DERMATOMUSCULOSKELETAL SYSTEM

Case 2

TUTOR GUIDE
Case 2
MR. Teten can SMILE AGAIN
Date:
30 Januari, 2 Februari 2015

Marlianti Hidayat, drg., MH.Kes.

ORAL AND DENTAL DEPARTMENT

FACULTY OF MEDICINE UNIVERSITAS
PADJADJARAN
BANDUNG
2014-2015
FRAME OF THINKING

Rational and Reasoning Behind the Case

Predisposition Factor
Poor Oral Hygiene
Defence Mechanism

Etiology
Caries

Pathophysiology
Mandible

Maxilla
Anterior teeth

Potential
Spaces

Canine Fossa

Posterior teeth

Temporal Fossa

Anterior teeth

*Submental
* Sublingual

Posterior teeth

* Submandibular

Acute Progressive Cellulitis =

Plegmon = Angina Von Ludwing
Hospitalization :
Airway & Breathing
General Condition
Surgical Treatment
(tooth extraction/tracheoctomy)

Note :
1. In Mr.Tetens case, tooth extraction can be conducted and become
the best choice of treatment.
2. Inappropriate or delayed treatment can cause the spread of
infection to the mediastinum space.

SPREAD OF ODONTOGENIC INFECTIONS

1

Caries

Superfisial
Media
Profunda
Necrotic Pulp
Gangren
Abses

Predisposition factor :
- Poor Oral Hygiene
- Defence Mechanism

Soft Tissue

Hard Tissue

Cellulitis

Osteomyelitis

Upper Jaw

Lower Jaw

Potential spaces

SubMental Spaces
SubMandibular Spaces
SubLingual Spaces

Dis.

= Acute Progresive Cellulitis

= Phlegmon
= Ludwigs Von Angina
Hospitalization :
Airway & Breathing
General Condition
Surgical Treatment
(Incision and drainage ,
tracheoctomy ,tooth extraction,

Dermatomusculoskeletal System

Tutor Guide Mr Teten Can Smile Again

System

: Dermatomusculo Skeletal System

Week Theme

: Head and Neck

Trigger Case

: Angina von Ludwig / Phlegmone

(SKDI competency level: 3A)

Differential Diagnose

:- Abcess Submandible
- Osteomyelitis of the Jaw

Week schedule

: Three meetings

General Learning Objectives :

At the end of this week, the students will be able to :
- Understand and explain the anatomy and physiology of the oral, maxillofacial and neck
region.
- Understand the pathogenesis and microbiology of the mouth due to infection of dental
origin.
- Understand and explain pathogenesis of caries dentis.
- understand and explain the phenomenom / nature ,epidemiology, characteristics and
spread of dentoalveolar infection in the oral cavity to facial spaces, hard and soft tissue
-Understand the predisposition factors of a progressive acute cellulites (Angina Von
Ludwig) due to dental origin.
-Know principles management therapy of dentoalveolar infection.
-Understand and explain pharmacology of antimicroba and analgetic for dentoalveolar
infection (classification , choosing the appropriate antibiotic, dose and write drug
prescription )

Dermatomusculoskeletal System

Case for Tutor Mr Teten Can Smile Again

TUTORIAL 1 part 1

You are a medical student observing at Puskesmas Jatinangor. Mr Teten, an 48 years old was
brought to Puskesmas by his wife. He has swelling of the neck area, and difficulty of
swallowing, opening mouth widely, breathing and speaks with weak voice. He can not eat
anything since 2 days ago except porridge, juice or drink water in small volume .According
to his wife, he drools a lot since yesterday. He is immediately admitted.

Instruction:
What are Mr Tetens problems?
Generate list of hypotheses and state a rationale for each problem.
What further information do you need?

Guiding lists for Tutorial 1 part 1

-Identify Mr Tetens Problems
(1)
(2)
(3)
(4)

Difficulty of : swallowing, breathing and speaking.

Swelling of the neck area.
Can not eat anything since 2 days.
Spontaneous drooling.

-Before discusing the problems of this case, please challenge the students to review and
explain :
(1) Anatomy of the skull, landmark and features of the mandible, muscle of mastication,
trigeminal nerve , anatomy and physiology of the teeth ,including the intended tissue
spaces around the jaw (anatomy).
(2) Mechanism of swallowing, breathing and speaking.(physiology).
(3) Why the patient has difficulty of swallowing, breathing, speaking and spontaneous
drooling.

1 A. Anatomy of the skull

1 B. Anatomy of the mandible

1 C.

Muscles of Mastication

The muscles of mastication is a collective term reserved for the masseter, temporalis,
medial and lateral pterygoid muscles. These muscles develop from the mesenchyme of the
first branchial arch, therefore receive the innervation from the mandibular branch of the
trigeminal nerve. Closely associated functionally and developmentally with the muscle of
mastication is the digastric muscle. The masseter and the temporalis muscles lie on the
superficial face, while the lateral and medial pterygoid muscles lie deeper within the infra
temporal fossa.

1 D.

Trigeminal Nerve

Lower Jaw

Upper Jaw

1 E. Anatomy and Physiology of teeth.

Each human has two sets of teeth. The first set of deciduous teeth are followed by the
permanent dentition. Twenty deciduous teeth erupting first are commonly called baby
teeth or primary teeth.The thirty two permanent teeth that erupt and replace the deciduous
teeth are commonly called secondary teeth.

Physiology of the Teeth

1.
2.
3.
4.
5.

Mastication
Fonetic
Esthetic
Self Confidence
Forensic

1 F. The important tissues spaces around the jaws

The primary spaces around the jaws
Lower Jaw
1. Submental space
2. Submandibular space

Upper Jaw
1. Buccal space
2. Canine space
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3. Sublingual space
4. Buccal space

3. Infratemporal space

Facial spaces
Fascial spaces are fascia-lined areas that can be eroded or distended by purulent exudat.
These areas are potential spaces that do not exist in healthy people but become filled during
infections. The spaces that are involved directly are known as the fascial spaces of primary
involvement:
A. The principal maxillary primary spaces:
1. Canine space is a thin potential space between the levator angulioris and the
levator labii superioris muscles.
2. Buccal space is bounded by overlying skin of the face on the lateral aspects and
the buccinator muscle on the medial aspect.
3. Infratemporal space lies posterior to the maxilla. It is bounded medially by the
lateral plate of the pterygoid process of the sphenoid bone and superiorly by the
base of the skull. Laterally, the infra temporal space is continuous with the deep
temporal space.
B. The principal mandibula primary spaces:
1. The submental space, lies between the anterior bellies of the digastric muscle and
between the mylohyoid muscle and the overlying skin.
2. The buccal space is bounded by the overlying skin of the face on the lateral aspect
and the buccinator muscle on the medial aspect.
3. The sublingual space, lies between the oral mucosa of he floor of the mouth and
the mylohyoid muscle. Its posterior border is open, and therefore it freely
communicates with the submandibular space and the secondary spaces of the
mandible to the posterior aspect.
4. The submandibular space, lies between the mylohyoid muscle and the overlying
skin and superficial fascia.
Secondary fascial spaces:
1. Masseteric space exists between the lateral aspect of the mandible and the medial
boundary of the masseter muscle.
2. Pterygomandibular space lies medial to the mandible and lateral to the medial
pterygoid muscle.

