Diseases of nerves and muscles of oral cavity

Diseases of the Nerves and
Muscles

DISEASES OF THE NERVES
 Pain is defined as "an unpleasant sensory and
emotional experience associated with actual or
potential tissue damage, or described in terms of
such damage" by the Task Force on Taxonomy of
the international Association for the Study of Pain.
 It is an experience rather than a sensation.
 A comprehensive understanding of the disorders
affecting the nerve pathways and the nerve supply
of the various anatomic sites and structures
associated with the oral cavity is essential for the
dentist to determine the true nature of the pain
and take appropriate measures to effect its relief.

DISTURBANCES OF FIFTH CRANIAL NERVE

Trigeminal Neuralgia (Tic Douloureux,
Trifacial Neuralgia, Fothergill's Disease)
 Trigeminal neuralgia is an archetype of orofacial
neuralgias which follows the anatomical distribution of the
fifth cranial nerve.
 It mainly affects the second and third divisions of the
trigeminal nerve
 almost always exhibits a trigger zone, stimulation of which
initiates paroxysm of pain.
 The pain is often accompanied by a brief facial spasm or
tic.
 Pain distribution is unilateral and lasts for a few seconds to
few minutes.
 Physical examination eliminates alternative diagnoses.
 Signs of cranial nerve dysfunction or other neurologic
abnormality exclude the diagnosis of idiopathic TN and
suggest that pain may be secondary to a structural lesion.

Aetiology
 The aetiology of trigeminal neuralgia is as much a mystery
 The causative mechanism of pain in this condition still remains
controversial
 The most accepted theory is atherosclerosis of the superior cerebellar
artery resulting in pressing and grooving the root of the trigeminal nerve.
 Uncommonly, an area of demyelination, such as may occur with multiple
sclerosis, may be the precipitant.
 In most cases, no organic lesion is identified and the aetiology is
labelled as idiopathic.
 Development of trigeminal neuralgia in a young person suggests the
possibility of multiple sclerosis.
 Lesions of the entry zone of the trigeminal roots within the pons may
cause a similar pain syndrome.
 Thus, although trigeminal neuralgia is typically caused by a dysfunction
in the peripheral nervous system (the roots or trigeminal nerve itself), a
lesion within the central nervous system may rarely cause similar
problems.
 Infrequently, adjacent dental fillings composed of dissimilar metals may
trigger attacks (galvanism).

Clinical Features
 most common cranial neuralgia
 affects person older than 50 years of age
 Females are more commonly affected (3:2)
 right side of the face is affected in more patients
than the left by a ratio of about 1.7:1.

 pain - searing, stabbing, or lancinating type which
patients describe as feeling like an electric shock
 Many times, the pain is initiated when the patient
touches a 'trigger zone' on the face
 The term 'tic douloureux' is properly applied only
when the patient suffers from spasmodic contractions
of the facial muscles.
 In the early stages of the disease, the pain is
relatively mild, but as the attacks progress over a
period of months or years, they become more severe
and tend to occur at more frequent intervals.

 The early pain has been termed 'pre-trigeminal neuralgia'
and is sometimes described as dull, aching, burning, or
resembling a sharp toothache.
 Later, the pain may be so severe that the patient lives in
constant fear of an attack and many sufferers have
attempted suicide to put an end to their torment.
 Each attack of excruciating pain persists for only a few
seconds to several minutes and characteristically
disappears as promptly as it arises.
 As the attack occurs, the patient may clutch his/her face as
if in terror of the dreaded pain.
 The patient is free of symptoms between the attacks, but
unfortunately the frequency of occurrence of the painful
seizures cannot be predicted

 The 'trigger zones', which precipitate an attack when touched, are
common on the vermilion border of the lips, the alae of the nose, the
cheeks, and around the eyes.
 Usually any given patient manifests only a single trigger zone.
 The patient learns to avoid touching the skin over the trigger area and
frequently goes unwashed or unshaven to forestall any possible
triggering of an attack
 In some cases, it is not necessary that the skin actually be touched to
initiate the painful seizure; exposure to a strong breeze, simply the act
of eating, or smiling has been known to precipitate it.
 Any portion of the face may be involved by the pain, depending upon
which branches of the fifth nerve are affected.
 The mandibular and maxillary divisions are more commonly involved
than the ophthalmic; in some instances, two divisions may be
simultaneously affected.
 The disease is unilateral in nearly all cases and seldom, if ever, does
the pain cross the midline.

Differential Diagnosis
 The unusual clinical nature of the disease is the
presence of a 'trigger zone', the fleeting, but severe
type of pain occasioned and the location of the pain
usually provides the key for establishing the diagnosis
of trigeminal neuralgia.
 migraine or migrainous neuralgia (Horton's syndrome,
histamine headache, and histamine cephalgia), but
this severe type of periodic headache is persistent, at
least over a period of hours, and has no 'trigger zone'.
 Sinusitis - the various clinical aspects of trigeminal
neuralgia should exclude this diagnosis.
 The so-called Costen' s syndrome has also been
reported to produce symptoms suggestive of
trigeminal neuralgia.

 Tumours of the nasopharynx - can produce a similar
type of pain, generally manifested in the lower jaw,
tongue, and side of the head with associated middle
ear deafness.
This symptom complex, caused by a nasopharyngeal
tumour, has been called Trotter's syndrome - 30% of a
series of patients
These patients also exhibit asymmetry and defective
mobility of the soft palate and affected side.
As the tumour progresses, trismus of the internal
pterygoid muscle develops and the patient is unable
to open his/her mouth.
The actual cause of the neuralgic pain in Trotter's
syndrome is involvement of the mandibular nerve in
the foramen ovale through which the tumour invades
the calvarium

 herpes zoster of the fifth nerve-Termed postherpetic
neuralgia, the pain usually involves the ophthalmic division
of the fifth cranial nerve, but commonly regresses within
two to three weeks
It may persist, however, particularly in elderly patients.
The history of skin lesions prior to the onset of the neuralgia
usually aids in the diagnosis.
 Finally, pain of dental origin may be of such a localized or
referred nature that it simulates this disease.
By careful observation and questioning of the patient;
however, one can usually establish the correct diagnosis.
However, an extremely diligent search is sometimes
necessary to establish the dental origin of pain, particularly
in cases of a split tooth or an interradicular periodontal
abscess.

Laboratory Findings
 elective MRI for all patients to exclude an
uncommon space occupying lesion or aberrant
vessel compression on the nerve roots.

