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Contents

. Summary ............................................... . Definition ..............................................

. History ...................................................

. Overview of Currently Used

Classification Systems and Terminology

. Currently Used Terms in Classification

of Osteomyelitis of the Jaws ..................

.. Acute/Subacute Osteomyelitis .... ..... .... .

.. Chronic Osteomyelitis .... .... ..... .... ..... .... .

.. Chronic Suppurative Osteomyelitis:

Secondary Chronic Osteomyelitis ..... .... .

.. Chronic Non-suppurative Osteomyelitis

.. Diffuse Sclerosing Osteomyelitis,

Primary Chronic Osteomyelitis,

Florid Osseous Dysplasia,

Juvenile Chronic Osteomyelitis .... .... .... .

.. SAPHO Syndrome, Chronic Recurrent

Multifocal Osteomyelitis (CRMO) .... .... ...

.. Periostitis Ossificans,

Garrès Osteomyelitis ............ .............. ...

.. Other Commonly Used Terms ..... .... .... ...

. Osteomyelitis of the Jaws:

The Zurich Classification System ...........

.. General Aspects of the ZurichClassification System ............ ............. ....

.. Acute Osteomyelitis and Secondary

Chronic Osteomyelitis ............ ............. ..

.. Clinical Presentation .................. ...........

.. Primary Chronic Osteomyelitis .... .... .... ..

. Differential Diagnosis ............................

.. General Considerations ..... .... ..... .... ..... ..

.. Differential Diagnosis of Acute

and Secondary Chronic Osteomyelitis ...

.. Differential Diagnosis of Primary

Chronic Osteomyelitis ............. ..............

2.1 Summary

Osteomyelitis o the jaws is still a airly common dis-ease in maxilloacial clinics and oces, despite the

introduction o antibiotics and the improvement o

dental and medical care. Te literature on this disease

is extensive. Dierent terminologies and classication

systems are used based on a variety o eatures such as

clinical course, pathological–anatomical or radiological

eatures, etiology, and pathogenesis. A mixture o these

classication systems has occurred throughout the liter-

ature, leading to conusion and thereby hindering com-

parative studies. An overview o the most commonly

used terms and classication systems in osteomyelitis o

the jaws is given at the beginning o this chapter.Te Zurich classication system, as advocated in this

textbook, is primarily based on the clinical course and

appearance o the disease as well as on imaging studies.

Subclassication is based on etiology and pathogenesis o

the disease. Mainly three dierent types o osteomyelitis

are distinguished: acute and secondary chronic osteo-

myelitis and primary chronic osteomyelitis. Acute and

secondary chronic osteomyelitis are basically the same

disease separated by the arbitrary time limit o 1 month

aer onset o the disease. Tey usually represent a true

bacterial inection o the jawbone. Suppuration, stulaormation, and sequestration are characteristic eatures

o this disease entity. Depending on the intensity o the

inection and the host bone response, the clinical pre-

sentation and course may vary signicantly. Acute and

secondary chronic osteomyelitis o the jaws is caused

mostly by a bacterial ocus (odontogenic disease, pulpal

and periodontal inection, extraction wounds, oreign

bodies, and inected ractures).

Primary chronic osteomyelitis o the jaw is a rare,

nonsuppurative, chronic infammation o an unknown

cause. Based on dierences in age at presentation,

5

2Osteomyelitis of the Jaws:

Definition and Classification

Marc Baltensperger and Gerold Eyrich



clinical appearance and course, as well as radiology and

histology, the disease may be subclassied into early-

and adult-onset primary chronic osteomyelitis. Cases

with purely mandibular involvement are urther distin-

guished rom cases associated with extragnathic derma-

toskeletal involvement such as in SAPHO syndrome or

chronic recurrent multiocal osteomyelitis (CRMO).

2.2 Definition

Te word “osteomyelitis” originates rom the ancient

Greek words osteon (bone) and muelinos (marrow)

and means inection o medullary portion o the bone.

Common medical literature extends the denition to an

infammation process o the entire bone including the

cortex and the periosteum, recognizing that the patho-

logical process is rarely conned to the endosteum. Itusually encompasses the cortical bone and periosteum as

well. It can thereore be considered as an infammatory

condition o the bone, beginning in the medullar cavity

and havarian systems and extending to involve the pe-

riosteum o the aected area. Te inection becomes es-

tablished in calcied portion o the bone when pus and

edema in the medullary cavity and beneath the perios-

teum compromises or obstructs the local blood supply.

Following ischemia, the inected bone becomes necrotic

and leads to sequester ormation, which is considered a

classical sign o osteomyelitis (opazian 1994, 2002).

Although other etiological actors, such as traumaticinjuries, radiation, and certain chemical substances,

among others, may also produce infammation o the

medullar space, the term “osteomyelitis” is mostly used

in the medical literature to describe a true inection o

the bone induced by pyogenic microorganisms (Marx

1991).

2.3 History

Te prevalence, clinical course, and management o os-

teomyelitis o the jawbones have changed prooundly

over the past 50 years. Tis is due to mainly one actor:

the introduction o antibiotic therapy, specically peni-

cillin. Te integration o antibiotics into the therapeu-

tic armamentarium has led to a complete renaissance

in the treatment o most inectious diseases, including

osteomyelitis (Hudson 1993). Further actors, such as

sophistication in medical and dental science as well as

the widespread availability or adequate treatment, have

additionally led to improvement in the management o this disease. Modern diagnostic imaging allows much

earlier treatment o bone inections at a more localized

stage.

In the preantibiotic era, the classical presentation o

jawbone osteomyelitis was an acute onset, usually ol-

lowed by a later transition to a secondary chronic pro-

cess (Wassmund 1935; Axhausen 1934). Massive clinical

symptoms with widespread bone necroses, neoosteo-

genesis, large sequester ormation, and intra- and ex-

traoral stula ormation were common presentations,

sometimes leading to signicant acial disgurement

(Fig. 2.1).Aer the introduction o antibiotics, acute phases

were oen concealed by these antimicrobial drugs with-

out ully eliminating the inection. Subacute or chronic

Fig. .a–c. Elder case o advanced secondary chronic

osteomyelitis o the let mandible. The massive aec-

tion o the let mandible demonstrates extraoral istula

and scar ormation (a). Intraoral view o the same patient

with large exposure o inected bone and sequestra (b).

Large sequester collected rom surgery (c) (Courtesy o

N. Hardt)

2

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Marc Baltensperger, Gerold Eyrich



orms o osteomyelitis have thereore become more

prominent, lacking an actual acute phase (Becker 1973;

Bünger 1984).

2.4 Overview of Currently Used

Classification Systemsand Terminology

One o the rst widely accepted staging systems or os-

teomyelitis in long bones was rst described by Wald-

vogel and Medo (1970) and Waldvogel et al. (1970a,b).

Te authors distinguished three categories o osteomy-

elitis: osteomyelitis rom hematogenous spread; rom a

contagious ocus; and due to vascular insuciency. Te

classication is primarily based on etiology and patho-

geneses o inection and does not readily lend itsel to

guiding therapeutic strategies such as surgery and an-

tibiotic therapy. A more comprehensive classication

proposed by Cieny et al. (1985) and Mader and Calhoun

(2000) is based upon the anatomy o the bone inec-

tion and the physiology o the host. It divides the dis-

ease into our stages combining our anatomical disease

types and three physiological host categories resultingin the description o 12 discrete clinical stages o osteo-

myelitis. Such a classication system, although it may be

important in dealing with numerous sites o the skeletal

system and allowing stratication o inection and the

development o comprehensive treatment guidelines or

each stage, is unnecessarily complex and impractical

when dealing with inections o the jawbones.

Because o its unique eature bearing teeth and

hence connecting to the oral cavity with the periodontal

membrane, osteomyelitis o the jaws diers in several

Table .. Classiication systems described in the literature or osteomyelitis o the jaws

Reference Classification Classification criteria

Hudson JW

Osteomyelitis o the jaws: a 50-year

perspective.

J Oral Maxillofac Su rg 1993 Dec;

51(12):1294-301

I. Acute orms o osteomyelitis (suppura-

tive or nonsuppurative)

A. Contagious ocus

1. Trauma

2. Surgery

3. Odontogenic Inection

B. Progressive

1. Burns2. Sinusitis

3. Vascular insuciency

C. Hematogenous(metastatic)

1. Developing skeleton (children)

II. Chronic orms o osteomyelitis

A. Recurrent multiocal

1. Developing skeleton (children)

2. Escalated osteogenic (activity

< age 25 years)

B. Garrè's

1. Unique prolierative

subperiosteal reaction

2. Developing skeleton (children

and young adults)C. Suppurative or nonsuppurative

1. Inadequately treated orms

2. Systemically compromised

orms

3. Reractory orms (chronic recur-

rent multiocal osteomyelitis

CROM)

D. Diuse sclerosing

1. Fastidious microorganisms

2. Compromised host/pathogen

interace

Classication based on clinical picture and

radiology.

The two major groups (acute and

chronic osteomyelitis) are dierenti-

ated by the clinical course o the

disease ater onset, relative to surgi-

cal and antimicrobial therapy. The

arbitrary time limit o 1 month is usedto dierentiate acute rom chronic

osteomyelitis (Marx 1991; Mercuri1991;

Koorbusch1992).

2

7

Osteomyelitis of the Jaws: Definition and Classification





Hudson JW


perspective.

J Oral Maxillofac Surg 1993

Dec;51(12):1294-301

I. Hematogenous osteomyelitis

II. Osteomyelitis secondary to a contigu-

ous ocus o inection

III. Osteomyelitis associated with or with-

out peripheral vascular disease

Classication based on pathogenesis.

From Vibhagool 1993

Hudson JW


perspective.

J Oral Maxillofac Surg 1993

Dec;51(12):1294-301

I. Anatomic Types

Stage I: medullar osteomyelitis –

involved medullar bone without

cortical involvement; usually

hematogenous

Stage II: supercial osteomyelitis –

less than 2 cm bony deect without

cancellous bone

Stage III: localized osteomyeli-

tis – less than 2 cm bony deect on

radiograph, deect does not appear

to involve both corticesStage IV: diuse osteomyelitis – de-

ect greater than 2 cm. Pathologic

racture, inection, nonunion

II. Physiological class

A host: normal host

B host: systemic compromised host,

local compromised host

C host: treatment worse than disease

Dual classication based on pathological

anatomy and pathophysiology

From Vibhagool 1993 and Cierny 1985

Mittermayer CH

Oralpathologie.

Schattauer, Stuttgart-New York 1976

I. Acute suppurative osteomyelitis (rar-

eactional osteomyelitis)

II. Chronic suppurative osteomyelitis

(sclerosing osteomyelitis)

III. Chronic ocal sclerosing osteomyelitis(pseudo-paget, condensing osteomy-

elitis)

IV. Chronic diuse sclerosing osteomyeli-

tis

V. Chronic osteomyelitis with proli-

erative periostitis (Garrè's chronic

nonsuppurative sclerosing osteitis,

ossiying periostitis)

VI. Specic osteomyelitis

1. Tuberculous osteomyelitis

2. Syphilitic osteomyelitis

3. Actinomycotic osteomyelitis

Classication based on clinical picture,

radiology, pathology, and etiology

important aspects rom osteomyelitis o long bones.