3. Superficial and deep temporal space is posterior and superior to the masseteric
and pterygomandibular space. It is divided into two portions by the temporalis
muscle: (1) a superficial portion that extends to the temporal fascia and (2) a deep
portion that is continuous with the infratemporal space.
4. Lateral pharyngeal space, extends from the base of the skull at the sphenoid bone
to the hyoid bone inferiorly. It is medial to the medial pterygoid muscle and
lateral to the superior pharyngeal constrictor on the medial side.
5. Retropharyngeal space lies behind the soft tissue of the posterior aspect of the
pharynx. It is bounded anteriorly by the superior pharyngeal constrictor muscle
and its investing facia and posteriorly by the alar layer of prevertebral fascia.
6. Prevertebral space extends from the pharyngeal tubercle on the base of the skull
to the diaphragm.

Canine Space

Buccal Space

Infratemporal Space

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2.

Mechanism of swallowing, breathing and speaking .(physiology).

(tutor guide from Department of Physiology)

3.

Please discuss : Why the patient has difficulty of swallowing, breathing, speaking
and spontaneous drooling.
Difficulty of swallowing, breathing and speaking in this case are caused by inflamation,
pushed upward and backward of the tongue, and other problems are caused by blockage
or disorders affecting the motions of swallowing.

4. Why the patient has difficulty of opening mouth widely? How does it refer to the
case?
Motor disturbance of the trigeminal nerve, especially spasm of the masticatory muscles,
with difficulty in opening the mouth (lockjaw). Difficulty of opening the mouth is called
trismus.
The relation to the case is due to the odontogenic infection.
5. Since due to e.g. pain, swelling, and trismus, Mr.Teten can not open his mouth
normally, what muscles are involved in the mastication process?
m.temporal

: muscle that elevates and lowers the jaw and can draw the mandible
backward.
m.masseter
: muscle that closes the mouth.
m.internal pterygoid : muscle thar raises the mandible to close the jaw.
m.external pterygoid: opens the jaw and thrusts the mandible forward. It assists with lateral

TUTORIAL 1 part 2
History of Present Illness :
Approximately a few years ago, Mr.Teten, was then 43 years old of age, had dental caries
on his right lower second molar . He never had a treatment as advised by his dentist. Two
weeks ago, he came with great pain and a swelling on his right mandible area. The dentist
on duty examined and cleaned the tooth followed by appropriate medication (antibiotics
and analgesic- anti inflamatory drugs). He was urged to continue his treatment three days
afterwards, but again he neglected it.
Investigation:
General Physical Condition
Conscious. The body temperature is 39,2 degrees Celsius.
Blood pressure 110/80 mmHg. Pulse 106 bpm. Respiratory rate 32x/m.
Shivering and pale.
Head & Neck: See local/oral examination
Thorax: Within normal limits.
Extra and Intra Oral Examination
There is a bilateral massive indurated edema of the tissues of the submandibular, as well as
the submental and sublingual region. The bull neck appearance is obviously characterized
11

by a tense skin, hard on pressure, shiny and reddish in color. There is no soft area that
might indicate suppuration, likewise it is hard like a massive board.
Intraorally, the tongue is pushed upward, dry and coated. The mucosa of the floor of the
mouth is raised upward. Trismus is detected, approximately one finger only (2 cm). The
tooth itself, though difficult to examine, it has deep caries with poor oral hygiene,gingiva
edema and hyperemi.
Kwadran 1

Calculus-plaque

Kwadran 2

8 7 6 5 4 3 2 1

1 2 3 4 5 6 7 8

8 7 6 5 4 3 2 1

1 2 3 4 5 6 7 8

Kwadran 4

= caries dentis
= radix

Kwadran 3

Calculus-plaque

Laboratory Examination
Complete urine and blood test are done. The result shows the white blood cell count was
18,700/mm3.
Radiology Examination
- Deep caries 4 7
- Caries media 1 6, 3 8
- Radix 2 4, 2 6, 3 6, 4 6
- Radiolucent at periapical area of 4 7

12

Radiolucent area
Note :
Inflamation process at periapical area of 4 7 make the osteoclast more active then osteoblast due
to resorbtion alveolar bone, thats why the radiology feature of area 4 7 is radiolucent.

Guiding questions for Tutorial 1 part 2

1. Please interpret the result of physical examination, extra & intra oral, result of
laboratory test . What does it mean to you?
-Signs of infection. ( body temperature > 37oC, massive indurated edema, reddish, shiny,
suppuration, white blood cell >>> ) .
-Panoramic foto : to know the tooth cause of infection/focus infection .
2. What is the cause of swelling at the neck area.
Abcess of the periapikal 4 7 spread to primary spaces around the mandible
(submaxillary/submandibulary space, sublingual space and submental space)
3. What is Oral Hygiene ?
How can the docter know Oral Hygiene of the patient ?
ORAL HYGIENE INDEX - S
( GREENE AND VERMILLION,1960 )
Dental Plaque is a filmy deposit on the surface of a tooth consisting of a mixture of mucus,
bacteria, food, etc. Also called bacterial.
Dental Calculus or Tartar is a form of hardened dental plaque. It is caused by the continual
accumulation of minerals from saliva on plaque on the teeth.
The oral Hygiene Index is composed of the combined Plaque/Debris Index and Calculus
Index, each of these index is in turn based on 6 numerical determinations representing the
13

amount of debris or calculus found of the buccal or lingual sufaces of each three segmen of
each dental arch, namely
1.The segment distal to the right cuspid ( see the picture ).
2. The segment distal to the left cuspid.
3. The segment mesial to the right and left first bicuspids.
The Maxillary and the Mandibular arches are each composed of three segment.
(These are illustrated above ).

Each segment is examined for debris or calculus. From segment one tooth is used for
calculating the individual index, for that particular segment. The tooth used for the
calculating must have the greatest area covered by either debris or calculus.
The method for scoring calculus is the same as that applied to debris, but additional
provisions are made for recording subgingival deposits.

Criteria for calssifying debris

Scores

Criteria

No debris or stain present

Soft debris covering not more than one third of the tooth surface, or
presence of extrinsic stains without other debris regardless of surface area
covered.

14

Soft debris covering more than one third, but not more than two thirds, of
the exposed tooth surface.

Soft debris covering more than two thirds of the exposed tooth surface.

Criteria for calssifying calculus

Scores

Criteria

No calculus present

Supragingival calculus covering not more than one third of the exposed
tooth surface.

Supragingival calculus covering more than one third, but not more than two
thirds, of the exposed tooth surface or the present of individual flecks of
subgingival calculus around the cervical portion of the tooth or both.

Supragingival calculus covering more than two thirds of the exposed tooth
surface or a continuos heavy band of subgingival calculus around the
cervical potion of the tooth ar both.

