitrate, which can especially be
recommended in achalasia
• Dietary modification is the key component in the general treatment program of dysphagia. A
diet of pureed foods is recommended for patients who have difficulties with the oral
preparatory phase of swallowing, who pocket food in the buccal recesses, or who have
significant pharyngeal retention of chewed solid foods.
• As patients' swallowing function improves, their dysphagic diet may be advanced to the next
level of soft and semisolid foods with regular consistencies. Recommend to patients that they
alternate bites with sips, bite or sip size, and the number of swallows per size.
• Diets for patients with dysphagia include the following:
• Dysphagia diet 1: Thin liquids (eg, fruit juice, coffee, tea)
• Dysphagia diet 2: Nectar-thick liquids (eg, cream soup, tomato juice)
• Dysphagia diet 3: Honey-thick liquids (ie, liquids that are thickened to a honey consistency)
• Dysphagia diet 4: Pudding-thick liquids/foods (eg, mashed bananas, cooked cereals, purees)
• Dysphagia diet 5: Mechanical soft foods (eg, meat loaf, baked beans, casseroles)
• Dysphagia diet 6: Chewy foods (eg, pizza, cheese, bagels)
• Dysphagia diet 7: Foods that fall apart (eg, bread, rice, muffins)
• Dysphagia diet 8: Mixed textures
 Complications
• Malnutrition, weight loss and dehydration.
Dysphagia can make it difficult to take in
adequate nourishment and fluids.
• Respiratory problems. Food or liquid entering
your airway when you try to swallow can
cause respiratory problems, such as
pneumonia or upper respiratory infections.
 Prognosis
• Stroke patients recover swallowing function gradually, and therapeutic
interventions for dysphagia generally are successful. At 6 months after stroke, 87%
of patients had returned to their prestroke diet.
• In conditions in which recovery is possible (eg, TBI, stroke), the normalization of
swallowing may take from 3 weeks to approximately 6 months or longer. Many
patients tolerate normal oral caloric intake 9 months after a stroke, while some
may require partial or nonoral caloric supplementation. In patients who have
sustained a stroke, continued swallowing dysfunction after 6 months is associated
with increased morbidity and mortality.
• In static or progressive conditions (eg, neuromuscular disorders, postpolio
syndrome), periodic evaluation of swallowing disorders is mandatory, especially
with the onset of new symptoms, and the appropriate strategies (the use of
nonoral feeding techniques or new compensatory mechanisms) should be
considered.
• Aspiration pneumonia
• Malnutrition
• Dehidration
 Prevention
• Although swallowing difficulties can't be
prevented, you can reduce your risk of
occasional difficulty swallowing by eating
slowly and chewing your food well. Early
detection and effective treatment of GERD can
lower your risk of developing dysphagia
associated with an esophageal stricture.
PROSEDUR DIAGNOSTIK
 Bercak putih
• White lesions of the oral mucosa are a
multifactorial group of disorders,the color of
which is produced by the scattering of the
light through an altered epithelial surface. The
diagnosis and differential diagnosis of oral
white lesions should be made on the basis of
the medical history, clinical features, and
laboratory tests.
 Tongue ulcers
• Tongue ulcers appear as light colored inflamed
areas on the tongue. In other cases, tongue
ulcers seem sunk on the tongue's surface and
are very sensitive to cold or hot substances.
There are several health issues that lead to
tongue ulcers.
 Karies Gigi
• Diagnosis ditegakkan berdasarkan
riwayat kesehatan, pemeriksaan klinis,
dan pemeriksaan radiologis. Paradigma
lama yang hanya mendeteksi ada
tidaknya kavitas, harus diubah, dengan
mendeteksi adanya kuman S. Mutans,
dan menentukan tingkat risiko
terjadinya karies. Berdasarkan
karakteristik karies gigi, maka diagnosis
ditegakkan dengan melihat lokalisasi
kavitas apakah terletak di permukaan
pits dan fissures, permukaan halus gigi
dan akar gigi.
Diagnosis karies pada pits dan
fissures
• Menegakkan diagnosis karies pada
permukaan pits dan fissures tidak mudah,
karena sulitnya membedakan karies yang
terjadi dengan anatomi normal gigi,
karena perubahan warna tidak selalu
berarti sebuah kavitas. Untuk menetapkan
diagnosis pits dan fissures ada tiga faktor
yang harus diperhatikan, yaitu dasar
kavitas pits atau fissures lunak, perubahan
warna di sekitar permukaan pits atau
fissures menjadi lebih putih sebagai tanda
adanya remineralisasi email & permukaan
email yg lunak pada pits atau fissures
dapat terangkat pada waktu dibersihkan.