Treatment
 peripheral neurectomy, sectioning of the nerve at
the mental foramen, or at the supraorbital or
infraorbital foramen
 The injection of alcohol either into a peripheral
nerve area or centrally into the gasserian
ganglion
 The injection of boiling water into the gasserian
ganglion
 Surgical sectioning of the trigeminal sensory root
by any of a number of techniques - the treatment
of choice when attempting to obtain a permanent

 phenytoin (dilantin)
 carbamazepine - this drug is frequently used as a
therapeutic challenge to the diagnosis of
trigeminal neuralgia. Thus, if a patient who is
presumed to have this disease does not respond
rapidly to carbamazepine in 24-48 hours, then the
diagnosis is seriously in doubt
 microsurgical decompression of the trigeminal
root- good results
 Gamma knife radiosurgery - very effective in
treating the cranial neuralgias

Paratrigeminal Syndrome (Raeder's Syndrome
Paratrigeminal Neuralgia)
 severe headache or pain in the area of the
trigeminal distribution with signs of ocular
sympathetic paralysis
 The sympathetic symptoms and homolateral pain
of deep, boring, nonpulsatile type in the head or
eye occur without vasomotor or trophic
disturbances
 These signs and symptoms usually appear
suddenly
 The disease appears to be most common in
males, chiefly those of middle age

Paratrigeminal Syndrome (Raeder's Syndrome
Paratrigeminal Neuralgia)
 Paratrigeminal syndrome presents some of the
signs of Homer's syndrome (q.v.), but can be
differentiated from it by the presence of pain and
little or no change in sweating activity on the
affected side of the face
 cause - unknown

Sphenopalatine Neuralgia (Sphenopalatine Ganglion
Neuralgia, Lower-Half Headache, Vidian Nerve
Neuralgia,Atypical Facial Neuralgia, Histamine Cephalgia,
Horton's Syndrome, Periodic Migrainous Neuralgia)
 known as cluster headache
 characterized by attacks of severe, strictly
unilateral pain in the orbital, supra orbital,
temporal or in any combination, often
accompanied by autonomic symptoms such as
eye watering, swelling around the eye, and nasal
congestion

Aetiology
 not understood entirely.
 Its typical periodicity has been attributed to
hypothalamic hormonal influences
 Pain is thought to be generated at the level of the
pericarotid/ cavernous sinus complex.
 This region receives sympathetic and
parasympathetic input from the brainstem, possibly
mediating occurrence of autonomic phenomena
during an attack.
 Cases of this syndrome affecting multiple members
within a single family have been reported, suggesting
that a genetic predisposition may exist in some
individuals.

Clinical Features
 unilateral paroxysms of intense pain in the region of the eyes,
the maxilla, the ear and mastoid, base of the nose, and beneath
the zygoma
 Sometimes, the pain extends into the occipital areas as well.
 rapid onset,
 persist for about 15 minutes to several hours and then disappear
as rapidly as they began
 no 'trigger zone'.
 50% of the patients described their pain as a toothache
 the disease has been referred to as alarm clock headache.
 It may awake individuals from sleep.
 After some weeks or months, the attacks disappear completely
and this period of freedom may persist for months or even years.
 However, there is a frequent subsequent recurrence of
paroxysms.

 Sneezing, swelling of the nasal mucosa and
severe nasal discharge often appear
simultaneously with the painful attacks, as well as
epiphora, or watering of the eyes, and bloodshot
eyes.
 Paresthetic sensations of the skin over the lower
half of the face
 attacks are precipitated in some patients by either
emotional stress or injudicious intake of alcohol.
 Men are affected more commonly than women
(5:1)
 before the age of 40 years.

Treatment
 cocainization of the sphenopalatine ganglion or
alcohol injection
 Resection of the ganglion has been carried out in
some instances as well as surgical correction of
septal defects
 ergotamine will often produce immediate and
complete relief of symptoms. In those cases where it
is not totally effective, combining it with methysergide,
an antiserotonin agent, appears to produce a
synergistic action usually providing total relief.
 All invasive nerve blocks and ablative neurosurgical
procedures have been implemented successfully in
refractory cases.

Burning Mouth Syndrome
 a burning or stinging of the mucosa, lips, and/ or
tongue, in the absence of visible mucosal lesions
 The main symptoms are located in the oral
mucosa with or without involvement of any other
part of the body
 no characteristic laboratory abnormalities
 strong female predilection and most female
patients being postmenopausal
 approximately 50 years
 causes of BMS are multifactorial and remain
poorly understood

Clinical Features
 protracted illness
 burning sensation may be felt either as a continuous or intermittent
discomfort which most frequently affects the tongue and sometimes the
lips or palate
 Other oral mucosal sites may also be involved
 sudden or gradual over months
 psychosomatic factors are associated with the onset of BMS
 No oral mucosal lesions will be detected on examination
 sensation of dry mouth
 increased thirst
 altered taste sensation either with reduction in taste perception or the
presence of a persistent unusual taste, most frequently bitter or metallic
 does not interfere with sleeping
 Drinking or eating may temporarily reduce the severity of symptoms
 associated anxiety or depression.

Treatment
 antidepressants,
 vitamins or dietary supplements such as alpha
lipoic acid;
 analgesic sprays or mouthwashes such as
benzydamine hydrochloride
 in postmenopausal female patients, hormone
replacement or topical oestrogen applied to the
oral mucosa
 saliva substitutes

Orolingual Paresthesia (Glossodynia or
Painful Tongue, Glossopyrosis or 'Burning'
Tongue)
 Paresthesia of the oral mucous membrane is a
common clinical occurrence
 represents a symptom rather than a disease
entity

Tongue)

Tongue)
Clinical Features
 tongue is the most frequent site
 pain, burning, itching, and stinging of the mucous
membranes
 appearance of the tissues is usually normal
 no apparent lesions
 women past the menopause

Tongue)
Treatment
 topical anaesthetics,
 analgesics,
 smooth-and skeletal-muscle relaxants,
 sedatives,
 antibacterial and antifungal agents,
 antihistamines,
 vitamins,
 enzyme digestants,
 CNS stimulants,
 salivary stimulants,
 vasodilators
 sex hormones

Auriculotemporal Syndrome
(Frey's Syndrome, Gustatory
Sweating)
 unusual phenomenon
 result of damage to the auriculotemporal nerve
and subsequent reinnervation of sweat glands by
parasympathetic salivary fibres.