Te specic local immunological and microbiological

aspects determine a major actor in the etiology and

pathogenesis o this disease, and hence also have a di-

rect impact on its treatment; thereore, to extrapolate

rom long bone inections to disease o the jaws is only

possible with limitations. Tis is refected by the long-

standing recognition o osteomyelitis o jawbones as a

clinical entity, which diers in many important aspects

rom the one ound in long bones; hence, a wide vari-

ety o classications, specically or the jawbones, have

been established by several authors in the medical lit-

erature. Classications proposed are based on dierent

aspects such as clinical course, pathological–anatomical

2

8




and/or radiological eatures, etiology, and pathogenesis.

A mixture o these classication systems has been used

in many instances, leading to conusion and thereby

hindering comparative studies and obscuring classica-

tion criteria. An overview o the most commonly cited

classications o jawbone osteomyelitis are listed in

ables 2.1–2.4.



Hjorting-Hansen E

Decortication in treatment o osteomy-

elitis o the mandible.

Oral Surg Oral Med Oral Pathol 1970

May;29(5):641-55

I. Acute/subacute osteomyelitis

II. Secondary chronic osteomyelitis

III. Primary chronic osteomyelitis


radiology

Marx RE

Chronic Osteomyelitis o the Jaws

Oral and Maxillofacial Surgery Clinics

of North America, Vol 3, No 2, May 91,

367-81

Mercuri LG

Acute Osteomyelitis o the Jaws

Oral and Maxillofacial Surgery Clinics

of North America, Vol 3, No 2, May 91,

355-65

I. Acute osteomyelitis

1. Associated with Hematogenous

spread*

2. Associated with intrinsic bone

pathology or peripheral vascular

disease*

3. Associated with odontogenic and

nonodontogenic local processes*

II. Chronic osteomyelitis

1. Chronic recurrent multiocal osteo-

myelitis o children

2. Garrè's osteomyelitis3. Chronic suppurative osteomyelitis

– Foreign body related

– Systemic disease related

– Related to persistent or resis-

tant organisms

4. True chronic diuse sclerosing

osteomyelitis


radiology, etiology, and pathophysiology

Classication o acute osteomyelitis by

Mercuri, classication o chronic os-

teomyelitis by Marx. The arbitrary time

limit o one month is used to dier

acute rom chronic osteomyelitis

* From Waldvogel and Medo 1970

Panders AK, Hadders HN

Chronic sclerosing infammations o

the jaw. Osteomyelitis sicca (Garre),

chronic sclerosing osteomyelitis with

ne-meshed trabecular structure, and

very dense sclerosing osteomyelitis.Oral Surg Oral Med Oral Pathol 1970

Sep;30(3):396-412

I. Primarily chronic jaw infammation

1. Osteomyelitis sicca (synonymous

osteomyelitis o Garrè, chronic

sclerosing nonsuppurative

osteomyelitis o Garrè, periostitis

ossicans)2. Chronic sclerosing osteomyelitis

with ne-meshed trabecular

structure

3. Local and more extensive very

dense sclerosing osteomyelitis

II. Secondary chronic jaw infammation

III. Chronic specic jaw infammations

– Tuberculosis

– Syphilis

– Lepra

– Actinomycosis


radiology

Classication o chronic osteomyelitis

orms only

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9






Schelhorn P, Zenk W

[Clinics and therapy of the osteomyelitis

of the lower jaw ].

Stomatol DDR 1989 Oct;39(10):672-6

I. Acute osteomyelitis

II. Secondary chronic osteomyelitis

III. Primary chronic osteomyelitis

IV. Special orms

– Osteomyelitis sicca (pseudo-paget

Axhausen)

– Chronic sclerosing osteomyelitis

Garrè

Classication based on clinical picture

Topazian RG

Osteomyelitis of the Jaws. In Topizan RG,

Goldberg MH (eds): Oral and Maxillofa-

cial Infections.

Philadelphia, WB Saunders 1994,

Chapter 7, pp 251-88

I. Suppurative osteomyelitis

1. Acute suppurative osteomyelitis

2. Chronic suppurative osteomyelitis

– Primary chronic suppurative osteo-

myelitis

– Secondary chronic suppurative

osteomyelitis

3. Inantile osteomyelitis

II. Nonsuppurative osteomyelitis1. Chronic sclerosing osteomyelitis

– Focal sclerosing osteomyelitis

– Diuse sclerosing osteomyelitis

2. Garrè's sclerosing osteomyelitis

3. Actinomycotic osteomyelitis

4. Radiation osteomyelitis and necro-

sis

Classication based on clinical picture,

radiology, and etiology

(specic orms such as syphilitic,

tuberculous, brucellar, viral, chemi-

cal, Escherichia coli and Salmonella

osteomyelitis not integrated in clas-

sication)

Bernier S, Clermont S, Maranda G,

Turcotte JY

Osteomyelitis of the jaws.

J Can Dent A ssoc 1995 May;61(5): 441-2,

445-8

I. Suppurative osteomyelitis

1. Acute suppurative osteomyelitis

2. Chronic suppurative osteomyelitis

II. Nonsuppurative osteomyelitis

1. Chronic ocal sclerosing osteomy-

elitis2. Chronic diuse sclerosing osteo-

myelitis

3. Garrè's chronic sclerosing osteomy-

elitis (prolierative osteomyelitis)

III. Osteoradionecrosis


radiology

Wassmund M

Lehrbuch der praktischen Chirurgie

des Mundes und der Kieer.

Meusser, Leipzig 1935

I. Exudative osteitis

II. Resorptive osteitis

III. Productive osteitis

IV. Acute necrotizing osteitis (osteomyeli-

tis)

V. Chronic osteomyelitis

1. Chronic course o an acute osteo-

myelitis

2. Occult osteomyelitis

3. Chronic necrotizing osteomyelitis

with hypertrophy

4. Chronic exudative osteomyelitis

5. Productive osteomyelitis


radiology

(note that classication was devel-

oped beore introduction o antibiotic

therapy)

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2.5 Currently Used Terms

in Classification of Osteomyelitis

of the Jaws

2.5.1 Acute/Subacute Osteomyelitis

Although acute orms o osteomyelitis are seen only rarely these days, most authors in common medical lit-

erature still describe this orm as an entity o its own.

Mercuri (1991) and Marx (1991) arbitrarily dened the

time element as being 1 month aer onset o symptoms.

Endurance past this arbitrary set time limit is then con-

sidered as chronic osteomyelitis refecting the inability

o host deense mechanisms to eradicate the responsible

pathogen. Many authors have agreed on this classica-

tion and have used the term likewise in their publica-

tions (Koorbusch et al. 1992; Hudson 1993; Schuknecht

et al. 1997; Schuknecht and Valavanis 2003; Eyrich et al.1999; Baltensperger et al. 2004).

Te term “subacute osteomyelitis” is not clearly de-

ned in the literature. Many authors use the term in-

terchangeably with acute osteomyelitis, and some use

it to describe cases o chronic osteomyelitis with more

prominent (subacute) symptoms. In some instances,

subacute osteomyelitis is reerred to as a transitional

stage within the time rame o acute osteomyelitis and

corresponds to the third and ourth week aer onset o

symptoms (Schuknecht et al. 1997; Schuknecht and Va-

lavanis 2003).

2.5.2 Chronic Osteomyelitis

Te classication o chronic osteomyelitis is incoherent

and conusing. Dierent disease processes have been

described by this one term in some instances, whereas

several terms have been designated or lesions that rep-

resent the same entity in other instances (Groot et al.

1996; Eyrich et al. 1999).

Many authors agree that chronic osteomyelitis in-

volving the jawbone may be divided in two major cat-egories: suppurative and nonsuppurative orms (Mit-

termayer 1976; Hudson 1993; opazian 1994, 2002;

Bernier et al. 1995).

2.5.3 Chronic Suppurative Osteomyelitis:

Secondary Chronic Osteomyelitis

Chronic suppurative osteomyelitis is an oen preerred

term in Anglo-American texts (Marx 1991; Bernier et

al. 1995; opazian 1994, 2002) and can mostly be used

interchangeably with the term “secondary chronic os-

teomyelitis,” which is predominantly used in literature

rom continental Europe (Hjorting-Hansen 1970; Pan-

ders and Hadders 1970; Schelhorn and Zenk 1989). It

is by ar the most common osteomyelitis type, which is

usually caused by bacterial invasion rom a contagiousocus. Most requent sources are odontogenic oci,

periodontal diseases and pulpal inections, extraction

wounds, and inected ractures. Pus, stula, and se-

questration are typical clinical ndings o this disease.

Clinically and radiographically, a broad spectrum rang-

ing rom an aggressive osteolytic putreactive phase to

a dry osteosclerotic phase may be observed (Eyrich et

al. 1999).

2.5.4 Chronic Non-suppurative Osteomyelitis

Te term “nonsuppurative osteomyelitis” describes a

more heterogenic group o chronic osteomyelitis orms,

which lacks the ormation o pus and stula. opazian

(1994, 2002) includes chronic sclerosing types o os-

teomyelitis, prolierative periostitis, as well as actino-

mycotic and radiation-induced orms to this group,

whereas Bernier et al. (1995) advocate a more restric-

tive use o this term. Hudson (1993) uses the term to

describe a condition o prolonged reractory osteomy-

elitis due to inadequate treatment, a compromised host,

or increased virulence and antibiotic resistance o theinvolved microorganisms. Tis classication thereore

also incorporates those cases in which a suppurative

orm o osteomyelitis can present as a nonsuppurative

orm in an advanced stage.

2.5.5 Diffuse Sclerosing Osteomyelitis,

Primary Chronic Osteomyelitis,

Florid Osseous Dysplasia,

Juvenile Chronic Osteomyelitis

One o the most conusing terms among the currently

used osteomyelitis nomenclature is “diuse sclerosing

osteomyelitis” (DSO). Tis term has apparently led to

great conusion in the medical literature. A variety o

denominations were used to describe this disease. One

o the rst descriptions was by Toma in 1944, who used

the term “ossiying osteomyelitis” and considered that

a disease which was caused by a subpyogenic inection

that could be ound in tertiary syphilis. Sclerosing os-

teomyelitis was later described and divided into a ocal

2

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and diuse types (Shaer 1957; Shaer et al. 1974; Pin-

dborg and Hjorting-Hansen 1974; Mittermayer 1976;

opazian 1994, 2002). Te ocal type, also known as

periapical osteitis/osteomyelitis or condensing osteitis,

is a rather common condition with a pathognomonic,

well-circumscribed radioopaque mass o sclerotic bone

surrounding the apex o the root. Since the inection inthese cases is limited to the apex o the root with the

absence o deep bone invasion, sucient endodontic

treatment with or without apex surgery or extraction o

the aected tooth usually leads to regression o these le-

sions or residual sclerosis may remain as a bone scar.

rue diuse sclerosing osteomyelitis, however, is a

rare disease o unknown etiology that can cause major

diagnostic and therapeutic problems (Jacobson 1984).

Te absence o pus, stula, and sequestration are char-

acteristic. Te disease shows an insidious onset, lacking

an acute state. It is thereore considered to be primary chronic and has been named primary chronic osteomy-

elitis by several authors, predominantly in the German

and continental European medical and dental literature

(Hjorting-Hansen 1970; Panders and Hadders 1970;

Schelhorn and Zenk 1989; Eyrich at al 1999). Periods

o onset usually last rom a ew days up to several weeks

and may demonstrate a cyclic course with symptom-

ree intervals. Pain, swelling, and limitation o mouth

opening, as well as occasional lymphadenopathy, domi-

nate the clinical picture.