Diagnosis karies di permukaan
halus gigi Diagnosis karies akar
• Karies pada permukaan halus gigi di sisi • Permukaan akar gigi yang
bukal/labial atau lingual dengan mudah terbuka biasanya terjadi karena retraksi
dapat dideteksi, namun karies yang gingiva, sehingga rentan untuk terjadi
letaknya proksimal sulit dideteksi karies. Perubahan warna pada
secara visual atau pada pemeriksaan permukaan akar gigi yang terbuka
klinis, sehingga diperlukan pemeriksaan merupakan tanda yang sering
radiologis. Hasil pemeriksaan radiologi ditemukan dan biasanya disertai proses
dengan foto bite-wing atau panoramik remineralisasi. Warna yang terjadi
dapat menunjukkan gambaran mulai dari coklat sampai hitam.
radiolusen pada sisi proksimal, di bawah Semakin gelap perubahan warna yang
titik kontak akibat proses terjadi berarti proses remineralisasi
demineralisasi. Penilaian klinis yang semakin kuat. Sebaliknya bila karies
tepat harus dilakukan untuk menilai akar aktif, ditandai dengan dasar kavitas
apakah sudah terbentuk kavitas atau lunak dan hanya menunjukkan sedikit
belum, sehingga preparasi dan restorasi perubahan warna.
dapat dilakukan.
 Gingivitis
• Gingivitis biasanya terjadi pada anak saat gigi erupsi gigi sulung
maupun gigi tetap dan menyebabkan rasa sakit. Pada anak usia 6-7
tahun saat gigi permanen sedang erupsi, gingival marginnya tidak
terlindungi oleh kontur mahkota gigi. Keadaan ini menyebabkan sisa
makanan masuk ke dalam gingiva dan menyebabkan peradangan.
Terjadi inflamasi gingiva tanpa adanya kehilangan tulang atau
perlekatan jaringan ikat. Tanda pertama dari inflamasi adanya
hiperamie, warna gingiva berubah dari merah muda menjadi merah
tua, disebabkan dilatasi kapiler, sehingga jaringan lunak karena
banyak mengandung darah. Gingiva menjadi besar (membengkak),
licin, berkilat dan keras, perdarahan gingiva spontan atau bila
dilakukan probing, gingiva sensitif, gatal-gatal dan terbentuknya
saku periodontal akibat rusaknya jaringan kolagen. Muncul
perlahan-lahan dalam jangka lama dan tidak terasa nyeri kecuali
ada komplikasi dengan keadaan akut. Bila peradangan ini dibiarkan
dapat berlanjut menjadi periodontitis
 Halitosis
• Oral malodor (bad breath) can be measured in a number of ways, including studies
using organoleptic intensity and organoleptic hedonic indices and instruments that
quantitate the amount of volatile compounds or bacterial enzymes that contribute
to the production of odiferous compounds.
• Organoleptic measurements or the use of one’s nose to smell and rank the
intensity of odors are considered the criterion standard for the measurement of
malodor. However, these tend to be subjective and are uncomfortable for both the
examiner and the test subject. Either a 5-point or a 10-point scale can be used and,
usually, 2 separate judges evaluate the degree of halitosis (bad breath). The
intensity of halitosis (bad breath) is based on the Rosenberg scale, which rates
odor intensity and is as follows:
• 0 - Odor cannot be detected
• 1 - Questionable malodor, barely detectable
• 2 - Slight malodor, exceeds the threshold of malodor recognition
• 3 - Malodor is definitely detected
• 4 - Strong malodor
• 5 - Very strong malodor
 Dry mouth
• To determine if you have dry mouth, your doctor or
dentist likely will examine your mouth and review your
medical history and all medications you're taking,
including over-the-counter medications.
• Sometimes you may need blood tests, imaging scans of
your salivary glands or tests that measure how much
saliva you produce to identify the cause of your dry
mouth. If your doctor suspects your dry mouth is
caused by Sjogren's syndrome, a small sample of cells
(biopsy) taken from salivary glands in your lip may be
sent for testing.
 Cracked lips
• To diagnose your condition, your doctor or
licensed health care practitioner will ask you
several questions related to your cracked lips
including:
• How long have you experienced cracked lips?
• Do your cracked lips worsen when you use
certain lip products, such as lipstick?
• Are you experiencing any other symptoms along
with your cracked lips?
• Are your cracked lips becoming worse or more
frequent?
 Cleft lip
• Preoperative tests
– Blood tests - CBC count
– Chromosomal studies, if indicated (eg, chromosome
band 22q11.2 deletion)
– Cardiac evaluation, including echocardiography, if cleft
is associated with cardiac anomalies
• Most cases of cleft lip and cleft palate are noticed
right away at birth and don't require special tests
for diagnosis. Increasingly, cleft lip and cleft
palate are seen on ultrasound before the baby is
born.
 Aphthous
• Diagnosis of recurrent aphthous stomatitis (RAS) is based on history and clinical features. No
specific tests are available; however, to exclude systemic disorders discussed above, the
following tests may be helpful:
• Complete blood cell count
• Hemoglobin test
• White blood cell count with differential
• Red blood cell indices
• Iron studies (usually an assay of serum ferritin levels)
• Red blood cell folate assay
• Serum vitamin B-12 measurements
• Serum antiendomysium antibody and transglutaminase assay (positive in celiac disease)
• Rarely, biopsy may be indicated in cases in which a different diagnosis is suspected.