Sweating)
Aetiology
 follows some surgical operation such as removal of a
parotid tumour or the ramus of the mandible, or a
parotitis of some type that has damaged the
auriculotemporal nerve
 After a considerable amount of time following surgery,
during which the damaged nerve regenerates, the
parasympathetic salivary nerve supply develops,
innervating the sweat glands, which then function
after salivary, gustatory or psychic stimulation
 Some cases of gustatory sweating appear to be due
to transaxonal excitation rather than to actual
anatomic misdirection of fibres

Sweating)
Clinical Features
 flushing and sweating of the involved side of the
face, chiefly in the temporal area, during eating
 increased by tart foods
 not a common condition
 always be considered after surgical procedures in
the area supplied by the ninth cranial nerve
Treatment
 intracranial division of the auriculotemporal nerve

DISTURBANCES OF SEVENTH CRANIAL NERVE

Bell's Palsy (Seventh Nerve
Paralysis, Facial Paralysis)
 most common neurologic disorders affecting the
cranial nerves
 abrupt, isolated, unilateral, peripheral facial nerve
paralysis without detectable causes
 most common cause of facial paralysis worldwide
 Bell's palsy is a diagnosis of exclusion

Aetiology
 idiopathic facial paralysis
 an infectious cause - Herpes simplex virus (HSV)
 more than one aetiologic agent with a shared
common pathway leading to facial neuropathy
 Actual pathophysiology is unknown
 A popular theory proposes that the inflammation of
the facial nerve with resultant oedema causes nerve
compression while it passes through the temporal
bone
 Various inflammatory, demyelinating, ischaemic, or
compressive processes may impair neural conduction
at this unique anatomic site.

Clinical Features
 abruptly as paralysis of the facial musculature, usually
unilaterally
 hereditary factors may play a role in the aetiology of
the disease
 Women
 middle-aged
 more frequently in the spring and fall than at other
times of the year
 may develop within a few hours or be present when
the patient awakens in the morning.
 preceded by pain on the side of the face which is
ultimately involved, particularly within the ear, in the
temple or mastoid areas, or at the angle of the jaw

Clinical Features
 muscular paralysis manifests - drooping of the corner
of the mouth, from which saliva may run, the watering
of the eye and the inability to close or wink the eye,
which may lead to infection
 When the patient smiles, the paralysis becomes
obvious, since the corner of the mouth does not rise
nor does the skin of the forehead wrinkle or the
eyebrow raise
 patient has a typical mask like or expressionless
appearance
 Speech and eating usually become difficult and
occasionally the taste sensation on the anterior
portion of the tongue is lost or altered

 mild cases-regresses spontaneously within several
weeks to a month
 Recurrent attacks of facial paralysis, identical with
Bell's palsy, associated with multiple episodes of
nonpitting, non-inflammatory painless oedema of the
face, cheilitis granulomatosa, and fissured tongue or
lingua plicata is known as the Melkersson Rosenthal
syndrome
 The facial oedema resembles angioneurotic oedema
and involves the upper lip, occasionally the lower, and
sometimes the nose, tongue or maxillary alveolar
process.
 The fissured or scrotal -25-40% of cases

Treatment
 no specific treatment for Bell's palsy
 vasodilator drugs, e.g.
 Administration of physiologic flushing doses of
nicotinic acid has produced excellent results
 In permanent paralysis, surgical anastomosis of
nerves has been carried out with some success
 An attempt should be made to prevent infection of
the involved eye

DISTURBANCES OF NINTH CRANIAL NERVE

Glossopharyngeal Neuralgia
 Pain similar to that of trigeminal neuralgia
 not as common as trigeminal neuralgia
 pain may be as severe and excruciating
 rare condition
 characterized by severe, paroxysmal episodes of pain
mainly localized to the external ear canal, pharynx, and
tongue, usually caused by a neurovascular conflict
between postero-inferior cerebellar artery and ninth cranial
nerve
 Sometimes, there is also compression of Vagus nerve(also
termed as vagoglossopharyngeal neuralgia- because of
the pain distribution along the vagal sensory nerve and
may be associated with bradycardia, asystole, mental
confusion, syncope, convulsions, hypotension, and cardiac
arrest)

Clinical Features
 No gender predilection
 middle-aged or older persons
 sharp, shooting pain in the ear, the pharynx, the
nasopharynx, the tonsil, or the posterior portion of the
tongue
 unilateral
 paroxysmal, rapidly subsiding type of pain
characteristic of trigeminal neuralgia is also a feature
here
 Numerous mild attacks may be interspersed by
occasional severe ones
 The patient usually has a 'trigger zone' in the posterior
oropharynx or tonsillar fossa-swallowing, talking,
yawning, or coughing
 The aetiology of glossopharyngeal neuralgia is

Treatment
 resection of the extracranial portion of the nerve
or intracranial section
 Periods of remission with subsequent recurrence
are common in this disease

MISCELLANEOUS DISTURBANCES OF NERVES

Neuritis
 Neuritis is inflammation of the nerve
 traumatic, bacterial, viral or toxic causes
 Symptoms depend on the type of nerve fibres
affected
 If sensory fibres are involved then pain is of the
presenting symptom-pricking or burning type and
localizable one which is often related to the site of
inflammation. It may also produce other sensory
defects like, hyperesthesia, hypoesthesia,
paraesthesia, dysaesthesia or anaesthesia
 If motor fibres are affected, it causes muscular tic,
weakness, or paralysis. The involvement of the
autonomic fibres produces various autonomic
effects.

Neuritis
Types
 include peripheral neuritis, herpes zoster, and post
herpetic neuralgia.
 Trigeminal neuritis most commonly involves alveolar
nerve branches.
 Pain, in and around the teeth, periodontal structures,
and oral mucogingival tissues is the frequent
complaint.
 Weakness and paralysis of masticatory muscles
occur when mandibular division is involved.
 Auriculotemporal neuritis may be mistaken for
masticatory pain.
 Facial nerve neuritis produces facial palsy.
 Glossopharyngeal neuritis is characterized by pain in
the throat, post mandibular, and auricular areas.

Neuritis
Management
 understanding the cause of the inflammation
 Antibiotics or antiviral
 administration of steroids helps in alleviating the
symptoms.

Migraine (Migraine
Syndrome)
 Migraine is a term applied to certain headaches
with a vascular quality
 dominantly inherited disorder characterized by
varying degrees of recurrent vascular headache,
photophobia, sleep disruption, and depression.

Migraine (Migraine
Syndrome)
Aetiology
 not completely understood
 reactive hyperaemia in response to
vasoconstriction-induced ischaemia during aura
 This explained the throbbing quality of the
headache, its varied localization, and the relief
obtained from ergots; however, it does not explain
the prodromal and associated features.