Te term DSO is primarily descriptive o the radio-

logical appearance o the pathological bone reaction;however, although the term is usually used synony-

mously with primary chronic osteomyelitis, it repre-

sents a description o a strictly radiological appearance

that can be caused by several similar processes. Tese

processes include primary and secondary chronic osteo-

myelitis, chronic tendoperiostitis, and ossiying perios-

titis or Garrè’s osteomyelitis (Hjorting-Hansen 1970; El-

lis et al. 1977; Eisenbund et al. 1981; Bünger 1984; Van

Merkestyn et al. 1990; Groot et al. 1992b, 1996; Eyrich

et al. 1999). Tis act has most likely contributed to this

diversity in nomenclature, as the terms are oen usedinterchangeably.

A urther pathological disease entity has been con-

used with diuse sclerosing osteomyelitis, since it may

mimic DSO radiographically by presenting scleros-

ing opaque and dense masses: forid osseous dysplasia

(FOD). Tese masses are, however, conned to the al-

veolar process o either or both jaws in cases o FOD.

Florid osseous dysplasia is mostly observed in black

women and in many cases lacks clinical symptoms.

Patients suering rom this disease, similar to true DSO,

may in some instances also experience cyclic episodes

o unilateral pain and mild swelling. Tis is usually the

case when superinection occurs (Schneider et al. 1990;

Groot et al. 1996)

As with all pathologies o the bone which compro-

mise local blood fow and host resistance, FOD makesthe jaw more susceptible to secondary inection. In

these instances pus and stula ormation may occur as

well as sequestration (Carlson 1994). Many cases like

these in the literature have, in retrospect, been incor-

rectly labeled as diuse sclerosing osteomyelitis where

these symptoms are by denition always absent. Te

FOD should thereore be considered more a bone pa-

thology acilitating osteomyelitis once inection o the

bone has been established and not equated with the in-

ection itsel.

As mentioned above, the exact etiology o true DSOremains unknown. A common theory is a low-grade in-

ection o some kind; however, most biopsy specimens

taken rom the enoral and extraoral approach have

ailed to be conclusive, showing either no growth in

cultures or growth only rom suspected contaminants

(Jacobson et al. 1982; Jacobson 1984; Van Merkesteyn

et al. 1988). A study by Marx et al. (1994) demonstrated

a high requency o Actinomyces, E. corrodens species,

Arachnia and Bacteroides spp. in cortical and medullar

samples rom patients with DSO. Tis study, like many

others, still demonstrated insuciencies regarding the

protocol or collecting bone specimens and thereorewas inconclusive. Moreover, a variety o antibiotics used

over a long period consistently ailed to ully eradicate

the disease or arrest the symptoms (Jacobson 1984; Van

Merkesteyn et al. 1988, 1990). Van Merkesteyn et al.

(1990) and Groot et al. (1992a) have advocated other

etiologies such as aberrant jaw positioning and para-

unction; however, their theory lacks an explanation or

those cases o true DSO in edentulous patients.

In our recent publications (Eyrich et al. 1999, 2003;

Baltesperger et al. 2004) we used the term “juvenile

chronic osteomyelitis,” which resembles the clinicaland radiological picture o Garrè’s osteomyelitis as used

by various authors. Heggie et al. (2000, 2003) made a

similar observation when analyzing his young osteomy-

elitis patients and used the term “juvenile mandibular

chronic osteomyelitis.” Tis disease usually peaks at

puberty and is characterized mostly by voluminous ex-

pansion o the mandibular body, periosteal apposition

o bone (“periostitis ossicans”), and a mixed sclerotic-

lytic appearance o the cancellous bone. Te clinical

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picture resembles primary chronic osteomyelitis, shar-

ing the lack o pus ormation, stulae, or sequestration.

Juvenile chronic osteomyelitis is thereore considered to

be an early-onset orm o primary chronic osteomyeli-

tis. A urther and more detailed description o this dis-

ease entity is described later in this chapter.

2.5.6 SAPHO Syndrome, Chronic Recurrent

Multifocal Osteomyelitis (CRMO)

In 1986 Chamot et al. described a syndrome associ-

ated with synovitis, acne, pustulosis, hyperostosis, and

osteitis (SAPHO syndrome). Soon, several case reports

and studies were published, concluding a possible re-

lationship between SAPHO syndrome and DSO o the

mandible (Brandt et al. 1995; Kahn et al. 1994; Garcia-

Mann et al. 1996; Suei et al. 1996; Schilling et al. 1999;Eyrich et al. 1999; Roldan et al. 2001; Fleuridas et al.

2002). Kahn et al. (1994) presented a small series o

seven patients with DSO o the mandible out o 85 cases

o SAPHO syndrome. Eyrich et al. (1999) presented a

series o nine patients with DSO, eight o which also

represented a SAPHO syndrome, supporting the hy-

pothesis o a possible association o the two.

Chronic recurrent multiocal osteomyelitis (CRMO)

is characterized by periods o exacerbations and re-

missions over many years. Tis rare disease is noted in

adults as in children, although it is predominant in the

latter group. In several articles published in the past ew years, a possible nosological relationship between di-

use sclerosing osteomyelitis and chronic recurrent mul-

tiocal osteomyelitis has been described (Reuland et al.

1992; Stewart et al. 1994; Suei et al. 1994, 1995; Flygare

et al. 1997; Zebedin et al. 1998; Schilling 1998; Schil-

ling et al. 1999). In correlation with advanced age, there

seems to be an increased association with palmoplantar

pustulosis, a part o the SAPHO syndrome (Shilling et

al. 2000). Because o its possible relationship with other

dermatoskeletal associated diseases, CRMO has been

integrated in the nosological heterogeneous SAPHOsyndrome by several authors (Chamot et al. 1994; Schil-

ling and Kessler 1998; Schilling et al. 2000).

2.5.7 Periostitis Ossificans,

Garrès Osteomyelitis

Strictly periostitis ossicans or ossiying periostitis is,

like diuse sclerosing osteomyelitis, a descriptive term

or a condition that may be caused by several similar

entities. It is merely a periosteal infammatory reaction

to many nonspecic stimuli, leading to the ormation

o an immature type o new bone outside the normal

cortical layer.

Probably the most conusing and misinterpreted

term regarding osteomyelitis is “Garrè’s osteomyelitis.”While most medical pathologists discard the term, it

has still enjoyed great acceptance in the medical and

dental literature, where occurrence in the jaws has

been termed unequivocally (Eversole et al. 1979). Many

terms have been used synonymously in the literature

and attributed to Garrè, such as periostitis ossicans,

chronic nonsuppurative osteomyelitis o Garrè, Garrè’s

prolierative periostitis, chronic sclerosing infamma-

tion o the jaw, chronic osteomyelitis with prolierative

periostitis, and many more. able 2.5 gives an overview

o the use o the term “Garrè’s osteomyelitis” in themedical and dental literature; however, in his histori-

cal article in 1893, Carl Garrè did not actually describe

a singular, specic type o osteomyelitis. Moreover he

described special orms and complications o a single

disease: acute inective osteomyelitis. He used 72 illus-

trative cases (98 sites) to discuss ten specic manies-

tations and complications o acute osteomyelitis. Tis

is a direct contradiction to those authors who assume

that he described a new orm o chronic osteomyelitis

(Wood et al. 1988).

2.5.8 Other Commonly Used Terms

2.5.8.1 Alveolar Osteitis (Dry Socket)

Te clinical term “dry socket” or alveolar osteitis may

also be regarded as a localized orm o inection. Vari-

ous authors have used this term dierently. Hjorting-

Hansen (1960) describes three principle orms o dry

socket: alveolitis simplex; alveolitis granulomatosa; and

an alveolitis sicca. Amler (1973) dierentiates among al-

veolar osteitis, suppurative osteitis, and brous osteitis.Te author concludes that the three types o osteitis cor-

respond to disturbances during the natural healing pro-

cess o an extraction alveolus. Meyer (1971) took great

eort in demonstrating the histopathological changes

in alveolar osteitis. He classies this condition accord-

ing to the degree o local invasion o the surrounding

bone and uses the terms “osteitis circumscripta super-

cialis”, “media” and “prounda”. Te term latter may be

seen as a localized orm o osteomyelitis; however, the

2

13




Table .. Use o the term Garrè’s osteomyelitis in medical and dental literature

Reference Term used Type of Publication

Batcheldor GD, Giansanti JS, Hibbard ED, Waldron CA (1)

Garrè’s osteomyelitis o the jaws: a review and report o

two cases

J Am Dent Assoc 1973;87:892- 7

Ellis DJ, Winslow JR, Indovina AA (2)

Garrè’s osteomyelitis o the mandible. Report o a case.

Oral Surg Oral Med Oral Pathol. 1977 Aug;44(2):183-9

Marx RE (3)

Chronic Osteomyelitis o the Jaws

Oral and Maxilloacial Surgery Clinics o North America,

Vol 3, No 2, May 91, 367-81

Garrè's osteomyelitis Case report (1 & 2)

Review article (3)

Perriman A, Uthman A

Periostitis ossicans.

Br J Oral Surg 1972; 10:211-6

Periostitis ossicans Review article

Smith SN, Farman AG.

Osteomyelitis with prolierative periostitis (Garrè's osteo-myelitis). Report o a case aecting the mandible.

Oral Surg Oral Med Oral Pathol. 1977 Feb;43(2):315-8

Osteomyelitis with prolierative periostitis Case report

Eisenbud L, Miller J, Roberts IL

Garrè's prolierative periostitis occurring simultaneously

in our quadrants o the jaws.

Oral SurgOral Med Oral Pathol. 1981 Feb;51(2):172-8

Garrè’s prolierativ e periostitis Case report

Panders AK, Hadders HN

Chronic sclerosing infammations o the jaw. Osteomy-

elitis sicca (Garrè), chronic sclerosing osteomyelitis with

nemeshed trabecular structure, and very dense scleros-

ing osteomyelitis.

Oral Surg Oral Med Oral Pathol 1970 Sep;30(3):396-412

Osteomyelitis sicca (synonymous osteomy-

elitis o Garrè, chronic sclerosing nonsup-

purative osteomyelitis o Garrè, periostitis

ossicans)

Review article

Mittermayer CH

Oralpathologie.

Schattauer, Stuttgart-New York 1976

Chronic osteomyelitis with prolierative

periostitis (Garrè's chronic nonsuppurative

sclerosing osteitis, ossiying periostitis)

Textbook

Schelhorn P, Zenk W

[Clinics and therapy o the osteomyelitis o the lower

jaw].

Stomatol DDR 1989 Oct;39(10):672-6

Bernier S, Clermont S, Maranda G, Turcotte JY

Osteomyelitis o the jaws

J Can Dent Assoc 1995 May;61(5):441-2, 445-8

Chronic sclerosing osteomyelitis Garrè,

Garrè's chronic sclerosing osteomyelitis

(prolierative osteomyelitis)

Review article

Topazian RG

Osteomyelitis o the Jaws. In Topizan RG, Goldberg MH

(eds): Oral and Maxilloacial Inections.

Philadelphia, WB Saunders 1994, Chapter 7, pp 251-88

Garrè's sclerosing osteomyelitis Textbook

2

4




term “alveolar osteitis” (dry socket) is generally used in

the medical and dental literature to describe an absence

o invasion into the bone. It should thereore not be re-

garded as a orm o osteomyelitis (Marx 1991). In alveo-

lar osteitis the commonly advocated theory suggests a

clot breakdown due to the release o brinolysins either

rom microorganisms or trauma. In both situations thebacteria remain on the surace o the exposed bone, and

an actual invasion does not occur. Although not consid-

ered a true inection, alveolar osteitis may lead to acute

or secondary chronic osteomyelitis once the bacterial

invasion into the medullar and cortical bone has oc-

curred and a deep bone inection has been established.