Calculation Example
After the scores for debris and calculus are recorded, the index values are calculated.For each
individual, the debris scores are totaled and divided by the number of segments scored.
Score : 1

1,2 good
1,3
3
moderate
3
>
bad
4. How does poor oral hygiene (due to plaque) contributes to the development of
infection?
Like dental caries, microbiota accumulate in the ginggival sulcus plaque. As the
microbiota multiply, they produce histolytic enzymes, toxic metabolites, exotoxins,
endotoxins, and immunosuppressive and antiphagocytic factors. These induce
inflammation, causes direct damage to the tissue, and inferences with host defense
mechanism.
5. Please explain of the normal oral microbiota in Oral Cavity and their role in dental
caries formation.
The Normal Oral Microbiota
The mouth contains the normal oral microbiota that have colonized and are continually
maintained on the teeth and soft tissues and in saliva. These microbes usually cause no
harm except when they are allowed to accumulate in the form of dental plaque or are
displaced from the mouth to deeper tissues such as the tooth pulp or to other body sites
such as the bloodstream.
The human mouth is usually first exposed to microorganism at birth during passage
Through the birth canal. Most of the mothers vaginal bacteria that enter the childs
15

mouth are transient (short lived) and do not establish themselves as regular members
of oral microbiota. With time, the child is exposed to microorganism from the
environment, and it appears that the main sources of microbes that colonize the
childs mouth are the mouths of other people, particularly the mother and other close
family members.
For microbes to become established members of the oral microbiota,they must attach
to oral surfaces and be able to multiply in the oral environment. Eruption of the primary
teeth results in a major change in this environment,now providing tooth surfaces, gingival
crevices , and more opportunity for bleeding into the mouth. New bacteria, such as
streptococcus mutans, appear that can survive only on the teeth. Anaerobes increase in
number because of the added anaerobic sites around the teeth. Thus, different sites in the
mouth ( tongue, buccal epithelium, supragingival tooth surfaces, subgingival tooth, and
crevicular epithelia surfaces) support different combinations of microbes. As one grows
older, more and more microorganism colonize the mouth and, in general, the composition
stabilizes by approximately the early teen years.
The normal oral microbiota consists mostly of bacteria, although approximately one
third of the population also has the yeast Candida Albicans in their mouth . The oral
microbiota is very complex, with approximately 30 genera of bacteria represented
( Look at table ), although not every person has all of these genera present all of the
time. Each genus may be represented by several species, resulting in a very complex
group of both gram-positive and gram negative bacteria.
A gram of dental plaque contains approximately 200 billion bacteria.And saliva contain
contains approximately 10 million to 100 million bacteria per milliliter.

16

What are the role of the normal mouth microbiota in dental caries formation?
Normal mouth microbiota could form a dental palque. Dental palque is a biofilm which
means an accumulation of microbes within a matrix. The biofilm protects bacteria from
environmental hazards. Inside dental plaque, the acid producing bacteria
(predominantly Streptococci and Lactobaccili) are adhere to the enamel surface. The
formation of large amounts of acid (pH <5.0) from carbohydrates by streptococci and
lactobacilli in the plaque will demineralize the adjoining enamel and initiate caries.
6. What is Caries? How does it happen?
Dental caries is an infection disease. It is caused by demineralisasi of tooth structure
by acids produced during metabolism of dietary surgar by bacteria associated with the
tooth surfaces.
Bacterial genera in the mouth
Gram - Negative
Bacterioides
Porphinomonas
Prevotela
Mitsuokella
Fusobacterium
Actinobasillus
Cpnocytophaga
Eikenella
Wolinella
Campylobacter
Treponema
Neisseria
Leptotrichia
Selenomonas
Centipeda
Haemophillus
Veillonella
Cardiobacterium
moraxella

Gram Positive
Streptococcus
Actinomyces
Lactobacillus
Arachnia
Propionibacterium
Bifidobacterium
Micrococcus
Peptostreptococcus
Eubacterium
Rothia
Corynebacterium

17

Phatogenesis of Dental Caries

Sugars in the
diet

Acidogenc bacteria
on the teeth

Susceptible
host

Acids produced by bacteria

On the teeth
Acids accumulate at tooth
Surface to yield low pH
(critical pH)
Deminaralzation
(loss of tooth structure)

Remineralization
(white spots)

Dental caries

Dental caries

TUTORIAL 2
The oral surgeon on duty tells you that the bilateral massive edema covers the
submandibular, sublingual and submental spaces, meaning the patient developed a
progressive acute cellulites known as Angina Von Ludwig (phlegmone) caused by the
second molar mandible infection with differential diagnosis Abcess Submandible and
Osteomyelitis of the jaw.
Two days after admission, the condition of Mr Teten was improved. He was able to breath
and swallow more easily, less drooling of saliva, and wider opening of the mouth. The
swelling seemed to decrease in size by day four upon admission. By the eighth day, the
swelling and difficulty of opening the mouth are reduced greatly. The patient is discharged
with multivitamin in addition to the same antibiotic and analgesic as prescribed during
admission. An advice for extraction of the right lower second molar on the next visit which
scheduled four days afterwards was done.
18

Instruction:
1. How does infection spread of tooth into available spaces in head and neck area?
Please explain the mechanism of the spread of dental infection origin from
caries to the submandible, submental, and sublingual spaces

Guiding questions for Tutorial 2

The diffrent between Angina von Ludwig (Phlegmone), Abcess Submandible and
Osteomyelitis of the jaw.
Phlegmone
Extra oral
Swelling
Fitule
Intra oral
Tongue
Fitule
Space area involve

Mobility of the
tooth
Radiografi feature
Of mandible

Abcess
Submandible

Osteomyelitis

bilateral
none

unilateral
none

unilateral
multiple

pushed upward
none
three spaces:
submandible
sublingual
submental
only tooth cause of
infection
normal

normal
none
one space:
submandible

normal
multiple
none

only tooth cause of

infection
normal

More than one

squester

19

1. The treatment planning of Angina von Ludwig (Phlegmone) :

Hospitalization.
-Airway, breathing, circulation,
-Semi reclining position.
-5% glucose and ringer lactat solution intravenously with antibiotic Penicillin : Amoxilin
1gr/8hour + 500mg/8hour Metronidazole or Clindamycin 300mg/8hour (if the patient alergy
of penicillin), Dexametasone and -Roborantia..
-Drainage after fluctuative (+).
-Extraction of the tooth after trismus (-).
Note :
-

In Mr. Tetens case, tooth extraction can be conducted and become the best choice of
treatment.
Inappropriate or delayed treatment can cause the spread of infection to the Mediastinum
space.

a. Why we have to use Antibiotic for this case ?

Antibiotic therapy is indicated primarily when drainage cannot be adequately establish,
when the infection has spread to the suraounding soft tissue , or when systemic
symptoms are evident.Early and aggressive treatment with both surgery and antibiotics is
indicated in immunocompromised patients in order to prevent proggresion of disease.
The period of infection and the risk of complications due to odontogenic infections ca be
minimized in all patient with the prompt initiation of antimicrobial therapy.
b. Please discuss the principles for choosing the appropriate antibiotic!!!
-

Identification of the causative organism.