Migraine (Migraine
Syndrome)
Clinical Features
 second decade of life
 common in professional persons
 affect women more than men
 frequency of attacks is extremely variable
 occur at frequent intervals over a period of years or on only
a few occasions during the lifetime of the patient
 A prodromal stage (pre-headache phenomenon) is noted
by some patients, consisting of lethargy and dejection
several hours before the headache
 Visual phenomena such as scintillations, hallucinations or
scotomas are often described
 Other less common prodromal phenomena include vertigo,
aphasia, confusion, unilateral paraesthesia or facial
weakness

Migraine (Migraine
Syndrome)
 The headache phase consists of severe pain in the
temporal, frontal and retro-orbital areas
 pain is usually unilateral, but may become bilateral
and generalized
 deep, aching, and throbbing type
 the patient may appear extremely ill
 The face is usually pale, sallow, and sweaty
 The patient is irritable and fatigued, and the memory
and concentration are impaired
 Anorexia and vomiting as well as a variety of visual
disturbances may occur
 Prolonged and painful contraction of head and neck
muscles is found in some patients.

Migraine (Migraine
Syndrome)
Treatment
 wide variety of drugs ranging from acetylsalicylic
acid and codeine to ergotamine, methysergide
and norepinephrine
 The prognosis of the disease is good, since the
condition is not dangerous and may undergo
complete and permanent remission.

Temporal/Giant Cell
Arteritis
 headache, which is frequently diagnosed erroneously
as 'atypical migraine
 uncommon condition
 focal granulomatous inflammation of arteries,
especially the cranial vessels, although in severe
cases arteries throughout the body may be involved
 The temporal arteries are particularly prone to
develop these lesions
 Occasionally, similar lesions are found throughout the
skeletal muscles related to their vasculature and this
condition has been termed 'polymyalgia arteritica'.

Temporal/Giant Cell
Arteritis
Aetiology
 disease of cellular immunity
 The vasculitic damage is mediated by activated
CD4+ T helper cells responding to an antigen
presented by macrophages
 The primary inflammatory response affects the
internal elastic lamina
 Multinucleated giant cells, which are a histologic
hallmark of this condition, may contain elastic
fibre fragments
 The actual inciting antigen remains unknown, but
elastin remains an important suspect.

Temporal/Giant Cell
Arteritis
Clinical Features
 ages of 55 and 80 years
 women
 slow and insidious or the disease may develop
suddenly with a headache or a burning, throbbing
type of pain, sometimes beginning elsewhere than
over the course of the temporal artery
 A general malaise, chills, fever, weight loss with
anorexia, nausea, and vomiting may precede any
manifestations of pain
 These are sometimes followed by aching and
stiffness of the muscles of the shoulders and hips,
which are often termed as 'polymyalgia rheumatica'.

Temporal/Giant Cell
Arteritis
 pain -frequently localized first in the teeth,
temporomandibular joint, scalp, or occiput
 tiredness, fatigue and pain on repetitive chewing
 there is localized inflammation or cellulitis over the
swollen, nodular, and tortuous artery
 Eye pain, photophobia, diplopia, and even blindness
may accompany the temporal symptoms and
permanent visual loss occurs in 25-50% of patients
 The erythrocyte sedimentation rate is markedly
elevated in the majority of these patients and a mild
leukocytosis may also be found

Temporal/Giant Cell
Arteritis
Histologic Features
 intimal proliferation with resulting luminal
stenosis,
 disruption of the internal elastic lamina by a
mononuclear cell infiltrate,
 invasion and necrosis of the media progressing to
panarteritic involvement by mononuclear cells,
 giant cell formation with granulomata within the
mononuclear cell infiltrate
 less consistently, intravascular thrombosis.

Temporal/Giant Cell
Arteritis
Treatment and Prognosis
 corticosteroid therapy is excellent and clinical
manifestations subside within a few days
 In occasional cases in which there is widespread
systemic vascular involvement, the course of the
disease may be progressively downhill and may
terminate fatally.

Complex Regional Pain Syndrome
(Causalgia, Reflex Sympathetic Dystrophy
Syndrome
 term applied to severe pain which arises after
injury to or sectioning of a peripheral sensory
nerve
 cases do occur after the extraction of teeth

Syndrome
Aetiology
 development of causalgia requires the following
triad of conditions:
1. an injury,
2. an abnormal sympathetic response, and
3. a predisposing personality

Syndrome
Clinical Features
 any age
 usually follows extraction of a multirooted tooth,
particularly when the extraction is difficult or
traumatic
 arises within a few days to several weeks after
the extraction
 typical burning
 develops locally at the site of the injury
 evoked by contact or by application of heat or
cold
 an attack may be elicited not only by actual touch
stimulation but also by emotional disturbances

Syndrome
 Pain may be intensified by
1. application of heat,
2. ingestion of alcohol,
3. during the menstrual periods,
4. when the patient became frustrated or upset

Syndrome
 local pain due to simple traumatic injury to soft
tissue or bone during the extraction procedure
 subacute thyroiditis

Syndrome
Treatment
 difficult one
 resection of the nerves in the retrogasserian
region

Atypical Facial Pain (Atypical
Facial Neuralgia, Facial Causalgia)
 group of conditions
 vague, deep, poorly localized pain in the regions
supplied by the fifth and ninth cranial nerves and the
second and third cervical nerves
 pain is not associated with trigeminal neuralgia,
glossopharyngeal neuralgia, postherpetic neuralgia,
or with diseases of the teeth, throat, nose, sinuses,
eyes, or ears
 distribution of this pain is nonanatomic, since it
involves portions of the sensory supply of two or more
nerves and may cross the midline
 pain, which lacks a trigger zone, is constant and
persists for weeks, months or even years

Aetiology
 without a specific cause
 injury of any peripheral or proximal branch of the
trigeminal nerve due to facial trauma or basal
skull fracture can produce the disorder

Treatment
 tricyclic antidepressants give best results;
 phenytoin is of intermediate effectiveness and
 carbamazepine is least effective

Atypical Odontolgia
 variant of atypical facial pain
 localized only to teeth
 ache, which may be continuous or extreme
sensitivity to thermal change, pressure, or
masticatory force
 localized to one or more teeth

Atypical Odontolgia
 women in the fourth or fifth decades of life.
 The exact cause of this condition is not known
 vascular, neurovascular and psychogenic are
suggested, the latter is most commonly accepted
one. Psychiatric assessment is needed
 Tricyclic antidepressant may be of help in many
patients
 Topical application of capsaicin to the site of the
painful tooth may resolve the symptom to certain
extent.