2.5.8.2 Osteoradionecrosis

and Radioosteomyelitis

Radiotherapy is considered a major column in the treat-ment o head and neck malignancies. Despite recent

advances in radiotherapy, such as using modern three-

dimensional techniques, as well as hyperractionation

or moderately accelerated ractionation and consequent

prophylactic dental treatment, osteoradionecrosis is still

an observed condition in maxilloacial units.

Aside rom its eect on the tumor cells, radiation

also has serious side eects on the so and hard tissues

adjacent to the neoplasm. Mucositis, atrophic mucosa,

xerostomia, and radiation caries are well-known side

eects o head and neck radiotherapy. Because o its

mineral composition, bone tissue absorbs more energy than so tissues and is thereore more susceptible to

secondary radiation. In cases where the bone is irradi-

ated exceeding a certain local dose, osteoradionecrosis

may develop, leading to marked pain in the patient and

possible loss o bone leading to unctional and aesthetic

impairment.

Osteoradionecrosis was once considered an inec-

tion initiated by bacteria, which invaded the radiation-

damaged bone; hence, the term “radiation-induced os-

teomyelitis” or radioosteomyelitis was commonly used.

Marx (1983) conclusively identied this condition as aradiation-induced avascular necrosis o bone. He was

able to demonstrate that radiation caused a hypoxic, hy-

pocellular, and hypovascular tissue, leading to a sponta-

neous or trauma-initiated tissue breakdown. Te result

is a chronic nonhealing wound, susceptible to superin-

ection. As in forid osseous dysplasia and other bone

pathologies, microorganisms are responsible or con-

tamination and, i invasion occurs, secondary inection

o the bone, resulting in osteomyelitis.

2.5.8.3 Osteochemonecrosis

Te medical literature describes several drugs and sub-

stances that acilitate or induce conditions known as

osteonecrosis o the jaws, such as corticosteroids and

other cancer and antineoplastic drugs. Exposure to

white phosphorous among workers in the matchmak-ing industry in the nineteenth century has led to un-

usual necroses o the jaws, which became known in the

literature as phossy jaw or phosphorous necrosis o the

jaw.

In the recent years bisphosphonate therapy has be-

come a widely accepted mainstay o therapy in various

clinical settings such as multiple myeloma, metastatic

cancer therapy, and treatment o advanced osteoporo-

sis. With the increased prescription o these drugs, the

incidence and prevalence o bisphosphonate-associated

complications o the jaw continues to be elucidated. Tistrend seems to be even more the case in patients receiv-

ing injectable bisphosphonates, such as pamidronate and

zoledronic acid, but cases involving osteochemonecrosis

o the jaw associated with chronic peroral administered

bisphosphonates have also been reported (Ruggiero et

al. 2004, 2006).

Te pathophysiological mechanisms leading to bis-

phosphonate-induced osteochemonecrosis o the jaws

are yet ar rom being ully understood; however, it seems

apparent that important dierences to the pathogenesis

o osteoradionecrosis do occur (Hellenstein and Marek

2005). In bisphosphonate-induced osteochemonecrosiso the jaws osteoclastic action is reduced, but osteoblas-

tic production continues, leading to an osteopetrosis-

like condition (Whyte et al. 2003). Tese alterations in

bone physiology with eventual increase o the medul-

lary bone as the disease progresses and the inability o

osteoclasts to remove superinected “diseased” bone are

regarded as causative actors. In contrast to osteoradi-

onecrosis, where a radiation-induced avascular necrosis

is the major cause, avascularity does not appear to be a

major coactor to date; however, inhibition o angiogen-

esis is currently being actively investigated (Fournieret al. 2002; Wood et al. 2002), and urther research will

hopeully help ully understanding its role in pathogen-

esis o this disease.

Regarding the current data and knowledge, we avor

the term “bisphosphonate-induced osteochemonecro-

sis o the jaw” because it is not restricted to a certain

pathogenesis. Te term “bisphosphonate osteomyelitis”

should not be used or the same reasons as the term

radioosteomyelitis should be abandoned. Te jawbone

2

15




with bisphosphonate-induced osteochemonecrosis is ar

more susceptible to bacterial invasion due to its strongly

altered physiology; however, inection o the bone is to

be considered a secondary phenomenon and not the

primary cause o this disease entity.

2.6 Osteomyelitis of the Jaws:

The Zurich Classification System

2.6.1 General Aspects

of the Zurich Classification System

Osteomyelitis o the jaw as a clinical entity has long

been recognized in the medical literature. As mentioned

previously, various classication systems and nomencla-

tures o the disease have evolved with time. Te hetero-

geneity o the classication systems is borne by the actthat several modalities are used to describe and dene

maxilloacial osteomyelitis. Tese modalities include

etiology and pathogenesis, clinical presentation and

course, radiology, and histopathology. Furthermore,

most classication orms represent a mixture o these

criteria, causing conusion, thereby hindering compara-

tive studies.

At the Department o Cranio-Maxilloacial Surgery

at the University o Zurich, the classication system

or osteomyelitis o the jaws uses a hierarchical order

o classication criteria. It is primarily based on clinical

appearance and course o the disease, as well as on ra-diological eatures. Based on these criteria, three major

groups o osteomyelitis can be distinguished:

. Acute Osteomyelitis (AO)

. Secondary Chronic Osteomyelitis (SCO)

. Primary Chronic Osteomyelitis (PCO)

Within these major groups, the clinical presentation

is similar in the majority o cases; however, as will be

described later, a certain variety o the clinical courseis noted, especially in cases o primary and secondary

chronic osteomyelitis.

Histopathology is considered a secondary classi-

cation criterion, taking into account that ndings are

mostly unspecic and nonconclusive when considered

by themselves; however, tissue examinations o biopsies

are irreplaceable or conrmation o the diagnosis in

cases o unclear and atypical clinical and radiological

appearance, and moreover in excluding possible dier-

ential diagnosis.

Furthermore, in some cases o osteomyelitis with anatypical appearance a synthesis o medical history, clini-

cal presentation, imaging studies, histopathology, and

other diagnostic tools may be necessary to achieve an

appropriate diagnosis.

Analysis o the osteomyelitis patients treated in the

Department o Cranio-Maxilloacial Surgery in Zurich

using the abovementioned major classication groups

showed a clear predominance o cases diagnosed as

secondary chronic osteomyelitis at the time o presenta-

tion, whereas cases o acute osteomyelitis and primary

chronic osteomyelitis were signicantly less oen diag-

nosed (able 2.6). In a small group o nine patients, de-spite meticulous work-up o all data including clinical

course and symptoms, diagnostic imaging, laboratory

Table .. Distribution o osteomyelitis cases treated at the Department o Cranio-Maxilloacial Surgery in Zurich,

1970–2000 (Baltensperger 2003)

Major groups of osteomyelitis of the jaws Cases

N %

Acute osteomyelitis (AO) 48 16.6%

Secondary chronic osteomyelitis (SCO) 203 70.0%

Primary chronic osteomyelitis (PCO) 30 10.3%

Not clearly classiable/questionable osteomyelitis 9 3.1%

Total 290 100.0%

2

6




ndings, and histopathology, no clear diagnosis was

possible. Most o these cases showed a chronic course

resembling primary chronic osteomyelitis or a (diuse)

sclerosing orm o secondary chronic osteomyelitis. In

some o these cases the diagnosis o osteomyelitis was

even questionable. Te problems in diagnosis o these

challenging cases and possible related dierential diag-nosis are outlined later in this chapter.

Further subclassication o these major osteomyeli-

tis groups is based on presumed etiology and pathogen-

esis o disease. Tese criteria are thereore considered

tertiary classication criteria. Tese tertiary criteria are

helpul in determining the necessary therapeutic strate-

gies which may dier somewhat among the subgroups.

Te nature o these subgroups are outlined in more de-

tail later in this chapter.

An overview o the Zurich classication o osteomy-

elitis o the jaws and the classication criteria are givenin Fig. 2.2 and able 2.7.

2.6.2 Acute Osteomyelitis

and Secondary Chronic Osteomyelitis

2.6.2.1 Definitions

Te basic terminology used in the Zurich classica-

tion o osteomyelitis o the jaws was promoted by HugoObwegeser, among others. Te general principles o

this classication system were described and published

by E. Hjorting-Hanson, a ormer sta member at the

Department o Cranio-Maxilloacial Surgery Zurich,

in 1970. Hjorting-Hanson, as many other authors be-

ore and aer him, gave an excellent description o the

clinical and radiological picture o acute and secondary

chronic osteomyelitis; however, he ell short o clearly

dening at what stage an acute/subacute osteomyelitis

should be considered chronic. o our knowledge, Marx

(1991) and Mercuri (1991) were the rst and only au-thors to dene the duration or an acute osteomyelitis

Table .. Classiication criteria upon which the Zurich classiication o osteomyelitis is based

Hierarchic order

of classification criteria

Classification criteria Classification groups

First Clinical appearance andcourse o disease

Radiology

Major GroupsAcute osteomyelitis (AO)

Secondary chronic osteomyelitis (SCO)

Primary chronic osteomyelitis (PCO)

Second Pathology (gross pathology

and histology)

Dierentiation o cases that cannot clearly be distinguished

solely on clinical appearance and course o disease; important

or exclusion o dierential diagnosis in borderline cases.

Third Etiology

Pathogenesis

Subgroups o AO, SCO, and PCO

Fig. .. The Zurich classii-

cation o osteomyelitis o the

jaws: since secondary chronic

osteomyelitis is a sequel o the

prolonged and chroniied acute

orm, both basically have the

same subclassiication groups

AcuteOsteomyelitis

Secondary ChronicOsteomyelitis

•Neonatal, tooth germ associated•Trauma/fracture related

•Odontogenic•Foreign body, transplant/implant induced• Associated with bone pathology and/or systemic disease•Other (not further classifiable) cases

Primary ChronicOsteomyelitis

• Early onset(juvenile chronic osteomyelitis)

• Adult onset•Syndrome associated

The Zurich classification of osteomyelitis of the jaws

Acuteosteomyelitis

Secondary chronicosteomyelitis

•

•

••

•

•

Primary chronicosteomyelitis

•

••

2

17




until it should be considered as chronic. Tey set an ar-

bitrary time limit o 4 weeks aer onset o disease. Path-

ological–anatomical onset o osteomyelitis corresponds

to deep bacterial invasion into the medullar and cortical

bone. Aer the period o 4 weeks, a persisting bone in-

ection should be considered as secondary chronic os-

teomyelitis (Fig. 2.3). Although the onset o the disease

is a debatable point in time, it is still a simple and clear

classication criterion and thereore o practical use or

the clinician. Tis same denition was later used by sev-

eral other authors (Eyrich et al. 1999; Schuknecht et al.1997; Koorbusch et al. 1992). Because o its simplicity

and clarity, this criterion is also used in the Zurich clas-

sication to dierentiate acute osteomyelitis rom sec-

ondary chronic osteomyelitis cases.

Te term “subacute osteomyelitis” is not clearly de-

ned in the literature. Most clinicians would probably

agree that this term describes a condition somewhat in

between acute and chronic osteomyelitis with relatively

moderate symptoms. o avoid conusion and keep the

classication as simple as possible, this term has been

abandoned in the Zurich classication.According to this denition, acute and secondary

chronic osteomyelitis are to be considered the same

disease at dierent stages o their course; hence, both

groups are presented and discussed together in this

chapter.