Use of a specific, narrow spectrum antibiotic.
Use the least toxic antibiotic.
Use of a bactericidal rather than a bacteriostatic drug.
Use the antibiotic with a proven history of success.
Cost of antibiotic.
Encourage patient compliance.

-Please summarize the case in terms of basic science principles you have learned!!
Pharmacological properties of drugs used for the treatment:
PENICILLIN
Chemistry
All penicillins have the basic structure shown in Figure 1. A thiazolidine ring (A) is attached
to a -lactam ring (B) that carries a secondary amino group (RNH). Substituents (R;
examples shown in Figure 1) can be attached to the amino group. Structural integrity of the
6-aminopenicillanic acid nucleus is essential for the biologic activity of these compounds.
Hydrolysis of the -lactam ring by bacterial -lactamases yields penicilloic acid, which lacks
antibacterial activity.

20

Figure 1

Penicillin have greatest activity against gram-positive organisms, gram-negative cocci, and
non--lactamase-producing anaerobes. However, they have little activity against gramnegative rods, and they are susceptible to hydrolysis by -lactamases.
Mechanism of Action
Penicillins, like all -lactam antibiotics, inhibit bacterial growth by interfering with the
transpeptidation reaction of bacterial cell wall synthesis. The cell wall is a rigid outer layer
unique to bacterial species. It completely surrounds the cytoplasmic membrane (Figure 2),
maintains cell shape and integrity, and prevents cell lysis from high osmotic pressure. The
cell wall is composed of a complex cross-linked polymer of polysaccharides and
polypeptides, peptidoglycan (murein, mucopeptide). The polysaccharide contains alternating
amino sugars, N-acetylglucosamine and N-acetylmuramic acid (Figure 3). A five-amino-acid
peptide is linked to the N-acetylmuramic acid sugar. This peptide terminates in D-alanyl-Dalanine. Penicillin-binding protein (PBP, an enzyme) removes the terminal alanine in the
process of forming a cross-link with a nearby peptide. Cross-links give the cell wall its
structural rigidity. -Lactam antibiotics, structural analogs of the natural D-Ala-D-Ala
substrate, covalently bind to the active site of PBPs. This inhibits the transpeptidation
reaction (Figure 4), halting peptidoglycan synthesis, and the cell dies. The exact mechanism
of cell death is not completely understood, but autolysins and disruption of cell wall
morphogenesis are involved. Penicillins and cephalosporins kill bacterial cells only when
they are actively growing and synthesizing cell wall.

21

Figure 2

22

Figure 3

23

Figure 4

Pharmacokinetics
Absorption of orally administered drug differs greatly for different penicillins, depending in
part on their acid stability and protein binding. Gastrointestinal absorption of nafcillin is
erratic, so it is not suitable for oral administration. Dicloxacillin, ampicillin, and amoxicillin
are acid-stable and relatively well absorbed, producing serum concentrations in the range of
48 mcg/mL following a 500 mg oral dose. Absorption of most oral penicillins (amoxicillin
being an exception) is impaired by food, and the drugs should be administered at least 12
hours before or after a meal.
Penicillin concentrations in most tissues are equal to those in serum. Penicillin is also
excreted into sputum and milk to levels 315% of those present in the serum. Penetration
into the eye, the prostate, and the central nervous system is poor. However, with active
inflammation of the meninges, as in bacterial meningitis, penicillin concentrations of 15
mcg/mL can be achieved with a daily parenteral dose of 1824 million units. These
concentrations are sufficient to kill susceptible strains of pneumococci and meningococci.
Penicillin is rapidly excreted by the kidneys; small amounts are excreted by other routes.
About 10% of renal excretion is by glomerular filtration and 90% by tubular secretion. The
normal half-life of penicillin G is approximately 30 minutes; in renal failure, it may be as
long as 10 hours. Ampicillin and the extended-spectrum penicillins are secreted more slowly
than penicillin G and have half-lives of 1 hour. For penicillins that are cleared by the kidney,
the dose must be adjusted according to renal function, with approximately one fourth to one
third the normal dose being administered if creatinine clearance is 10 mL/min or less

24

Adverse Reactions
The penicillins are remarkably nontoxic. Most of the serious adverse effects are due to
hypersensitivity. All penicillins are cross-sensitizing and cross-reacting. The antigenic
determinants are degradation products of penicillins, particularly penicilloic acid and
products of alkaline hydrolysis bound to host protein. A history of a penicillin reaction is not
reliable; about 58% of people claim such a history, but only a small number of these will
have an allergic reaction when given penicillin. Less than 1% of persons who previously
received penicillin without incident will have an allergic reaction when given penicillin.
Because of the potential for anaphylaxis, however, penicillin should be administered with
caution or a substitute drug given if there is a history of penicillin allergy. The incidence of
allergic reactions in small children is negligible.
CLINDAMYCIN
Clindamycin is a chlorine-substituted derivative of lincomycin, an antibiotic that is
elaborated by Streptomyces lincolnensis.

Antibacterial Activity
Streptococci, staphylococci, and pneumococci are inhibited by clindamycin, 0.55 mcg/mL.
Enterococci and gram-negative aerobic organisms are resistant (in contrast to their
susceptibility to erythromycin). Bacteroides sp and other anaerobes, both gram-positive and
gram-negative, are usually susceptible. Clindamycin, like erythromycin, inhibits protein
synthesis by interfering with the formation of initiation complexes and with aminoacyl
translocation reactions. The binding site for clindamycin on the 50S subunit of the bacterial
ribosome is identical with that for erythromycin. Resistance to clindamycin, which generally
confers cross-resistance to macrolides, is due to (1) mutation of the ribosomal receptor site;
(2) modification of the receptor by a constitutively expressed methylase (see section on
Erythromycin Resistance, above); and (3) enzymatic inactivation of clindamycin. Gramnegative aerobic species are intrinsically resistant because of poor permeability of the outer
membrane.
Pharmacokinetics
Oral dosages of clindamycin, 0.150.3 g every 8 hours (1020 mg/kg/d for children), yield
serum levels of 23 mcg/mL. When administered intravenously, 600 mg of clindamycin
every 8 hours gives levels of 515 mcg/mL. The drug is about 90% protein-bound.
Clindamycin penetrates well into most tissues, with brain and cerebrospinal fluid being
important exceptions. It penetrates well into abscesses and is actively taken up and
concentrated by phagocytic cells. Clindamycin is metabolized by the liver, and both active
drug and active metabolites are excreted in bile and urine. The half-life is about 2.5 hours in
normal individuals, increasing to 6 hours in patients with anuria. No dosage adjustment is
required for renal failure.
25