Horner's Syndrome (Sympathetic
Ophthalmoplegia)
 Horner' s syndrome is a condition characterized
by:
• Miosis, or contraction of the pupil of the eye due
to paresis of the dilator of the pupil.
• Ptosis, or drooping of the eyelid due to paresis of
the smooth muscle elevator of the upper lid.
• Anhidrosis and vasodilatation over the face due to
interruption of sudomotor and vasomotor control.

Horner's Syndrome (Sympathetic
Ophthalmoplegia)
 exact features of the syndrome depend upon the
degree of damage of sympathetic pathways to the
head and the site of this damage
 Preganglionic fibres in the anterior spinal roots to the
sympathetic chain in the low cervical and high
thoracic area are rather commonly involved by
infection, trauma or pressure as by aneurysm or
tumour to produce Homer's syndrome
 Finally, involvement of the carotid sympathetic plexus
by lesions of the gasserian ganglion or an aneurysm
of the internal carotid artery may produce the typical
facial sweating defect as well as facial pain and
sensory loss.

Multiple Sclerosis (Disseminated
Sclerosis)
 idiopathic inflammatory demyelinating disease of
the central nervous system (CNS).
 Patients commonly present with an individual
mixture of neuropsychological dysfunction, which
tends to progress over years.

Sclerosis)
Aetiology
 autoimmune process
 isolated or additive environmental effect and/ or
inadvertent activation and dysregulation of
immune processes by a retroviral infection that
was perhaps acquired in childhood.
 Human herpes virus-6 (HHV-6) and Chlamydia
pneumoniae are implicated as causative agents.
 Polygenic inheritance accounts for a familial rate
of 10-20%

Sclerosis)
Clinical Features
 ages of 20 and 40 years
 female gender predilection (2:1)
 familial incidence
 The disease is characterized by:
1. A variety of ocular disturbances, including visual
impairment as a manifestation of retrobulbar neuritis,
nystagmus, and diplopia
2. Fatigability, weakness, and stiffness of extremities with
ataxia or gait difficulty involving one or both legs
3. Superficial or deep paraesthesia
4. Personality and mood deviation toward friendliness and
cheerfulness
5. Autonomic effect or derangements, such as bladder and/
or rectal retention or incontinence

Sclerosis)
 Charcot' s triad -diagnostic triad characteristic of
multiple sclerosis
1. intention tremor,
2. nystagmus, and
3. dysarthria or scanning speech, an imperfect
speech articulation
 Facial and jaw weakness
 staccato type of speech

Sclerosis)
Treatment
 There is no treatment for MS
 Although remissions of the disease frequently
occur, patients usually follow an ingravescent
course leading to death, often from supervening
infection.

DISEASES OF THE MUSCLES
 Diseases of the skeletal muscles of the face and
oral cavity occur with sufficient frequency
 generalized muscular involvement so that facial
and oral manifestations constitute only a minor
portion of the clinical problem
 Secondary diseases of muscle are seen with
somewhat greater frequency and they also
present difficulties in diagnosis and clinical
management

Dystrophies
 Muscular dystrophy is a primary, progressively
degenerative disease of skeletal muscle.
 The basic disorder lies within the muscle fibre
itself, since the muscular nerves and nerve
endings at the neuromuscular junction are
normal.

Dystrophies
 Actually, a number of different diseases fall within this category,
all characterized by:
1. Symmetric distribution of muscular atrophy
2. Retention of faradic excitability in proportion to the remaining
power of contraction
3. Intact sensibility and preservation of cutaneous reflexes
4. Liability to heredofamilial incidence
5. Unknown aetiology
 The important forms of muscular dystrophy include:
1. Severe generalized familial muscular dystrophy
2. Mild restricted muscular dystrophy
3. Myotonic dystrophy
4. Ophthalmoplegic dystrophy
5. Late distal muscular dystrophy

Severe Generalized Familial Muscular
Dystrophy (Pseudohypertrophic Muscular
Dystrophy of Duchenne)
 rapidly progressive muscle disease
 usually beginning in early childhood,
 presenting strong familial transmission usually
through unaffected females
 occurring predominantly in males with or without
pseudohypertrophy
 most common form of muscular dystrophy

Clinical Features
 before the age of 6 years and rarely after 15 years
 inability to walk or run,
 the children falling readily,
 muscular enlargement and weakness
 muscles of the extremities are generally those first
affected, but even the facial muscles may be involved
 ultimately proceeds to atrophy
 limbs appear flaccid
 waddling gait
 muscles of mastication, facial and ocular muscles, and
laryngeal and pharyngeal muscles are usually involved
only late in the course of the disease

Histologic Features
 There is gradual disappearance of muscle fibres
as the disease progresses
 ultimately no fibres may be recognized
 g replaced entirely by connective tissue and fat
 Persistent fibres show variation in size in earlier
stages of the disease, some being hypertrophic,
but others atrophic

Laboratory Findings
 The serum creatine phosphokinase (CPK) level is
elevated in all males who are affected by this
disease and in about 70% of the female carriers
as well
 CPK elevation occurs prior to the clinical
manifestations of the disease in the males

Treatment
 There is no treatment for this disease
 the disease remains incurable
 die by the time they are 30 years of age, usually
as a result of cardiopulmonary failure

Mild Restricted Muscular Dystrophy
(Facioscapulohumeral Dystrophy,
Landouzy-Dejerine Dystrophy)
 slowly progressive proximal myopathy
 primarily involves the muscles of the shoulder and
face
 has a weak familial incidence
 frequently presents long remissions and sometimes
complete arrests.
Aetiology
 It is an autosomal dominant disease in 70-90% of
patients
 sporadic in the rest
 One of the causative genes has been localized to
chromosome band 4q35

Clinical Features
 2-60 years-majority of cases is in the first two decades of life
 Frequency of occurrence is higher in males
 no familial history can be found
 autosomal dominant trait
 earliest signs of the condition may be inability to raise the arms
above the head and inability to close the eyes even during sleep
as a result of weakness of facial muscles
 lips develop a characteristic looseness and protrusion which
have been described as 'tapir-lips', a part of the 'myopathic
facies', and the patients are unable to whistle or smile
 scapular muscles become atrophic and weak, with subsequent
alteration in posture, as do the muscles of the upper arm
 Cardiac abnormalities including cardiomegaly and tachycardia
are often present and many patients die of sudden cardiac
failure.

Histologic Features
 No specific microscopic findings
 There is some variation in the size of muscle
fibres
 moderate infiltration of fibre bundles by
connective tissue
 Individual fibres ultimately become atrophic

Treatment
 no treatment for the disease
 temporary periods of remission or even complete
arrest
 mild disability
 possibility of cardiac failure is always present.