2.6.2.2 Predisposing Factors,

Etiology, and Pathogenesis

2.6.2.2.1 General Considerations

As mentioned previously, there are several etiological

actors, such as traumatic injuries, radiation, and cer-

tain chemical substances, among others, which may

cause infammation in the medullar space o the bone;

however, acute and secondary chronic osteomyelitis,

as these terms are generally used in the medical anddental literature and in this textbook, represent a true

inection o the bone induced by pyogenic microorgan-

isms.

Te oral cavity harbors a large number o bacteria,

among which many may be identied as possible patho-

gens to cause inection o the jawbone. Regarding the

high requency and sometimes severity o odontogenic

inections in the daily dental and oral surgery practice,

and the intimate relationship o dental roots apices with

the medullar cavity o the jawbone, it is remarkable that

osteomyelitis cases are not more requently observed.Explanation or the low incidence o osteomyelitis o

the jawbones can be explained by our primary actors

which are responsible or deep bacterial invasion into

the medullar cavity and cortical bone and hence estab-

lishment o the inection:

. Number o pathogens

. Virulence o pathogens

. Local and systemic host immunity

. Local tissue perusion

Fig. .. Deinition o acute

and secondary chronic os-

teomyelitis o the jawbone

(Adapted rom Marx and Mer-

curi 1991)

O n s e t o f d i s e a s e

4 w e e k s

Acute

osteomyelitis

Secondary

chronic osteomyelitis

Onset of Disease

(=deep bacterial invasion into

medullar and cortical bone)

t

Onset of disease

(�deep bacterial invasion into

medullar and cortical bone)

2

8




Fig. .. Chronic inection o the periapical bone as a

sequel o endodontic disease. This requently observed

condition represents a classical equilibrium between mi-

crobiological aggressors and host actors hindering ur-

ther spread o the bacteria. I this balance is disturbed and

shits toward the side o the microorganisms, deep inva-

sion into the medullar and cortical bone may occur and

osteomyelitis is established

Close interaction o these actors, as shown in Fig. 2.5,

determine the pathological pathway o disease orma-

tion. In the healthy individual with sucient host im-

munity mechanisms these actors orm a careully bal-

anced equilibrium. I this equilibrium is disturbed by

altering one or more o these actors, deep bone inec-

tion will be established (Figs. 2.4, 2.5).

2.6.2.2.2 Local and Systemic Host Immunity

Te oral cavity, like no other part o the human body,

is constantly exposed to various potential aggressors.

Many o these bacteria, given the chance, may cause se-

vere inection and damage to the tissue i they are not

kept at distance. Due to its unique environment, many

potent strategies have been developed to prevent deep

tissue invasion o bacteria. Specic local immunological

mechanisms, potent barrier systems, such as the peri-odontal membrane and a rich local vascular supply, are

the most important. A more detailed description o these

and other deense systems is provided extensively in spe-

cic literature and is beyond the scope o this book.

Every systemic disease with concomitant alterations

in host deenses may infuence prooundly the onset and

course o acute and secondary chronic osteomyelitis.

An alteration o some extent is probably the reason why

osteomyelitis o the jaws develops in most cases, regard-

less o whether or not such deciencies can be detected.

Although the data is limited and lacks evidence-based

criteria in most instances, osteomyelitis has been asso-ciated with a variety o systemic diseases and pathologi-

cal conditions. A list o such diseases and conditions,

as well their mechanisms, are given in ables 2.8 and

2.9. In our retrospective study o 244 cases o acute and

secondary chronic osteomyelitis o the jaws, alcohol and

tobacco consumption were observed in 33.2 and 47.5%

o the cases, respectively, while other conditions, as

shown in able 2.8, were only observed in a scarce num-

ber o patients (Baltensperger 2003); however, more

important in this study than the mentioned systemic

actors seemed to be the high prevalence o local inec-tion in the examined patients with acute and secondary

chronic osteomyelitis. Especially periodontal disease,

which leads to a breakdown o the periodontal barrier

membrane, acilitating deep invasion pathogens, seems

to be an important condition leading to osteomyelitis.

Signicant periodontal disease was ound in 51% o the

patients o the same study.

It is important or the treating physician to consider

host compromise and treat any compromising condi-

tion, when easible, concomitantly with the inection.

2.6.2.2.3 Local and Systemic Alterations

in Bone Vascularity

Compromise o local blood supply must be considered

a critical actor in the establishment o osteomyelitis.

Systemic and local conditions that alter the vascularity

o bone predispose the development o osteomyelitis. In

these conditions immune cells and oxygen cannot reach

the target area in an adequate manner. Tis acilitates

the growth and spread o microorganisms, especially

anaerobes, leading to establishment and progression o

osteomyelitis. An overview o conditions compromising

2

19




blood supply o the jawbone is given in able 2.10. In

many cases o acute and secondary chronic osteomyeli-

tis none o these actors may be apparent or detected;

however, they must always be considered, looked or,

and ultimately treated (Baltensperger 2003).

2.6.2.2.4 Microbiology

Acute and secondary chronic osteomyelitis are consid-

ered true inections o the bone induced by pyogenic

microorganisms. As shown in Fig. 2.5, the number and

virulence o these pathogens are important actors in

the establishment o a bone inection.

Although until recently involvement o S. aureus,

S. epidermidis, and Actinomyces were still discussed

as the major pathogens in cases o osteomyelitis o the

jaws, more recent studies avor the concept o a poly-

microbic inection with several responsible pathogens.Tis shi in doctrine is explained mainly by modern,

sophisticated culture methods, especially involving

anaerobic media, which enable identication o pos-

sible pathogens more accurately. Consequently, many

pathogens, which are mostly ound in the healthy oral

fora, have been associated with cases o jawbone os-

teomyelitis; however, prolonged antibiotic therapy

prior to harvesting o the specimen and possible oral

contamination complicate the interpretation o each

result.

A more detailed overview and in-depth inormation

on this topic is provided in Chap. 7.

2.6.2.2.5 Etiology and Pathogenesis,

Subclassification Groups

According to the classication criteria stated previously,

subclassication o acute and secondary chronic osteo-

myelitis is based on presumed etiology and pathogene-

sis o disease (ables 2.7 and 2.11). Acute and secondary chronic osteomyelitis are initiated by a contagious ocus

o inection or by hematogenous spread. In osteomyeli-

tis o long bones, hematogenous spread is the leading

cause, especially in inants and children, because o the

distinct anatomy o the metaphyseal region. In most o

these cases a single responsible pathogen can be isolated

(Mader and Calhoun 2000). Staphylococcus spp. are the

most common organisms isolated in adults and are also

prominent in children and inants.

Osteomyelitis o the jaws induced by hematogenous

spread has become a rarity since the introduction o an-tibiotics; however, in regions o limited medical access

these orms may still be noted. Especially one orm o os-

teomyelitis o hematogenous spread merits special men-

tion: neonatal or tooth-germ-induced acute osteomyeli-

tis o the jaws. Because o its risks o involvement o the

eye, spreading to the dural sinuses and creating loss o

teeth and acial bone deormities i treated inadequately,

this type o osteomyelitis should be remembered. Neo-

natal or tooth-germ-induced acute osteomyelitis occurs

most ofen within the rst ew weeks afer birth, aecting

the upper jaw in most instances. Tis inection showed

a mortality rate o up to 30% beore the advent o an-

Fig. .. Schematic illustra-

tion showing the interaction

o host and pathogens. I the

balance is shited to the ad-

vantage o the aggressor, deep

bone inection will be estab-

lished (Modiied ater Marx

1999 and Mercuri 1999)

Pathogenesis of acute &secondary chronic osteomyelitis

Number of pathogens x Virulence of pathogens

Local and systemic host immunity x

local tissue perfusion

Deep bacterial invasion into

medullar and cortical bone

2

0




Table .. Systemic host actors acilitating development o acute and secondary chronic osteomyelitis o the jaw-

bone due to impairment o immune response mechanisms (Modiied rom Marx 1991; Mercuri 1991; Sanders 1978; Bar-

baglio et al. 1998; Battaglia et al. 1991; Bishop et al. 1995; Cheung et al. 1999; Exner et al. 1995; Groot et al. 1995; Hovi et

al. 1996; Lawoyin et al. 1988; Melrose et al. 1976; Podlesh et al. 1996; Shroyer et al. 1991; Topazian 1994, 2002; Diktaban

1992; Koorbush et al. 1992; Eversole et al 1979; Meer et al. 2006)

Systemic factors altering host immunity

• Diabetesmellitus

• Autoimmunedisorders

• AIDS

• Agranulocytosis

• Anemia(especiallysicklecell)

• Leukemia

• Syphilis

• Malnutrit ion

• Chemotherapy

• Corticosteroidandotherimmunosuppressivetherapy

• Alcoholandtobacco

• Drugabuse

• Priormajorsurgery

• Herpessimplexvirus(Zoster)andcytomegalovirusinfection

Table .. Host actors acilitating development o acute and secondary chronic osteomyelitis o the jawbone due

to compromise o local blood supply (Modiied rom Marx 1991; Mercuri 1991; Sanders 1978; Barbaglio et al. 1998;

Battaglia et al. 1991; Bishop et al. 1995; Cheung et al. 1999; Exner et al. 1995; Groot et al. 1995; Hovi et al. 1996; Lawoyin

et al. 1988; Melrose et al. 1976; Podlesh et al. 1996; Shroyer et al. 1991; Topazian 1994, 2002; Diktaban 1992; Koorbush

et al. 1992; Eversole et al 1979)

Local and systemic factors altering bone vascularity

• Smoking

• Diabetesmellitus

• Floridosseousdysplasia

• Fibrousdysplasia

• Paget’sdisease

• Osteopetrosis(Albers–SchonbergDisease)

• Osteoporosis

• Bisphosphonateinducedosteochemonecrosis

• Otherformsofosteonecrosis(mercury,bismuth,arsenic)

• Tobacco

• Radiationtherapyandosteoradionecrosis

• Bonemalignancy(primaryormetastatic)

Table .. Mechanisms o systemic diseases/conditions predisposing to osteomyelitis (Adapted rom Marx 1991)

Disease Mechanism facilitating bone infection

Diabetes Diminished leukocyte chemotaxis, phagocytosis, and liespan; diminished vascu-larity o tissue due to vasculopathy, thus reducing perusion and the ability or an

eective infammatory response; slower healing rate due to reduced tissue peru-

sion and deective glucose utilization

Leukemia Decient leukocyte unction and associated anemia

Malnutrition Reduced wound healing and reduction o immunological response

Cancer Reduced wound healing and reduction o immunological response

Osteopetrosis (Albers–Schonberg disease) Reduction o bone vascularization due to enhanced mineralization, replacement o

hematopoietic marrow causing anemia and leukopenia

Severe anemia (particularly sickle-cell anemia) Systemic debilitation, reduced tissue oxygenation, bone inarction (sickle cell

anemia), especially in patients with a homozygous anemia trait

IV drug abuse Repeated septic injections, spreading o septic emboli (especially with harboring

septic vegetation on heart valves, in skin or within veins)

AIDS Impaired immune response

Immunosuppression (steroids, cytostatic drugs) Impaired immune response

2

21




tibiotics. Te route o inection is considered by most

clinicians to be hematogenous (Bass 1928; Lacey and En-

gel 1939; Heslop and Rowe 1956; Nade 1983), although

a local inection caused by perinatal trauma o the oral

mucosa and local trauma to the overlying mucosa o the

alveolar ridge (Hitchin and Naylor 1957; Nade 1983; o-

pazian 1994, 2002), as well as extension o inection romadjacent teeth or sof tissues, are also discussed (Loh and

Ling 1993). Staphylococcus aureus has been implicated as

the organism responsible or this type o acute osteomy-

elitis (Asherson 1939; Haworth 1947; McCasch and Rowe

1953; Niego 1970; Nade 1983; Loh and Ling 1993).