Clinical Uses
Clindamycin is indicated for treatment of anaerobic infection caused by bacteroides and
other anaerobes that often participate in mixed infections. Clindamycin, sometimes in
combination with an aminoglycoside or cephalosporin, is used to treat penetrating wounds of
the abdomen and the gut; infections originating in the female genital tract, eg, septic abortion
and pelvic abscesses; and aspiration pneumonia. Clindamycin is now recommended rather
than erythromycin for prophylaxis of endocarditis in patients with valvular heart disease who
are undergoing certain dental procedures. Clindamycin plus primaquine is an effective
alternative to trimethoprim-sulfamethoxazole for moderate to moderately severe
Pneumocystis jiroveci pneumonia in AIDS patients. It is also used in combination with
pyrimethamine for AIDS-related toxoplasmosis of the brain.
Adverse Effects
Common adverse effects are diarrhea, nausea, and skin rashes. Impaired liver function (with
or without jaundice) and neutropenia sometimes occur. Severe diarrhea and enterocolitis
have followed clindamycin administration. Administration of clindamycin is a risk factor for
diarrhea and colitis due to Clostridium difficile.
METRONIDAZOLE
Metronidazole is a nitroimidazole antiprotozoal drug (see Chapter 53) that also has potent
antibacterial activity against anaerobes, including bacteroides and clostridium species. It is
well absorbed after oral administration, is widely distributed in tissues, and reaches serum
levels of 46 mcg/mL after a 250-mg oral dose. Metronidazole can also be given
intravenously or by rectal suppository. The drug penetrates well into the cerebrospinal fluid
and brain, reaching levels similar to those in serum. Metronidazole is metabolized in the liver
and may accumulate in hepatic insufficiency.
Metronidazole is indicated for treatment of anaerobic or mixed intra-abdominal infections,
vaginitis (trichomonas infection, bacterial vaginosis), C difficile colitis, and brain abscess.
The typical dosage is 500 mg three times daily orally or intravenously (30 mg/kg/d).
Vaginitis may respond to a single 2-g dose. A vaginal gel is available for topical use.
Adverse effects include nausea, diarrhea, stomatitis, and peripheral neuropathy with
prolonged use. Metronidazole has a disulfiram-like effect, and patients should be instructed
to avoid alcohol. Although teratogenic in some animals, metronidazole has not been
associated with this effect in humans. Other properties of metronidazole are discussed in
Chapter 53.
A structurally similar agent, tinidazole, is a once-daily drug approved for treatment of
trichomonas infection, giardiasis, and amebiasis. It also is active against anaerobic bacteria,
but is not FDA-approved for treatment of anaerobic infections.
DEXAMETHASONE
Anti-inflamatory Effect
Glucocorticoids dramatically reduce the manifestations of inflammation. This is due to their
profound effects on the concentration, distribution, and function of peripheral leukocytes and
to their suppressive effects on the inflammatory cytokines and chemokines and on other
mediators of inflammation. Inflammation, regardless of its cause, is characterized by the
extravasation and infiltration of leukocytes into the affected tissue. These events are
mediated by a complex series of interactions of white cell adhesion molecules with those on
endothelial cells and are inhibited by glucocorticoids. After a single dose of a short-acting
26

glucocorticoid, the concentration of neutrophils in the circulation increases while the

lymphocytes (T and B cells), monocytes, eosinophils, and basophils decrease. The changes
are maximal at 6 hours and are dissipated in 24 hours. The increase in neutrophils is due both
to the increased influx into the blood from the bone marrow and decreased migration from
the blood vessels, leading to a reduction in the number of cells at the site of inflammation.
The reduction in circulating lymphocytes, monocytes, eosinophils, and basophils is primarily
the result of their movement from the vascular bed to lymphoid tissue.
Glucocorticoids also inhibit the functions of tissue macrophages and other antigen-presenting
cells. The ability of these cells to respond to antigens and mitogens is reduced. The effect on
macrophages is particularly marked and limits their ability to phagocytose and kill
microorganisms and to produce tumor necrosis factor-, interleukin-1, metalloproteinases,
and plasminogen activator. Both macrophages and lymphocytes produce less interleukin-12
and interferon-, important inducers of TH1 cell activity, and cellular immunity.
In addition to their effects on leukocyte function, glucocorticoids influence the inflammatory
response by reducing the prostaglandin, leukotriene, and platelet-activating factor synthesis
that results from activation of phospholipase A2. Finally, glucocorticoids reduce expression
of cyclooxygenase-2, the inducible form of this enzyme, in inflammatory cells, thus reducing
the amount of enzyme available to produce prostaglandins
Dosage
Oral, IV and IM (injections as sodium phosphate):
0.75 to 9 mg per day in divided doses every 6 to 12 hours

EPILOGUE
Seven days after the extraction was done, he was control to Puskesmas Mr. Teten was very
happy because he can smile and eat his favorite spicy food again. He promised to himself and
his wife to take good care of his oral health. The dentist told him to have a regular teeth
examination twice a year.

References
1. Chow AW, Infections of Oral Cavity, Neck and Head.las In : Mandell GL, Douglas RG,
Bennett JE, editors Principles and Practice of Infectious Toronto: Churchill Livingstone,
2000.
2. J.V. Soames, J.C Southam : Oral Pathology, 4 th Ed, Oxford, 2005.
3. Neville, Damm, Allen, Bouquot : Oral and Maxillofacial Pathology, W.B. saunders Co,
1995.
4. Newman, Takei, Carranza : Clinical Periodontology, 9 th Ed, W.B. Saunders Co, 2002.
5. Oral and Maxillofacial Anatomy.
6. Sand T, Pynn BR, Katsikeris N. Odontogenid Infections : Microbiology, Antibiotics, and
Management. Oral Health, 1995.
7. Topazian, Goldberg, Hupp : Oral and Maxillofacial Infection, 4 th Ed, W.B Saunders Co,
2002.
27

TUTOR GUIDE
DERMATO MUSKULO SKELETAL SYSTEM
SWALLOWING, BREATHING, SPEAKING

By :
Jimmy S., dr., M.Kes, AIF.
Ronny, dr., M.Kes, AIFO.
Nova, dr.
Hendarsyah, drs., M.Sc, M.Kes, AIF.

PHYSIOLOGY DEPARTEMENT
UNIVERSITY PADJADJARAN
JATINANGOR

28

A.