Myotonias
 failure of muscle relaxation after cessation of
voluntary contraction
 three chief forms:
1. dystrophic,
2. congenital, and
3. acquired myotonia
 Paramyotonia is a disorder related to the other
myotonias, but differing from them in several
important aspects.

Dystrophic Myotonia (Myotonic
Dystrophy Dystrophia Myotonica)
 steadily progressive, familial, distal myopathy with
associated weakness of the muscles of the face,
jaw and neck, and levators of the eyelids, a
tendency for myotonic persistence of contraction
in the affected parts, and testicular atrophy
 autosomal dominant characteristic

Clinical Features
 Atrophy of muscles is a characteristic feature - muscles of the
hands and forearms
 he third decade of life
 Alterations in the facial muscles are one of the prominent
features of the disease
 ptosis of the eyelids and atrophy of the masseter and
sternocleidomastoid muscles
 masseteric atrophy produces a narrowing of the lower half of the
face which, with the ptosis and generalized weakness of the
facial musculature, gives the patient a characteristic 'myopathic
facies' and 'swan neck'
 muscles of the tongue commonly show myotonia but seldom
atrophy
 Pharyngeal and laryngeal muscles in patients with dystrophic
myotonia also exhibit weakness manifested by a weak,
monotonous, nasal type of voice and subsequent dysphagia
 Recurrent dislocation of the jaw is also reported to be common in
this disease

 testicular atrophy, which is so common as to be
considered an integral part of the syndrome;
 Cataracts-even in a high percentage of young
patients;
 hypothyroidism with coldness of extremities, slow
pulse and loss of hair
 functional cardiac changes

Histologic Features
 Enlargement of scattered muscle fibres
 presence of centrally placed muscle nuclei in long
rows
 True hypertrophy of some fibres
 isolated fibres which show extreme degenerative
changes, including nuclear proliferation, intense
basophilic cytoplasmic staining and phagocytosis
 advanced muscular atrophy-fibres appear small
and there may be interstitial fatty infiltration

 progresses inevitably over a period of many
years, producing disability and ultimately death

Congenital Myotonia (Thomsen's
Disease, Myotonia Congenita)
 an anomaly of muscular contraction
 inheritance pattern -25% cases
 an autosomal dominant trait but with incomplete
penetrance in some families
 characteristic feature of the disease is myotonia
associated with muscular hypertrophy

Clinical Features
 early in childhood
 difficulties in learning to stand and walk
 generally severe
 affects all skeletal muscles, especially those of
the lower limbs
 Muscular contraction induces severe, painless
muscular spasms, actually a delay in relaxation
 Electrical or physical stimulation of a muscle
produces characteristic prolonged contraction or
'percussion contraction'

 The muscles are large
 patients with this disease are described as presenting a
Herculean appearance
 muscles of the thighs, forearms and shoulders are
especially affected, as well as the muscles of the neck and
the masseter muscles of the face
 Blinking with strong closure of the eyes will sometimes
produce a prolonged contraction of the lids
 Spasms of the extraocular muscles may lead to
convergent strabismus.
 Interestingly, a sudden movement such as sneezing often
produces a prolonged spasm of the muscles of the face,
tongue, larynx, neck and chest, and there may be
respiratory embarrassment
 A subjective increase in disability following exposure to
cold has been described by many patients with this
disease

Histologic Features
 Muscle biopsy reveals no alterations from normal
except for hypertrophy of all muscle fibres.
 There is no specific treatment of the disease, but
the prognosis is good
 some regression of the disease occurs in
occasional patients

Acquired Myotonia
 spasms of muscles
 more intense than those occurring in typical
myotonia.
 If these spasms are intermittent, the condition is
called clonus (myoclonic contractions);
 if constant, the term trismus is applied (myotonic
contractions)

Acquired Myotonia
 Spasm involving the facial muscles is seen in a
variety of situations such as epilepsy, diseases of
the CNS and tetany
 Such spasms on a local basis are far more
common; and these occur in a variety of
conditions such as pericoronal infection,
especially of third molars; infectious myositis; and
hysteria (hysterical trismus)
 The spasms, which are usually painful, may be
transitory or may persist for a period of several
days or until the cause of the disease is treated

Hemifacial Spasm (Facial
Myoclonus, Facial Dystonia)
 repeated, rapid, painless, irregular, non-rhythmic,
uncontrollable, and unilateral contractures of the
facial muscles
 adults, chiefly women
 cause – unknown
 appears to be a peripheral facial nerve lesion
 may be compression of the facial nerve in the
facial canal adjacent to the stylomastoid foramen

Clinical Features
 usually begins in the periorbital muscles, but soon
spreads to the entire half-face
 brief transitory twitching, but may progress to
sustained spasms
 triggered by fatigue, tension or facial activity
 brief duration, usually only a few seconds
 continue through sleep and even awaken the patient
 long-standing hemifacial spasm-mild facial
contracture as well as lid closure and lip pursing may
occur
 Hemifacial spasm must be differentiated from
emotional tics and focal convulsive seizures

 decompression of the facial nerve
 progressive, nonfatal illness

Periodic Paralyses (Paramyotonia
Congenita)
 episodes of flaccid muscle weakness occurring at
irregular intervals
 hereditary
 more episodic than periodic
 They can be divided conveniently into primary and
secondary disorders
 General characteristics of primary PP include the
following:
1. They are hereditary
2. Most are associated with alteration in serum
potassium levels
3. Myotonia sometimes coexists
4. Both myotonia and PP result from defective ion
channels

Congenita)
Clinical Features
 cramping, stiffness and weakness of the muscles
of the face and neck, fingers and hands upon
exposure to cold
 eyelids are closed
 face assumes a mask-like appearance
 tongue may exhibit a similar cramping after
drinking cold liquids
 speech becomes slurred
 myotonia of the tongue may be induced by
percussion
 weakness may persist for several days

Congenita)
Histologic Features
 There are no significant histologic changes in
muscle fibres.
 There is no specific treatment for paramyotonia,
but the prognosis is excellent with frequent
improvement during adult life.