Te vast majority o cases o acute and secondary

chronic osteomyelitis involving the jaws are usually

caused by inection primarily spreading by a contagious

ocus. Te most common oci are odontogenic, origi-

nating rom inected pulp or periodontal tissue or in-

ected pericoronal tissue rom retained teeth, especially third molars.

rauma, especially compound ractures, is also a

major condition, which i not treated or treated inade-

quately, acilitates the development o osteomyelitis. But

also every type o jawbone surgery, including surgical

removal o impacted third molars, inevitably leads to a

certain degree o local trauma to the bone, which causes

local ischemia and may acilitate deep invasion o bacte-

ria into the medullar cavity; hence, osteomyelitis can be

established. Especially additional trauma to a preexist-

ing chronic local inection carries a great risk o causing

deep bone inection. Foreign bodies as well as the varioustransplants and implants used in maxilloacial and den-

tal surgery also may harbor microorganisms and hence

acilitate urther spreading to the surrounding bone.

Several types o bone pathologies and systemic con-

ditions, as mentioned previously, infuence local tissue

perusion and immunity and thereore are important

coactors in establishing bone inection. In rare cases,

inections derived rom periostitis aer gingival ulcer-

ation, uruncles, and acial and oral lacerations may also

be considered causative.

In some instances the etiology and pathogenesis re-

mains unclear or can only be speculated. Tese cases are

subclassied as “other” in the classication system pro-

posed in this book.A distribution o acute and secondary chronic os-

teomyelitis cases, according to their etiology and patho-

genesis, and their subclassication, respectively, is given

in able 2.12.

Te distribution o acute and secondary chronic

osteomyelitis shows a clear predominance o the man-

dible. In our patient data rom 251 cases o acute and

secondary chronic osteomyelitis only 16 patients (6.4%)

demonstrated involvement o the upper jaw, whereas

in the vast majority o cases (n=235; 93.6%) the man-

dible was the inected bone (Baltensperger 2003). Tedierent anatomy o maxilla and mandible is probably

the most important actor explaining the distribution

o osteomyelitis involving the jawbones. Te maxillary

blood supply is more extensive than in the mandible.

Additional thin cortical plates and the paucity o med-

ullary tissues in the maxilla preclude connement o

inections within the bone and permit dissipation o

edema and pus into the so tissues o the midace and

the paranasal sinuses (opazian 1994, 2002). Maxillary

osteomyelitis with tooth exoliation aer herpes zoster

reactivation and concomitant cytomegalovirus inec-

tion has recently gained attention based on a review o the literature and 27 previous reports o herpes zoster-

induced jaw inections (Meer et al. 2006).

Te mandible is like a squashed long bone which has

been shaped in a U-orm. Like all long bones there is

a clear distinction o a medullary cavity, dense cortical

plates, and a well-dened periosteum on the outer bor-

der o the cortical bone. Te medullary cavity is lined by

Table .. Subclassiication o acute and secondary chronic osteomyelitis o the jaws

Subclassification of acute and secondary chronic osteomyelitis of the jaws

Induced by hematogenous spread:

Neonatal, tooth germ associated

Extension rom a local inection:

Trauma/racture related

Odontogenic

Foreign body, transplant/implant induced

Associated with bone pathology and/or systemic disease

Other

2

2




the endosteum, which, like the periosteum, is a mem-

brane o cells containing large numbers o osteoblasts.

Within the medullary cavity a large variety o cells, such

as reticuloendothelial cells, erythrocytes, granulocytes,

platelets, and osteoblastic precursors, are harbored, as

well as cancellous bone, at, and blood vessels. Bone

spicules radiate centrally rom cortical bone to producea scaold o interconnecting trabeculae (Copehaver et

al. 1978). Te architecture o mandibular cortical bone

resembles that o other long bones. Longitudinally ori-

entated haversian systems (osteons), each with a central

canal and blood vessel that provide nutrients by means

o canaliculi to osteocytes contained within lacunae.

Tese canals communicate with adjunct haversian sys-

tems as well with the periosteum and the marrow space

by Volkmann’s canals, thus orming a complex inter-

connecting vascular and neural network that nourishes

bone and enables bone metabolism, necessary or re-pair, regeneration, and unctional adaptation.

Acute and secondary chronic osteomyelitis o the

mandible aects most commonly the body o the man-

dible, ollowed by the symphysis, angle, ascending ra-

mus, and condyle (Calhoun et al. 1988; Baltensperger

2003).

Te compromise o local blood supply is the critical

actor and nal common pathway in the establishment

o acute and secondary chronic osteomyelitis (Fig. 2.7).

Wannors and Gazelius (1991) demonstrated by means

o laser Doppler fowmetry (LDF) that long-standing

local infammation o the mandible was associated witha persistent reduction in blood fow.

Except or the coronoid process, which is supplied

primarily rom the temporalis muscle and the mandibu-

lar condyle, which is supplied in part by vessels rom

the lateral pterygoid muscle and the temporomandibu-

lar joint (MJ) capsule, the major blood supply o the

rest o the mandible consists o the inerior alveolar ar-

tery (Fig. 2.6). A secondary source is provided by the

vessels o the periosteum. Tese vessels are organized

in a reticular manner and run alongside o the corticalsurace, giving o small nutrient vessels that penetrate

the cortical bone and anastomose with branches o the

inerior alveolar artery (Fig. 2.6; Castelli 1963; Cohen

1959); however, the value o the periosteal circulation

probably cannot be seen as ull replacement o the vas-

cular supply o the marrow space. Hence, despite this

adjunctive vascularization o the mandible through the

periosteum, the main blood supply is derived rom the

inerior alveolar artery which, especially in elderly pa-

tients, is a vessel o small caliber and most susceptible to

damage. Tis context can be transerred to the clinicalappearance o osteomyelitis o the mandible, where oc-

clusion o the inerior alveolar artery inevitably boosts

the progress o the inection even i an intact perios-

teum is still present.

In most incidences periapical and periodontal inec-

tions are localized by a protective pyogenic membrane

or so tissue abscess wall which serves as a certain bar-

rier (Schroeder 1991). As mentioned above, this con-

dition represents a careully balanced equilibrium be-

tween microorganisms and host resistance preventing

urther spreading o the inection. I the causative bac-

teria are sucient in number and virulence, this barriercan be destroyed. Furthermore, permanent or tempo-

rary reduction o host resistance actors or various rea-

sons mentioned previously acilitate deep bone invasion

Table .. Etiology and pathogenesis o acute and secondary osteomyelitis cases treated at the Department o Cran-

io-Maxilloacial Surgery in Zurich, 1970-2000, according to Baltensperger (2003)

Subclassification groups of acute and secondary chronic

osteomyelitis

Cases

N° %

Induced by hematogenous spread

Neonatal, tooth germ associated

2 0.80

Extension rom a local inection

Trauma/racture related

Odontogenic

Foreign body, transplant/implant induced

Associated with bone pathology and/or systemic disease

Other

42

173

13

5

16

16.73

68.92

5.18

1.99

6.37

Total 251 100.00

2

23




o the microorganisms. Tis invasion induces a cascade

o infammatory host responses causing hyperemia,

increased capillary permeability, and local infamma-

tion o granulocytes. Proteolytic enzymes are released

during this immunological reaction creating tissue ne-

crosis, which urther progresses as destruction o bacte-

ria and vascular thrombosis ensue. Accumulation o pusinside the medullary cavity, consisting o necrotic tissue

and dead bacteria within white blood cells, increases in-

tramedullary pressure. Tis leads to vascular collapse,

venous stasis, thrombosis, and hence local ischemia (A

in Fig. 2.7; opazian 1994, 2002). Pus travels through

the haversian and nutrient canals and accumulates be-

neath the periosteum, elevating it rom the cortical

bone and thereby urther reducing the vascular supply

(B in Fig. 2.7; opazian 1994, 2002). Elevation o the pe-

riosteum is usually observed more extensively in chil-

dren, presumably because the periosteum is less rmly

attached to the cortical bone than in adults. When pus

accumulates continually underneath the periosteum,

peroration may occur, leading to mucosal and cutane-

ous abscesses, and stulas may develop.

In mandibular osteomyelitis, the increased intramed-

ullary pressure also leads to direct compression o theneurovascular bundle, accelerating thrombosis and isch-

emia resulting in dysunction o the inerior alveolar

nerve, known as Vincent’s symptom. Te mandibular ca-

nal is also an anatomical pathway with no barrier unc-

tion, alongside which pus can spread quickly (Fig. 2.8).

2.6.2.2.6 Chronification of Bone Infection

Te chronication o the disease refects the inability o

the host to eradicate the pathogen due to lack o treat-

Fig. .. a Condylar process

arteries o an injected human

head. Mandible sot parts

were discarded ater injec-

tion was perormed through

the common carotid artery. A

artery coming rom the lateral

pterygoid muscle, B artery com-

ing rom vessels o the tem-

poromandibular joint capsule

(Teichmann’s paste injection;decalciied and cleared). b Cor-

onoid process arterial vessels.

Two arterioles ( A and A’ ) are

present, both coming rom the

temporalis muscle (China-ink

solution injection; decalciied

and cleared). c Overall view o

injected inerior alveolar artery

(Teichmann’s paste injection;

decalciied and cleared). (From

Castelli 1963)

2

4




ment or inadequate treatment, resulting in ailure to

reestablish the careully balanced equilibrium between

host actors and pathogens ound in a healthy oral en-

vironment.

Aer the acute infammatory process occurs and

local blood supply is compromised, necrosis o the en-

dosteal bone takes place. Te bone ragments die andbecome sequestra (Fig. 2.9). Osteoclastic activity is then

responsible or separating the dead bone rom vital

bone. Devital bone tissue clinically appears dirty, whit-

ish-gray with an opaque appearance. Its atty tissue has

been destroyed and it does not bleed i scraped (Marx

1991). In some instances the bone sequester can dem-

onstrate considerable dimensions (Fig. 2.10).

Te elevated periosteum involved in the infamma-

tory process still contains vital cells. Tese cells, once

the acute phase has passed, orm a new bony shell (in-

volucrum) covering the sequester. Te involucrum may be penetrated by sinuses called cloacae, through which

pus discharges, elevating the periosteum or orming

stula. As chronication progresses this scenario may

be repeated (Figs. 2.11, 2.12). Te involucrum tends to

hinder sequester rom extruding, which perpetuates the

process because the whole area is bathed in increasing

amounts o pus unless treated promptly and adequately

(Killey and Kay 1970).

In secondary chronic osteomyelitis o the jaws, even-

tually a new equilibrium is established between the host

and the aggressor causing the inection. Te nature o

this newly ormed equilibrium is dependent on host im-munity supported by medical therapy and the causative

bacteria. It dictates the urther course o the inection:

I adequate therapy is administered on time, balance•

is shied in avor o the host, resulting in complete

healing o the inection.

I no or inadequate therapy is provided, the disease•

may progress slowly or aster depending on the num-

ber and virulence o the bacteria and the remaining

host deenses.

I the number and virulence o the bacteria are small,•

host mechanisms may overwhelm, but still ail to

ully eradicate the pathogen. In these instances a

strong and diuse sclerosis o the bone with or with-

out a signicant periosteal reaction can be noted. Te

clinical and radiological picture may then resemble

primary chronic osteomyelitis.