SWALLOWING
The motility associated with the pharynx and esophagus is swallowing. Most of
us think of swallowing as the limited act of moving food out of the mouth into
the esophagus. However, swallowing actually is the entire process of moving
food from the mouth through the esophagus into the stomach.
SWALLOWING IS A SEQUENTIALLY PROGRAMMED ALL OR NONE REFLEX
Swallowing is inisiated when bolus, or ball of chewed or liquid food, is voluntarily
forced by the tongue to the rear of the mouth into pharynx. The pressure of the
bolus stimulates pharyngeal pressure receptors, which send afferent impulses to
the swallowing center located in the medulla of the brain stem. The swallowing
center then reflexly activates in the appropriate sequence the muscles involved
in swallowing . Swallowing is the most complex reflex in the body. Multiple highly
coordinated responses are triggered in a specific all or none pattern over a
period of time to accomplish the act of swallowing. Swallowing is initiated
voluntary, but once begun it cannot be stopped. Perhaps you have experienced
this when a large piece of hard candy inadvertently slipped to the rear of your
throat, triggering an unintentional swallow.
DURING THE OROPHARYNGEAL STAGE OF SWALLOWING, FOOD IS PREVENTED
FROM ENTERING THE WRONG PASSAGEWAYS
Swallowing is divided into the oropharyngeal stage and the esophageal stage.
THE OROPHARYNGEAL STAGE
Last about 1 second and consist of moving the bolus from the mouth through the
pharynx and into esophagus. When the bolus enters the pharynx, it must be
directed into the esophagus and prevented form entering the other opening that
communicate with the pharynx. In the other words, food must be kept from reentering the mouth, from entering the trachea. All of this is managed by the
following coordinated activities.
- The position of the tongue against the hard palate keeps food from reentering the mouth during swallowing
- The uvula is elevated and lodges against the back of the throat, sealing off
the nasal passage from the pharynx so that food does not enter the nose.
- Food is prevented from entering the trachea primarily by elevation of the
larynx and tight closure of the vocal fold across the laryngeal opening, or
glottis. The first part of the trachea is the larynx, or voice box, across
which are strechted the vocal folds. During Swallowing, the vocal folds
serve a purpose unrelated to speech. Contraction of laryngeal muscle
aligns the vocal cord in tight apposition to each other, thus sealing the
glottis entrance. Also bolus tilt

Pharynx - Three pharyngeal constrictors (Groher, fig 1.4)

o

Superior pharyngeal constrictor - The elevation and contraction of

the velum results in the complete closure of the velopharyngeal
port, this action is facilitated by the contraction of the spc, which
narrow the pharynx.

Medial and inferior pharyngeal constrictors-Initiation of pharyngeal

peristalsis occurs. The bolus is carried by sequential peristaltic
action of the middle and inferior pharyngeal constrictors into and
through the pharynx to the cricopharygneal sphincter.

29

thyroid cartilage - fibers of the inferior constrictor attach to the sides of

the thyroid cartilage anteriorly, a space is formed between these fibers
and the sides of the thyroid cartilage.

pyriform sinuses - These spaces are known as the pyriform sinuses. These
end inferiorly at the cricopharyngeus muscle, which is the most inferior
structure of the pharynx and serves as the valve at the top of the
esophagus. Pharyngeal constrictors insert into throid cartilage anteriorly
to form pyriform sinuses

pharyngoesphageal sphincter or juncture (P-E segment) upon contraction

prevents air from entering the esophagus during respiration and material
from refluxing back up the esophagus and into the pharynx.

larynx
o

vocal folds

Structures

Lateral cricoarytenoid muscle and oblique interarytenoid

muscles adduct (close) vocal folds.

Posterior cricoarytenoid muscles abduct (open) vocal folds.

vocal fold closure

epiglottis (Logemann, fig 2-5) - The topmost structure of the larynx is the
epiglottis, which rests against the base of the tongue. The wedge-shaped
space formed between the base of the tongue and epiglottic is the
valleculae. The valleculae and the pyriform sinuses are known as the
pharyngeal recesses or side pockets, into which food may fall and reside
before or after the swallowing reflex triggers.

trachea

Esophagus - consists of a hollow muscular tube 23 to 25 cm long with a

sphincter at each end.

Physiology - UMD Tutorial

Oral Preparatory Phase

o

Movement patterns depend on consistency of material swallowed

Liquid Bolus has a certain degree of cohesiveness that may be

maintained as bolus is held between tongue and anterior hard
palate.

Lip Closure

Facial tone helps with labial seal.

30

Rotary, lateral jaw movement

Rotary, lateral tongue movement

Anterior pulling of soft palate and rests against the back of the
tongue, which is elevated serving to keep material in the oral cavity.

Oral Phase (1 sec)

o

Intact labial seal

Anterior to posterior tongue movement

Pharyngeal Phase-Pharyngeal Response (1 sec)

o

Triggering of the swallowing response occurs at the anterior faucial

arch.

elevation and retraction of the velum and complete closure

of

velopharyngeal port to prevent material from entering the

nasal cavity.

initiation of pharyngeal peristalis to pick up the bolus as it

passes the anterior faucial arch and carry it by sequential
peristalic (squeezing) action of the pharyngeal constrictors
into and through the pharynx to the cricopharyngeal
sphincter at the top of the esophagus.

elevation and closure of the larynx at all three sphincters

(epiglottis/aryepiglottic folds, false vocal folds, and true vocal
folds) to prevent material from entering the airway.

relaxation of the cricopharyngeal sphincter to allow material

to pass from pharynx into the esophagus.

laryngeal elevation and cricopharngeus relaxation

Transit time can be measuered from the point where the bolus
moves from the point at which the reflex is triggered at the anterior
faucial arch through the cricopharyngeal juncture into the
espohagus.

Esophageal Phase (8-20 sec) transit times can be measured from the point
where the bolus enters the esophagus at the crico-esophageal juncture
until it passes into the stomach at the gastro-esophageal juncture.

Neural Regulation of Swallowing

Swallowing is initiated by sensory impulses transmitted as a result of

stimulation of receptors on the fauces, tonsils, soft palate, base of the
tongue, and posterior pharyngeal wall.

31

Sensory impulses reach the brainstem primarily through the 7th, 9th, and
10 cranial nerves, while the efferent (motor) function is mediated through
the 9th, 10th, 12th cranial nerves.Cricopharyngeal sphincter opening is
reflexive, relaxation occurring at the time when the bolus reaches the
posterior pharyngal wall prior to reaching this sphincter.

Cranial Nerves
o

CN V -- Trigeminal

contains both sensory and motor fibers that innervate the

face

important in chewing

CN VII -- Facial

contains both sensory and motor fibers

important for sensation of oropharynx & taste to anterior 2/3

of tongue

CN IX -- Glossopharyngeal

contains both sensory and motor fibers

important for taste to posterior tongue, sensory and motor

functions of the pharynx

CN X -- Vagus

contains both sensory and motor fibers

important for taste to oropharynx, and sensation and motor

function to larynx and laryngopharynx.

important for airway protection

CN XII -- Hypoglossal

contains motor fibers that primarily innervate the tongue

B. BREATHING
Mechanics of Breathing
This explanation of the physiology of breathing shows how our health
improves through the conscious connected breathing that we do in
Transformation Breathwork.