Hypotonia
 reduction or complete absence of tonus in
muscles
 many causes of hypotonia and delay in motor
development in infants
 this condition should be regarded only as a
symptom which may be found in many diseases

Hypotonia
 Certain congenital diseases may result in
hypotonia, such as:
• Diseases of the central nervous system (e.g.
atonic diplegia)
• Lipoid and glycogen storage diseases (e.g. Tay-
Sachs disease)
• Mongolism
• Cretinism
• Achondrodysplasia

Hypotonia
 Hypotonia also may result from strictly
neuromuscular diseases including:
• Infantile muscular atrophy
• Infantile muscular dystrophy
• Amyotonia congenita
• Congenital nonprogressive myopathy
• Neonatal myasthenia gravis

Hypotonia
 Many of these latter diseases, all occurring in infancy,
have certain features in common, including hypotonia,
reduced tendon reflexes, and muscular weakness
 Because of the difficulty encountered in their
separation, the term 'floppy infant syndrome' has
sometimes been applied to describe the chief clinical
manifestation of these unfortunate children
 infants have a generalized weakness so that their
bodies hang limply with inability to sit, stand or walk
 hypotonia involves the muscles of the face and
tongue as well, but these findings are secondary to
the generalized condition

Myasthenia
 Myasthenia is an abnormal weakness and fatigue
in muscle following activity
 constitute a group of diseases in which there is a
basic disorder of muscle excitability and
contractility
1. myasthenia gravis,
2. familial periodic paralysis, and
3. aldosteronism

Myasthenia Gravis
 acquired autoimmune disorder
 weakness of skeletal muscles and fatigability of
striated muscles on exertion
Aetiology
 idiopathic in most patients
 autoimmunity
 The antibodies in myasthenia gravis are directed
toward the acetylcholine receptor (at the
neuromuscular junction of skeletal muscles)

Myasthenia Gravis
Clinical Features
 adults –middle age group
 predilection for women
 rapidly developing weakness in voluntary muscles
following even minor activity
 muscles of mastication and facial expression are
involved before any other muscle group
 difficulty in mastication and in deglutition and
dropping of the jaw
 Speech is often slow and slurred

Myasthenia Gravis
Clinical Features
 Disturbances in taste sensation occur in some
patients
 Diplopia and ptosis, along with dropping of the
face, lend a sorrowful appearance to the patient
 neck muscles may be so weak that the head
cannot be held up without support
 Patients with this disease rapidly become
exhausted, lose weight, become further
weakened and may eventually become bedfast
 Death frequently occurs from respiratory failure

Myasthenia Gravis
 Some patients enter an acute exacerbation of
their disease and succumb very shortly, but
others live for many years with only the slightest
evidence of disability
 On this basis, two forms of the disease are now
recognized:
1. steadily progressive type
2. a remitting, relapsing type

Myasthenia Gravis
Histologic Features
 no demonstrable changes in the muscle
 Occasionally, focal collections of small
lymphocytes, or 'lymphorrhages', are found
surrounding small blood vessels in the interstitial
tissue of affected muscles
 few cases-foci of atrophy or necrosis of muscle
fibres

Myasthenia Gravis
Treatment
 drug of choice used in treatment of myasthenia
gravis & the diagnostic test for the disease-
Physostigmine, an anticholinesterase,
administered intramuscularly, improves the
strength of the affected muscles in a matter of
minutes
 No 'cure' for the disease is known, even though
the prognosis is good in the relapsing type.

Myositis
 inflammation of muscle tissue
 entirely non-specific, since a great many
bacterial, viral, fungal or parasitic infections, as
well as certain physical and chemical injuries may
give rise to the condition
 a variety of diseases of unknown aetiology may
produce or at least be associated with myositis

Dermatomyositis (juvenile Dermatomyositis,
Childhood Dermatomyositis, Polymyositis)
 idiopathic inflammatory myopathy (IIM) with
characteristic cutaneous findings (5 findings)
1. progressive proximal symmetrical weakness,
2. elevated muscle enzymes,
3. an abnormal finding on electromyograph
4. an abnormal finding on muscle biopsy
5. compatible cutaneous disease

Aetiology
 cause – unknown
 DM is probably caused by complement-mediated
(terminal attack complex) vascular inflammation,
while proliferative myositisis caused by the direct
cytotoxic effect of CD8+ lymphocytes on muscle

Clinical Features
 the fifth decade of life
 no sex predilection
 more acute form of the disease-more commonly
in children,
 erythematous skin eruption, oedema, tenderness,
swelling, and weakness of the proximal muscles
of the limbs
 skin lesions frequently calcify and form calcium
carbonate nodules with a foreign body reaction
 known as calcinosis cutis, whereas the term
calcinosis universalis is applied when these
calcified masses are found generalized

 The chronic form of the disease is similar, but may not
show dermal involvement (polymyositis only)
 Raynaud' s phenomenon or paroxysmal digital
cyanosis may be an early manifestation
 muscular stiffness and weakness are often symmetric
in distribution
 cutaneous lesions usually consist of a diffuse
erythema with desquamation, although other types of
rashes have been described
 rash is most frequently seen on the face, eyelids,
ears, anterior neck, and overlying articulations

Oral Manifestations
 diffuse stomatitis and pharyngitis, are extremely
common
 Telangiectatic lesions of the vermilion border of
the lips and cheeks may also occur
 involvement of the muscles of the jaws, tongue,
and pharynx may pose problems in eating and
phonation

Histologic Features
 muscle fibres in OM exhibit widespread degeneration
and hyalinization
 advanced cases the muscle fibres disappear, leaving
only the fibrous stroma
 Many fibres show vacuolization, granulation, and
fragmentation with phagocytosis of disintegrating
fibres
 Diffuse leukocytic infiltration is also frequently
pronounced
Laboratory Findings
 mild anaemia or leukocytosis
 creatinuria is a constant finding
 elevated levels of serum transaminase and aldolase

Treatment
 no specific treatment for the disease
 symptomatic treatment may be of considerable
benefit to the patient
 more acute forms of the disease, death may
occur rapidly
 other cases, there may be recovery, sometimes
with a residual disability

Heterotopic Ossification
 The term heterotopic ossification describes bone
formation at an abnormal anatomical site, usually
in soft tissue
 three types:
1. myositis ossificans progressiva
2. traumatic myositis ossificans
3. neurogenic heterotopic ossification

Myositis Ossificans
Progressiva
 unknown aetiology
 affects the interstitial tissues of muscles as well
as tendons, ligaments, fascia, aponeuroses and
even the skin
 Basically, masses of fibrous tissue and bone
occur within these structures with secondary
atrophy
 destruction of the associated muscles due to
pressure and inactivity

Myositis Ossificans
Progressiva
Clinical Features
 young children or adolescents
 development of soft, fluctuant or firm nodular
swellings anywhere on the body but frequently on
the neck or back
 may develop spontaneously or after minor trauma
 vary considerably in size and shape
 may disappear or become transformed into bony
nodules
 usually painless
 covered by a reddened skin which may ulcerate
as a result of pressure from the underlying mass

Myositis Ossificans
Progressiva
 skeletal muscle of the trunk and proximal limbs
are most frequently involved
 certain muscles tend to escape involvement: the
tongue, larynx, diaphragm, and perineal muscles
 entire groups of muscles become transformed
into bone with resulting limitation of movement
 masseter muscle is often involved so that fixation
of the jaw occurs
 patient becomes transformed into a rigid
organism sometimes encountered in circuses as
the 'petrified man'

Myositis Ossificans
Progressiva
Differential diagnosis
 calcinosis universalis, which usually occurs in
relation to scleroderma or polymyositis
 In calcinosis, calcium deposition is noted in the
skin, subcutaneous tissues, and connective
tissue sheaths around muscles, as opposed to
within muscles.