Acute Inflammation

(edema, pus formation)

Increased

intramedullary pressure

Vascular collapse

(stasis, thromosis, ischemia

of bone)

Avascular bone

Pus,

organism extension

Haversian system / nutrient

canal involvement

Elevation

of periosteum

Disrupted blood supply

Sequester formation

Compromisedlocal blood supply

A B

Acute inflammation

(edema, pus formation)

Increased

intramedullary pressure

Vascular collapse

(stasis, thrombosis, ischemia

of bone)

Avascular bone

Pus,

organism extension

Haversian system/nutrient

canal involvement

Elevation

of periosteum

Disrupted blood supply

Sequester formation

Compromised local blood supply

A B

Fig. .. Pathogenesiso acute and secondary chronic

osteomyelitis o the jaws.

Pathway A shows the role

o inlammation and pathway B

the role o pus ormation in

compromising blood supply

o the inected bone, which can

be considered as the inal com-

mon pathway in the ormation

o sequestra (Modiied rom

Topazian 1994, 2002)

2

25




2.6.3 Clinical Presentation

2.6.3.1 Demographics

Acute and secondary chronic osteomyelitis may aect

all ages and both sexes. In our retrospective analysis o

251 cases o acute and secondary chronic osteomyelitis

there was a male predominance with a 2:1 ratio (Balten-

sperger 2003). Koorbush et al. (1992) described a male

to emale ratio o 3:1 in a survey o 35 patients. An equal

gender distribution was noted by Daramola et al. (1982)

in a larger Arican patient population.

Te mean age o onset o disease in our studied cases

was almost the same in cases o acute and secondary

chronic osteomyelitis: 42.9 years (range 1–81 years)

and 44.1 years (range 6–89 years; Baltensperger 2003),

respectively. Tese gures are comparable with those

described by previous investigators (Adekeye 1985; Cal-

houn 1988; Koorbush 1992; Daramola 1982).

Fig. .a,b. Patient with acute osteomyelitis, beginning

secondary chronic osteomyelitis o the right mandible ol-

lowing extraction o the lower right second molar. Her chie

complaint was a marked hypoesthesia o the right inerior

alveolar nerve (Vincent’s symptom), which was document-

ed preoperatively in a. b The intraoperative view ater re-

moval o the buccal cortical plate by decortication: notethe granulation tissue alongside the inerior alveolar nerve

(arrows) as a primary pathway or spread o the inection.

(This case is described in detail in Chap. 12, case report 4)

Fig. .. a An OPG o a secondary chronic osteomyeli-

tis case demonstrates osteolysis in the mandibular corpus

around the alveolar region o the right irst molar. A se-

quester is noted at the base o the right mandibular cor-

pus with adjacent periosteal reaction. b Surgical specimen

o the case shown in a: multiple sequesters and necrotic

bone collected during debridement surgery

2

6




2.6.3.2 Acute Osteomyelitis

Te clinical appearance o acute osteomyelitis o the

jaws may show a great variety, depending on the in-

tensity o the disease and the magnitude o imbalance

between the host and the microbiological aggressors.

Tree principal types o clinical courses o acute osteo-

myelitis can be distinguished:

Acute suppurative•

Subacute suppurative•

Clinically silent with or without suppuration•

Cases o acute osteomyelitis o the jawbone with an

acute suppurative clinical course usually show impres-

sive signs o infammation. Pain can be intense and is

mostly described by a deep sensation within the bone

by the patient, which may be a valuable clue in the pa-

tient’s history. Local swelling and edema due to abscess

ormation can also be substantial causing trismus and

limitation o jaw unction. Te patients experiences a

general malaise caused by high intermittent ever with

temperatures reaching up to 39–40°C, oen accompa-

Fig. .a–c. The CT scans o a patient with secondary

chronic osteomyelitis o the let mandible developing a gi-

ant sequester on the bases o the mandibular corpus. The

progressive inection has weakened the bone and hence apathological racture has resulted. Sagittal CT scan (a) and

3D reconstructions (b,c). (Courtesy o N. Hardt)

Fig. .. Axial CT scan o an extended secondary

chronic osteomyelitis o the let mandible. A strong pe-

riosteal reaction with neoosteogenesis has ormed an in-

volucrum over several sequestra. (This case is described in

detail in Chap. 12, case report 6)

2

27




nied by regional lymphadenopathy. In some instances

paresthesia or anesthesia o the lower lip is described

(Vincent’s symptom), indicating involvement o the

inerior alveolar nerve. In most cases the cause o in-

ection is odontogenic (able 2.12) and can easily be

identied. Pus may exude around the gingival sulcus

and through mucosal and, possibly cutaneous, stulas

(Figs. 2.13–2.15). A etid oral odor caused by anaerobic

pyogenic bacteria oen is present. eeth in the aected

region may demonstrate increased mobility even lead-

ing to malocclusion and show decreased or loss o sen-sitivity. Sequester ormation and appositional neoosteo-

genesis are limited, i not absent, due to the short period

since establishment o deep bone inection, which is the

denition o acute osteomyelitis (Fig. 2.16).

Neonatal or tooth-germ-induced acute osteomyelitis

o the jaws, as described previously, is a classical rep-

resentative o this group, although this orm o osteo-

myelitis has become a rarity in modern maxilloacial

practice. But also in elderly patients this orm o acute

osteomyelitis has been seen much less requently since

the introduction o antibiotics and sophistication o medical and dental practice.

In cases o a subacute or silent course, with or with-

out suppuration, the clinical presentation is by deni-

tion less impressive. Tis can make an early diagnosis

increasingly dicult, and in many instances these cases

are not detected until they have become secondary

chronic.

An overview o symptoms at initial presentation o

our patient data is given in able 2.13.

2.6.3.2.1 Laboratory Findings

Depending on the intensity o the inection, labora-

tory results in acute osteomyelitis may demonstrate

a wide range. While in cases with little infammation

the laboratory will only reveal moderate evidence o

acute inection, cases which are accompanied by ab-

scess ormation will show more pronounced ndings.

Examination o our own patient data is demonstrated

in able 2.14.

2.6.3.3 Secondary Chronic Osteomyelitis

As a sequel o acute osteomyelitis, the clinical presenta-

tion o secondary chronic osteomyelitis o the jaws may

also show a great variety, depending on the intensity o

the disease and the magnitude o imbalance between

the host and the microbiological aggressors and the

time (Fig. 2.16). Following an acute or subacute clini-

cal phase with suppuration, the chronication o the

disease is refected by the clinical course and ndings.

Most symptoms, such as pain and swelling, are usually less extensive in the chronic than in the acute stage. Te

deep and intense pain requently observed in the acute

stage is replaced by a more dull pain. Painul swelling

caused by local edema and abscess ormation in the

acute stage is subsided by a harder palpable tender-

ness caused by periosteal reaction (see Figs. 2.11, 2.12).

Other symptoms are somewhat more predominant in

advanced stages, such as sequester and stula orma-

tion, and are regarded as classical signs o secondary

Fig. .. Coronal view corresponding to axial CT scan

shown in Fig. 2.11. (This case is described in detail in

Chap. 12, case report 6)

Fig. .. Acute odontogenic osteomyelitis with mas-

sive suppuration. Oral examination at initial presentation

revealed pus in the sulci o the anterior incisors and ca-

nines on both sides, extending distally to the molars in the

right lower jaw with multiple istula ormation

2

8




chronic osteomyelitis (see Figs 2.10, 2.11, 2.12). Te

noted etid odor oen noted in cases o acute abscess

ormation is less requent in patients with secondary

chronic osteomyelitis. A disturbed occlusion can some-

times be noted when teeth o an aected region become

more mobile and elongate due to rise o intraosseous

pressure or a racture present as a result or initiator o

the osteomyelitic process.

An overview o symptoms at initial presentation o

our patient data is given in able 2.15.

In cases where the acute phase was clinically silent,secondary chronic osteomyelitis may begin as a hid-

eous disease with little and somewhat unspecic clinical

symptoms. In such instances the cause o the inection

is considered to be a low-grade inection, which, how-

ever, cannot be ully eradicated by host deenses. Tese

cases o secondary chronic osteomyelitis demonstrate

less pus, stula, and sequester ormation, or may even

lack these symptoms at a certain (progressive) stage o

the disease. Furthermore, their radiological appearance

may predominantly show a diuse sclerosis with little

to no osteolysis. Probably a large portion o the casesdescribed in the literature as diuse sclerosing osteo-

myelitis (DSO) alls into this category. A dierentiation

rom primary chronic osteomyelitis may be dicult, i

not impossible, in such cases (Figs. 2.17, 2.18); hence,

it is most important to review the whole course o the

disease and possibly obtain repeated imaging over time

in such cases to establish the correct diagnosis.

2.6.3.3.1 Actinomycotic and Other Rare Secondary

Chronic Osteomyelitis of the Jaws

Specic clinical ndings can be ound in acute and es-

pecially in secondary chronic osteomyelitis caused by

Actinomyces, Nocardia, and Mycobacteria. While Actino-myces is inrequently observed, the other pathogens are

rarely associated with osteomyelitis o the jaws; however,

i they are the causative pathogen, the clinical picture is

somewhat atypical and hence deserves special recogni-

tion. In our studied cases we identied 5 patients with

actinomycotic secondary chronic osteomyelitis, while

osteomyelitis cases associated with Nocardia and Myco-

bacteria were not observed (Baltensperger 2003).

Fig. .. OPG at initial

presentation (same patient as

shown in Fig. 2.13). Osteolysis

o the neighboring bone, de-

rived rom apical pathology, is

noted in the incisor and canine

region on both sides as well as

in the molar region on the right

side

Fig. .. Corresponding axial CT scan to OPG shown in

Fig. 2.14 with a more detailed view o the osteolysis in the

anterior and right sided alveolar bone

2

29




Local and systemic host immunity x local tissue perfusion x t

N ° P a t h o g e n s x V

i r u l e n c e p a t h o g e n s Abscess formation

Fistula formation

Sequester formation

Periosteal reactionneoosteogenesis

Predominant osteolysis

Predominant sclerosis

Fig. .. Clinical and radio-

logical eatures o acute and

secondary chronic osteomyeli-

tis o the jaws: the ormation

o certain clinical and radio-

logical indings is dependent

on the intensity o the disease

and the magnitude o imbal-

ance between the host and the

microbiological aggressors, as

well as the time rame

Table .. Acute osteomyelitis: clinical symptoms at initial presentation at the Department o Cranio-Maxilloacial

Surgery in Zurich (Baltensperger 2003)

Clinical Symptoms Cases

N° %

Pain 48 100.0

Swelling 43 89.6

Hypoesthesiaa 25 52.1

Clinical abscess/pus ormation 30 62.5

Extraoral stula ormation 0 0.0

Intraoral stula ormation 7 14.6

Sequester ormationb 3 6.3

Exposed bone 3 6.3

Limited mouth opening 24 50.0

Lymphadenopathy 5 10.4

Fracture evidentc 12 25.0

Myoacial, temporomandibular joint pain 1 2.1

aHypoesthesia o the inerior alveolar nerve (Vincent’s symptom)

bOnly clinically diagnosed sequester ormation without use o imaging

cCases o trauma/racture-related acute osteomyelitis

2

0




Table .. Acute osteomyelitis: laboratory indings at initial presentation at the Department o Cranio-Maxilloacial

Surgery in Zurich (From Baltensperger 2003)

Cases

N° %

Erythrocyte sedimentation rate

Data available 23 100.0

Normal (♂ ≤15; ♀ ≤20) 4 17.4

Elevated (♂>15;♀ >20) 19 82.6

C-reactive protein


Normal (<5) 5 33.3

Markedly elevated (>50) 5 33.3

Moderately elevated (3–50) 5 33.3

Leukocyte count


Normal

(age 2–3 years: 6000–17000;

age 4–12 years: 5000–13000;

adults: 3800–10500)