32

Humans need a continuous supply of oxygen for cellular respiration, and they
must get rid of excess carbon dioxide, the poisonous waste product of this
process. Gas exchange supports this cellular respiration by constantly supplying
oxygen and removing carbon dioxide. The oxygen we need is derived from the
Earth's atmosphere, which is 21% oxygen. This oxygen in the air is exchanged in
the body by the respiratory surface. In humans, the alveoli in the lungs serve as
the surface for gas exchange.
Gas exchange in humans can be divided into five steps:
1. Breathing
2. External Respiration
3. Gas Transport
4. Internal Respiration
5. Cellular Respiration
Other factors involved with respiration are:

Adaptations of Diving Mammals

Bohr Shift

Control of Breathing

Partial Pressure

Structure of Respiratory System

Structure of the Human Respiratory System

The Nose - Usually air will enter the respiratory system through the nostrils.
The nostrils then lead to open spaces in the nose called the nasal passages.
The nasal passages serve as a moistener, a filter, and to warm up the air before
it reaches the lungs. The hairs existing within the nostrils prevents various
foreign particles from entering. Different air passageways and the nasal
passages are covered with a mucous membrane. Many of the cells which
produce the cells that make up the membrane contain cilia. Others secrete a
type a sticky fluid called mucus. The mucus and cilia collect dust, bacteria, and
other particles in the air. The mucus also helps in moistening the air. Under the
mucous membrane there are a large number of capillaries. The blood within
these capillaries helps to warm the air as it passes through the nose. The nose
serves three purposes. It warms, filters, and moistens the air before it reaches
the lungs. You will obviously lose these special advantages if you breath through
your mouth.
Pharynx and Larynx - Air travels from the nasal passages to the pharynx, or
more commonly known as the throat. When the air leaves the pharynx it passes
into the larynx, or the voice box. The voice box is constructed mainly of
cartilage, which is a flexible connective tissue. The vocal chords are two pairs of
membranes that are stretched across the inside of the larynx. As the air is

33

expired, the vocal chords vibrate. Humans can control the vibrations of the
vocal chords, which enables us to make sounds. Food and liquids are blocked
from entering the opening of the larynx by the epiglottis to prevent people from
choking during swallowing.
Trachea - The larynx goes directly into the trachea or the windpipe. The
trachea is a tube approximately 12 centimeters in length and 2.5 centimeters
wide. The trachea is kept open by rings of cartilage within its walls. Similar to
the nasal passages, the trachea is covered with a ciliated mucous membrane.
Usually the cilia move mucus and trapped foreign matter to the pharynx. After
that, they leave the air passages and are normally swallowed. The respiratory
system cannot deal with tobacco smoke very keenly. Smoking stops the cilia
from moving. Just one cigarette slows their motion for about 20 minutes.
The tobacco smoke increases the amount of mucus in the air passages. When
smokers cough, their body is attempting to dispose of the extra mucus.
Bronchi - Around the center of the chest, the trachea divides into two cartilageringed tubes called bronchi. Also, this section of the respiratory system is lined
with ciliated cells. The bronchi enter the lungs and spread into a treelike fashion
into smaller tubes calle bronchial tubes.
Bronchioles - The bronchial tubes divide and then subdivide. By doing this
their walls become thinner and have less and less cartilage. Eventually, they
become a tiny group of tubes called bronchioles.
Alveoli - Each bronchiole ends in a tiny air chamber that looks like a bunch of
grapes. Each chamber contains many cup-shaped cavities known as alveoli.
The walls of the alveoli, which are only about one cell thick, are the respiratory
surface. They are thin, moist, and are surrounded by several numbers of
capillaries. The exchange of oxygen and carbon dioxide between blood and air
occurs through these walls. The estimation is that lungs contain about 300
million alveoli. Their total surface area would be about 70 square meters. That is
40 times the surface area of the skin. Smoking makes it difficult for oxygen to
be taken through the alveoli. When the cigarette smoke is inhaled, about onethird of the particles will remain within the alveoli. There are too many particles
from smoking or from other sources of air pollution which can damage the walls
in the alveoli. This causes a certain tissue to form. This tissue reduces the
working area of the respiratory surface and leads to the disease called
emphysema.

Breathing
Breathing consists of two phases, inspiration and expiration. During inspiration,
the diaphragm and the intercostal muscles contract. The diaphragm moves
downwards increasing the volume of the thoracic (chest) cavity, and the
intercostal muscles pull the ribs up expanding the rib cage and further increasing
this volume. This increase of volume lowers the air pressure in the alveoli to
below atmospheric pressure. Because air always flows from a region of high
pressure to a region of lower pressure, it rushes in through the respiratory tract
and into the alveoli. This is called negative pressure breathing, changing the
pressure inside the lungs relative to the pressure of the outside atmosphere. In
contrast to inspiration, during expiration the diaphragm and intercostal muscles
relax. This returns the thoracic cavity to it's original volume, increasing the air
pressure in the lungs, and forcing the air out.

34

External Respiration
When a breath is taken, air
passes
in
through
the
nostrils, through the nasal
passages, into the pharynx,
through the larynx, down the
trachea, into one of the main
bronchi, then into smaller
bronchial tubules, through even smaller bronchioles, and into a microscopic air
sac called an alveolus. It is here that external respiration occurs. Simply put, it
is the exchange of oxygen and carbon dioxide between the air and the blood in
the lungs. Blood enters the lungs via the pulmonary arteries. It then proceeds
through arterioles and into the alveolar capillaries. Oxygen and carbon dioxide
are exchanged between blood and the air. This blood then flows out of the
alveolar capillaries, through venuoles, and back to the heart via the pulmonary
veins. For an explanation as to why gasses are exchanged here, see partial
pressure.

Gas Transport
If 100mL of plasma is exposed to an atmosphere
with a pO2 of 100mm Hg, only 0.3mL of oxygen
would be absorbed. However, if 100mL of blood is
exposed to the same atmosphere, about 19mL of
oxygen would be absorbed. This is due to the
presence of haemoglobin, the main means of
oxygen transport in the body. The respiratory
pigment haemoglobin is made up of an ironcontaining porphyron, haem, combined with the
protein globin. Each iron atom in haem is attached
to four pyrole groups by covalent bonds. A fifth
covalent bond of the iron is attached to the globin
part of the molecule and the sixth covalent bond is available for combination
with oxygen. There are four iron atoms in each hemoglobin molecule and
therefore four heam groups.
Oxygen Transport In the loading and unloading of oxygen, there is a cooperation between these
four haem groups. When oxygen binds to one of the groups, the others change
shape slightly and their attraction to oxygen increases. The loading of the first
oxygen, results in the rapid loading of the next three (forming oxyhemoglobin).
At the other end, when one group unloads it's oxygen, the other three rapidly
unload as their groups change shape again having less attraction for oxygen.
This method of cooperative binding and release can be seen in the dissociation
curve for hemoglobin. Over the range of oxygen concentrations where the curve
has a steep slope, the slightest change in concentration will cause hemoglobin to
load or unload a substantial amount of oxygen. Notice that the steep part of the
curve corresponds to the range of oxygen concentrations found in the tissues.