Occasionally, for example, pemphigus may mimic RAS. Occasional RAS can mimic a neoplasm,
necrotizing sialometaplasia, or TUGSE (traumatic ulcerative granuloma with stromal
eosinophilia).
 Lymphadenopathy
• The laboratory evaluation of lymphadenopathy must be directed by the history
and physical examination and is based on the size and other characteristics of the
nodes and the overall clinical assessment of the patient. When a laboratory
evaluation is indicated, it must be driven by the clinical evaluation.
• The following studies should be considered for chronic lymphadenopathy (>3 wk):
• CBC count, including a careful evaluation of the peripheral blood smear
• Lactate dehydrogenase (LDH) and uric acid
• Chest radiography
• B henselae (catscratch) serology if exposed to a cat
• Tuberculosis skin test (TST) and interferon-gamma release assay (eg, Quantiferon
Gold)
• Evaluation of hepatic and renal function and a urine analysis are useful in
identifying underlying systemic disorders that may be associated with
lymphadenopathy. When evaluating specific regional adenopathy, lymph node
aspirate for culture may be important if lymphadenitis is clinically suspected.
• Titers for specific microorganisms may be indicated, particularly if generalized
adenopathy is present. These may include Epstein-Barr virus, cytomegalovirus
(CMV), Toxoplasma species, and human immunodeficiency virus (HIV).
 Oral leukoplakia
• Oral leukoplakia is a white patch or plaque
that cannot be rubbed off, cannot be
characterized clinically or histologically as any
other condition, and is not associated with
any physical or chemical causative agent
except tobacco.
 Aphthous
• Recurrent aphthous stomatitis (RAS) is a
common condition, restricted to the mouth,
that typically starts in childhood or
adolescence as recurrent small, round, or
ovoid ulcers with circumscribed margins,
erythematous haloes, and yellow or gray
floors.
 Mucosal candidiasis
• Candidosis (candidiasis) describes a group of
yeast-like fungal infections involving the skin and
mucous membranes, including the mouth.
Infection is caused by Candida species, typically,
Candida albicans. C albicans is ubiquitous and is
found mainly on oral or genital mucosae; it may
also be transmissible between consorts. Candidal
infection is less common and typically occurs
where the local ecology is disturbed, or where
there is an immune defect.
 Odynophagia
• Odynophagia: Pain on swallowing food and
fluids, a symptom often due to disease of the
esophagus.
 Reflux esophagitis
• Reflux esophagitis is an esophageal mucosal
injury that occurs secondary to retrograde flux
of gastric contents into the esophagus.
Clinically, this is referred to as
gastroesophageal reflux disease (GERD).
Typically, the reflux disease involves the distal
8-10 cm of the esophagus and the
gastroesophageal junction. The disease is
patchy in distribution.
 Ludwig’s angina
• Ludwig's angina is an infection of the floor of
the mouth under the tongue. It is due to
bacteria. Ludwig's angina is a type of skin
infection that occurs on the floor of the
mouth, under the tongue. It often develops
after an infection of the roots of the teeth
(such as tooth abscess) or a mouth injury.
• This condition is uncommon in children.
 Glossitis
• Glossitis is a problem in which the tongue is
swollen and changes color, often making the
surface of the tongue appear smooth.
Geographic tongue is a type of glossitis.
 Esophageal atresia
• Esophageal atresia is a disorder of the
digestive system in which the esophagus does
not develop properly. The esophagus is the
tube that normally carries food from the
mouth to the stomach
 Achalasia
• Achalasia is a disorder of the esophagus, the
tube that carries food from the mouth to the
stomach. This condition affects the ability of
the esophagus to move food into the stomach.
 Mouth ulcers
• Mouth ulcers are painful round or oval sores that
form in the mouth, most often on the inside of
the cheeks or lips.
• They're usually white, red, yellow or grey in
colour and are inflamed (red and swollen) around
the edge.
• Although mouth ulcers can be uncomfortable,
especially when you eat, drink or brush your
teeth, they are usually harmless.
• Most mouth ulcers will clear up by themselves
within a week or two.
 Parotitis
• Salivary gland infections affect the glands that
produce saliva (spit). The infection may be due
to bacteria or viruses.
• Parotid glands. These are the two largest
glands. One is located in each cheek over the
jaw in front of the ears. Inflammation of one
or more of these glands is called parotitis, or
parotiditis.
 Caries dentis
• Cavities are permanently damaged areas in
the hard surface of your teeth that develop
into tiny openings or holes. Cavities, also
called tooth decay or caries, are caused by a
combination of factors, including bacteria in
your mouth, frequent snacking, sipping sugary
drinks, and not cleaning your teeth well.