Myositis Ossificans
Progressiva
Histologic Features
 The muscle is gradually replaced by connective
tissue which undergoes osteoid formation and
subsequently ossification
 In some cases cartilage formation may also be
evident
 Characteristically, intact muscle fibres may be
found within the bony tissue

Myositis Ossificans
Progressiva
 no treatment for the disease
 It is progressive until death results, usually from a
pulmonary infection secondary to the respiratory
difficulties arising from involvement of the
intercostal muscles

Traumatic Myositis
Ossificans
 painful area develops in muscle or soft tissue
following a single blow to the area, a muscle tear,
or repeated minor trauma
 gradually develops masses of cartilaginous
consistence
 within 4-7 weeks, a solid mass of bone can be felt
 Common sites include the pectoralis major,
biceps, and thigh muscles
 A non-traumatic type of myositis ossificans also
may exist

Traumatic Myositis
Ossificans
 The exact mechanism of the ossification is not entirely clear
 Possible theories have include the following:
1. Traumatization of the periosteum of an adjacent bone with the
displacement of osteoblasts into the muscle and subsequent
formation of bone
2. Activation of periosteal implants already present in muscle by
trauma or haemorrhage
3. Metaplasia of the pluripotential intermuscular connective tissue
into bone
4. Metaplasia of fibrocartilage, a normal constituent of many
muscle tendons, into bone
 It is recognized that this typical ossifying lesion can occur in
superficial tissue away from muscle and is termed as 'fasciitis
ossificans'.

Traumatic Myositis
Ossificans
Clinical Features
 Acute cases-firm, painful mass in the injured
muscle within 1-4 weeks
 motion is limited
 Chronic cases of myositis ossificans are usually
asymptomatic and may be discovered
accidentally
 mild discomfort associated with a progressive
limitation of motion

Traumatic Myositis
Ossificans
Oral Manifestations
 muscles of the face- the masseter and temporal
muscles occurs usually following a single acute
traumatic injury
 Growth of the calcified lesions is rapid
 when the maximum size is obtained, the lesion
remains static or even diminishes in size
 Some difficulty in opening the mouth may be
experienced by patients with myositis ossificans
of the masseter muscle

Traumatic Myositis
Ossificans
Radiographic Features
 may appear either as a feathery type of
calcification in muscle, following ossification of a
haematoma which dissected along muscle
bundles, or as a solitary irregular calcified mass
occurring in a simple haematoma
 radiopaque calcification may be first seen within
two to three weeks of the traumatic experience
and show a progressive increase in radiodensity

Traumatic Myositis
Ossificans
Histologic Features
 varying stages from haemorrhage, degeneration of
muscle and connective tissue hyperplasia to
chondrification and, ossification
 The osteoid and bone trabeculae formed often trap
viable muscle fibres, but these may ultimately
disappear
 trabecular pattern is often extremely bizarre, and with
the cartilage and myxomatous tissue present may
resemble callus formation
 The more mature tissue is usually found on the
periphery of the lesion
 rapidly proliferating bony tissue often produces a
sufficiently atypical microscopic picture to confuse the
lesion with osteosarcoma

Traumatic Myositis
Ossificans
 surgical excision
 Recurrence has been reported in some cases,
but this is not characteristic
 prognosis is good, since the lesion is a localized
and inflammatory one

Neurogenic Heterotopic
Ossification
 fairly common sequela of spinal cord injury,
especially after traumatic cord injury
 also has been described with lesser frequency in
other severe neurologic disorders (e.g. closed
head injuries, stroke, encephalitis, polio, tetanus,
tabes dorsalis, syringomyelia, and anoxic
encephalopathy) as well as following severe
burns

Proliferative Myositis
 a pseudosarcomatous process of muscle
characterized by an ill-defined proliferation of
basophilic giant cells and fibroblasts chiefly
involving the perimysium, epimysium and
neighbouring fascia
 mechanical trauma may play a role in the
development of proliferative myositis, there may
be other causes as well.

Clinical Features
 early 20s to the early 80s, with a median age of
50 years
 Males
 a firm solitary nodule that is deep-seated and not
attached to overlying skin
 grows rapidly, but is seldom tender or painful

Histologic Features
 poorly demarcated fibroblastic proliferation
involving the epimysium, perimysium, and
endomysium and by the presence of large,
basophilic giant cells resembling ganglion cells or
rhabdomyoblasts
 process affects primarily stromal tissue and
leaves muscle fibres virtually uninvolved
 never complete replacement of muscle tissue
over a large circumscribed area

Treatment
 Proliferative myositis is treated by simple local
excision and has no tendency to recur.

Focal Myositis
 benign inflammatory pseudotumour of skeletal
muscle
 actual aetiology is unknown, but even though a
history of trauma is absent in most cases, it is
speculated that a subclinical injury, such as a
muscle tear, might initiate the condition

Focal Myositis
Clinical Features
 rapidly enlarging mass within a single skeletal
muscle
 lower leg, thorax, abdomen, and forearm;
however, involvement of perioral musculature and
submandibular and buccal mucosa
 no apparent gender predilection
 age range has been from 10 to over 65 years of
age
 While lesions have a duration of only a few
weeks, some lesions are present a year or longer
 Some cases are asymptomatic; others are
characterized by a dull and aching pain

Focal Myositis
Histologic Features
 There are microscopic changes in random muscle
fibres, rather than grouped bundles, consisting of
atrophy, hypertrophy, necrosis with phagocytosis,
and regeneration
 Lymphocytic infiltration is usually present in the
interstitial tissue, as is an increase in fibrous
connective tissue in endomysial and perimysial
locations

Focal Myositis
 benign or malignant neoplasm within muscle
 nodular fasciitis
 proliferative myositis
 myositis ossificans
 Polymyositis
 in the oral region, a salivary gland lesion
Treatment
 The lesion should be excised; it does not recur.

Diseases of nerves and muscles of oral cavity

Diseases of nerves and muscles of oral cavity

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