35

When the cells in a particular location begin to work harder, e.g. during exercise,
oxygen concentration dips in that location, as the oxygen is used in cellular
respiration. Because of the cooperation between the haem groups, this slight
change in concentration is enough to cause
a large increase in the amount of oxygen
unloaded.
As with all proteins, hemoglobin's shape
shift is sensitive to a variety of
environmental conditions. A drop in pH
lowers the attraction of hemoglobin to
oxygen, an effect known as the Bohr shift.
Because carbon dioxide reacts with water
to produce carbonic acid, an active tissue
will lower the pH of it's surroundings and
encourage hemoglobin to give up extra
oxygen, to be used in cellular respiration.
Hemoglobin is a notable molecule for it's ability to transport oxygen from
regions of supply to regions of demand.
Carbon Dioxide Transport - Out of the carbon dioxide released from respiring
cells, 7% dissolves into the plasma, 23% binds to the multiple amino groups of
hemoglobin (Caroxyhemoglobin), and 70% is carried as bicarbonate ions.
Carbon dioxide created by respiring cells diffuses into the blood plasma and
then into the red blood cells, where most of it is converted to bicarbonate ions.
It first reacts with water forming carbonic acid, which then breaks down into H +
and CO3-. Most of the hydrogen ions that are produced attach to hemoglobin or
other proteins.
Internal Respiration
The body tissues need the oxygen
and have to get rid of the carbon
dioxide, so the blood carried
throughout the body exchanges
oxygen and carbon dioxide with
the
body's
tissues.
Internal
respiration
is
basically
the
exchange of gasses between the
blood in the capillaries and the
body's cells.
Control of Breathing
The respiratory center is gray
matter in the pons and the upper
Medulla, which is responsible for rhythmic respiration. This center can be divided
into an inspiratory center and an expiratory center in the Medulla, an apneustic
center in the lower and midpons and a pneumotaxic center in the rostral-most
part of the pons. This respiratory center is very sensitive to the pCO 2 in the
arteries and to the pH level of the blood. The CO2 can be brought back to the
lungs in three different ways; dissolved in plasma, as carboxyhemoglobin, or as
carbonic acid. That particular form of acid is almost broken down immediately by
carbonic hydrase into bicarbonate and hydrogen ions. This process is then
reversed in the lungs so that water and carbon dioxide are exhaled. The Medulla
Oblongata reacts to both CO 2 and pH levels which triggers the breathing process
so that more oxygen can enter the body to replace the oxygen that has been

36

utilized. The Medulla Oblongata sends neural impulses down through the spinal
chord and into the diaphragm. The impulse contracts down to the floor of the
chest cavity, and at the same time there is a message sent to the chest muscles
to expand causing a partial vacuum to be formed in the lungs. The partial
vacuum will draw air into the lungs.
There are two other ways the Medulla Oblongata can be stimulated. The first
type is when there is an oxygen debt (lack of oxygen reaching the muscles),
and this produces lactic acid which lowers the pH level. The Medulla Oblongata
is then stimulated. If the pH rises it begins a process known as the Bohr shift.
The Bohr shift is affected when there are extremely high oxygen and carbon
dioxide pressures present in the human body. This factor causes difficulty for the
oxygen and carbon dioxide to attach to hemoglobin. When the body is exposed
to higher altitudes the oxygen will not attach to the hemoglobin properly,
causing the oxygen level to drop and the person will black out. This theory also
applies to divers who go to great depths, and the pressure of the oxygen
becomes poisonous. These pressures are known as pO 2 and pCO2, or partial
pressures. The second type occurs when the major arteries in the body called
the aortic and carotid bodies, sense a lack of oxygen within the blood and they
send messages to the Medulla Oblongata.

C. VOICE SPEAKING
Physiology of the Voice
The Three Subsystems of Voice

Voice production is a complex action, and involves practically all

systems of the body. Voice production begins with respiration
(breathing). Air is inhaled as the diaphragm (the large, horizontal
muscle below the lungs) lowers. The volume of the lungs expands and
air rushes in to fill this space. We exhale as the muscles of the rib

37

cage lower and the diaphragm raises, essentially squeezing the air
out.
In order to produce sound, adductor muscles (the "vocal cord
closers") are activated, providing resistance to exhaled air from the
lungs. Air then bursts through the closed vocal cords. As the air
rushes through the vocal cords, the pressure between the cords
drops, sucking them back together. This is known as the "Bernoulli
Effect." This vibration, or the action of the vocal cords being blown
apart and then "sucked" back together, is repeated hundreds or even
thousands of times per second, producing what we hear as voice. This
sound, created at the level of the vocal cords, is then shaped by
muscular changes in the pharynx (throat) and oral cavity (including
the lips, tongue, palate, and jaw) to create speech.

The larynx (lar-inks), commonly called the "voice box," is a tube

shaped structure comprised of a complex system of muscle, cartilage,
and connective tissue. The larynx is suspended from the hyoid bone,
which is significant in that it is the only bone in the body that does not
articulate with any other bone. The framework of the larynx is
composed of three unpaired and three paired cartilages. The thyroid
cartilage is the largest of the unpaired cartilages, and resembles a
shield in shape. The most anterior portion of this cartilage is very
prominent in some men, and is commonly referred to as an "Adam's
apple." The second unpaired cartilage is the cricoid cartilage, whose
shape is often described as a "signet ring." The third unpaired
cartilage is the epiglottis, which is shaped like a leaf. The attachment
of the epiglottis allows it to invert, an action which helps to direct
food and liquid into the esophagus and to protect the vocal cords and
airway
during
swallowing.

38

The three paired cartilages include the arytenoid, cuneiform, and

corniculate cartilages. The arytenoids are shaped like pyramids, and
because they are a point of attachment for the vocal cords, allow the
opening and closing movement of the vocal cords necessary for
respiration and voice. The cuneiform and corniculate cartilages
are very small, and have no clear-cut function.

There are two primary groups of laryngeal muscles, extrinsic and

instrinsic. The extrinsic muscles are described as such because
they attach to a site within the larynx and to a site outside of the
larynx (such as the hyoid bone, jaw, etc.). There are eight
extrinsic laryngeal muscles, and they are further divided into the
suprahyoid group (above the hyoid bone) and the infrahyoid group
(below the hyoid bone).
The suprahyoid group includes the
stylohyoid,
mylohyoid,
geniohyoid,
and
digastric muscles.
The suprahyoid extrinsic laryngeal muscles work together to raise the
larynx. The infrahyoid group includes the sternothyroid, sternohyoid,
thyrohyoid, and omohyoid muscles. The infrahyoid extrinsic laryngeal
muscles work together to lower the hyoid bone and larynx.
The intrinsic laryngeal muscles are described as such because both of
their attachments are within the larynx. The intrinsic muscles include
the interarytenoid, lateral cricoarytenoid, posterior cricoarytenoid,
cricothyroid, and thyroarytenoid (true vocal cord) muscles. All of the
intrinsic muscles are paired (that is, there is a right and left muscle)
with the exception of the transverse interarytenoid. All of the
intrinsic laryngeal muscles work together to adduct (close) the vocal
cords with the exception of the posterior cricoarytenoid, which is the
only muscle that abducts (opens) the vocal cords.

39

The larynx houses the vocal cords, two elastic bands of tissue (right
and left) that form the entryway into the trachea (airway). Above and
to the sides of the true vocal cords are the false vocal cords, or
ventricular cords. The false vocal cords do not usually vibrate during
voicing, but are often seen coming together (adducting) in individuals
with muscle tension dysphonia, a common voice disorder
characterized by excessive muscular tension with voice
production. The true vocal cords open (abduct) when we are breathing
and close (adduct) during voicing, coughing, and swallowing.

40