23 60.5

Moderately elevated

(age 2–3 years: 17000–20000;age 4–12 years: 13000–15000;

adults: 10500-13000)

4 10.5

Markedly elevated

(age 2–3 years: >20000;

age 4–12 years: >15000;

adults: >13000)

11 28.9

Body temperature


Normal temperature (≤37°C) 20 46.5

Subebrile temperature (37°–38°C) 17 39.5

Febrile temperature (≥38°C) 6 14.0

2

31




Table .. Secondary chronic osteomyelitis: clinical symptoms at initial presentation at the Department o Cranio-

Maxilloacial Surgery in Zurich (Baltensperger 2003)

Clinical symptoms Cases

N° %

Pain 178 87.7

Swelling 162 79.8

Hypoesthesiaa 78 38.4

Clinical abscess/pus ormation 117 57.6

Extraoral stula ormation 15 7.4

Intraoral stula ormation 27 13.3

Sequester ormationb 30 14.8

Exposed bone 38 18.7

Limited mouth opening 42 20.7

Pathological racture due to secondary

chronic osteomyelitis

4 2.0

Lymphadenopathy 29 14.3

Pseudarthroses c 3 1.5

Fracture evidentc 29 14.3

Myoacial, temporomandibular joint pain 6 3.0

aHypoesthesia o the inerior alveolar nerve (Vincent’s symptom)

bOnly clinically diagnosed sequester ormation without use o imaging

cCases o trauma/racture-related acute osteomyelitis

Fig. .. Patient with secondary chronic osteomyelitis. Ater an initial phase o

pus and istula ormation with local surgical drainage and prolonged antibiotic ther-

apy, the process advanced with little clinical symptoms and demonstrated a diuse

sclerosing pattern o the let and right mandibular corpus and symphyseal region in

the urther course mimicking primary chronic osteomyelitis

2

2




Cervicoacial actinomycosis is a slowly progressive

inection with both granulomatous and suppurativeeatures. Te disease predominantly aects the so tis-

sue o the head and neck with primary involvement o

nearly every structure (Lerner 1988); however, in some

instances the underlying bone, predominantly the man-

dible, can be inected by direct extension to the under-

lying bone or hematogenous spread (opazian 1994,

2002).

As in most cases o secondary chronic osteomyeli-

tis, inection with Actinomyces is mostly o endogenous

origin, since the pathogen is known to be an oral sap-

rophyte, present in periodontal pockets, carious teeth,

tonsillar crypts, and other structures. Local inection,as well as surgical or nonsurgical trauma, acilitates

penetration o the mucosal and periodontal barrier

structures and allows penetration o deep tissue and

bone (Bowden 1984). Advanced cervicoacial Actino-

mycosis spreads without regard or ascial planes and

typically appears on cutaneous, rather than mucosal,

suraces.

Firm so tissue masses are present on the skin with

purplish to dark-red oily areas and occasionally small

zones o fuctuance (see Fig. 9.1, 9.2, Chap. 9). Spon-

taneous drainage o serous fuid containing granularmaterial may occur. When placed on a piece o gauze,

these granular, yellowish substances, also called sulur

granules, can be seen clearly and represent colonies o

bacteria (opazian 1994, 2002). Te underlying aected

bone demonstrates the clinical and radiological picture

o secondary chronic osteomyelitis with zones o oste-

olysis, delayed healing o extraction sites, and sclerosis

on radiographs. Occasionally sequester ormation is

also noted.

Nocardiosis is also a chronic disease that may re-

semble actinomycotic inection. Although the primary

target is usually the lungs, rom where hematogenous

spread leads the pathogen to other organs, the cervico-

acial region, including bone, is occasionally involved

(Schwartz and io 1987).

uberculosis is still a widespread inectious diseaseworldwide with also an increasing incidence again in

countries with poor socio-economic conditions, con-

comitant with the AIDS pandemic. Te etiology, patho-

genesis, diagnosis, and treatment o tuberculosis are

well described in other textbooks and are beyond the

scope o this book.

Osteomyelitis o the jaws caused by inection with

Mycobacterium tuberculosis is uncommon and, in most

described instances, the tuberculosis inection is rarely

conned to the bone. Adults are predominantly a-

ected, although cases o aected children are also de-scribed (Bhatt and Jayakrishnan 2001; Hock-Liew et al.

1996; Kothari et al. 1998; Dimitrakopoulos et al. 1991;

Fukuda et al. 1992). Oral tuberculous lesions are gen-

erally quite rare, despite the act o high incidence o

systemic involvement. A possible reason or this obser-

vation may be the inhibition o Mycobacterium tubercu-

losis by saliva and intact oral mucosa (Hock-Liew et al.

1996; McCarthy and Shklar 1980). Te mechanisms o

spread o inection are, in analogy to other osteomyelitis

cases, caused by other bacteria, by direct inoculation,

through tooth-extraction sockets, through any breach

in the mucosa during tooth eruption, spread rom adjacent so tissue sites, or by hematogenous spread

(Mishra and Bhoyar 1986). Te clinical and radiological

picture may resemble that o regular secondary chronic

osteomyelitis with eatures similar to a dento-alveolar

abscess; however, cervical lymphadenopathy, producing

discrete or matted masses which are usually nontender,

may be a distinctive presenting eature in some patients

(Lee and Schecter 1995). Tis resemblance to conven-

tional osteomyelitis cases underlines the importance o

considering tuberculous osteomyelitis in the dierential

diagnosis o jaw lesions, especially i the patient’s medi-cal history is suspicious or possible inection (Bhatt

and Jayakrishnan 2001).

Candida albicans has also been described as a po-

tential microorganism to cause osteomyelitis in vari-

ous bones o the skeleton, especially in conjunction

with prosthesis. In the acial skeleton, however, docu-

mented cases o osteomyelitis caused by Candida albi-

cans are extremely rare, despite the act that Candida

is known commensal o the oral cavity. Arranz-Caso

Fig. .. Same as Fig. 2.17

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et al. (1996) report o a case o Candida albicans os-

teomyelitis o the zygomatic bone probably caused by

sel-inoculation o spores rom muguet plaques on

the oral mucosa to the exposed bone tissue by hand

contact. Te authors conclude that such a mechanism

should be considered especially in patients who re-

quently have oral candiasis (e.g., diabetic, cancer, andHIV patients).

Cases o acute and secondary chronic osteomyelitis

o the jaws have also been reported by bacteria which

are rarely or not considered to be oral commensals.

Tese cases, however, are extremely scarce, and hence

the literature on these inections consists mainly o case

reports.

2.6.3.3.2 Secondary Chronic Osteomyelitis

Masquerading Malignancy

Te clinical and radiological signs o secondary chronic

osteomyelitis may share many similarities with ma-

lignancy complicated by secondary bone inection

(Figs. 2.19, 2.20). Tis may lead to delay denite diag-

nosis and appropriate treatment in certain instances

(Vezeau et al. 1990).

Lesions believed to be osteomyelitis that do not

respond to treatment as expected within a short time

should be viewed with concern. Te patient’s medical

history, determining possible risk actors or develop-

ing oral carcinoma such as smoking, alcohol abuse, and

poor oral hygiene, may be indicative, but imaging stud-ies and representative biopsies should be perormed to

establish the diagnosis (opazian 1994, 2002).

As much as the presence o a malignancy with inva-

sion into the underlying jawbone may acilitate second-

ary inection, the opposite pathway may also be the case

in rare instances. Ongoing bone inection may also lead

to malignancy by neoplastic conversion o inectious tis-

sue (Lemière et al. 2000; Niederdellmann et al. 1982).

2.6.3.3.3 Secondary Chronic Osteomyelitis

Associated with Bone Pathology

As mentioned previously, there are several conditions

which acilitate bone inection in the jaw. A summary

o the most requently involved pathological conditions

enhancing the incidence o osteomyelitis o the jaws is

given in able 2.10; however, theoretically every patho-

logical condition which alters bone physiology and/or

vascularization o bone tissue may jeopardize host tis-

sue deense mechanisms and hence may promote sec-

ondary inection. Te unique location o the jawbones

with their proximity to the heavily contaminated oral

cavity makes them particularly vulnerable.

Depending on the nature o the underlying bone

pathology, the clinical picture o succeeding second-

ary chronic osteomyelitis may dier rom the average

osteomyelitis inection established in “healthy bone.”

Te initiation o inection is, like in regular acute andsecondary chronic osteomyelitis, oen a trauma such

as extraction o a tooth or a dental inection leading to

breakdown o the periodontal and/or mucosal barrier

and promoting contamination and deep bone inva-

sion o the jawbone. Te urther course o the disease

is, however, strongly dependent on the reactive mecha-

nisms o the host tissue (e.g., bone). In general, under-

lying bone pathology will reduce the deensive abilities

o the host tissue and inection may spread aster than

in healthy bone. Clinical and radiological signs refect-

ing suppurative inection, such as abscess and stulaormation, are similar to osteomyelitis cases without

associated bone pathology. Bone reaction to inection,

like osteolysis, sclerosis, sequester ormation, and pe-

riosteal reaction, however, may strongly dier, making

correct diagnosis and determining the extent o the

inection more challenging (Fig. 2.21). In cases were

necrotic bone is exposed to the oral cavity, secondary

colonization o the bone and eventual deep bone inva-

sion may occur (Fig. 2.22).

2.6.3.3.4 Laboratory Findings

In analogy to the clinical symptoms, the laboratory

ndings in secondary chronic osteomyelitis o the jaws

are usually less prominent than in acute osteomyelitis.

Te overall moderate systemic reactions are refected

by these results and indicate a more localized inec-

tious process, especially in secondary chronic osteomy-

elitis cases. Tis is especially true in cases with little or

mild clinical symptoms where laboratory ndings can

be almost normal and hence are o little diagnostic or

monitoring value. Examination o our own patient data

is demonstrated in able 2.16.

2.6.4 Primary Chronic Osteomyelitis

2.6.4.1 Definition

Acute and secondary chronic osteomyelitis o the jaw,

as being the same disease at a dierent stage, share the

same etiology, a bacterial or, in rare cases, a ungal in-

ection. In the literature acute and secondary chronic

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Fig. .a,b. Histology

samples o the same patient

shown in Figs. 2.19a and b.

Hematoxylin and eosin stains.

a Iniltration o bone by moder-

ately dierentiated squamous

cell carcinoma. Keratinization

in center o tumor cell islands

(arrow ). Peritumoral ibrosis

and iniltration by inlammatory

cells are present (arrowheads)

osteomyelitis are oen summarized by the term “sup-

purative osteomyelitis,” indicating a true bacterial inec-

tion with ormation o pus.

Te term “primary chronic osteomyelitis,” as used in

the Zurich classication o osteomyelitis o the jaws, re-

ers to a rare infammatory disease o unknown etiology.

It is characterized as a strictly nonsuppurative chronicinfammation o the jawbone with the absence o pus

ormation, extra- or intraoral stula, or sequestration.

Te absence o these symptoms represents a conditio sine

qua non and clearly dierentiates primary rom acute

and secondary chronic osteomyelitis in most cases. Te

term “primary chronic osteomyelitis” also implies that

the patient has never undergone an appreciable acute

phase and lacks a denitive initiating event.

Te disease tends to a rise de novo without an ac-

tual acute phase and ollows an insidious course. In

most cases o primary chronic osteomyelitis, periodic

episodes o onset with varying intensity last rom a ew days to several weeks and are intersected by periods o

silence where the patient may experience little to no

clinical symptoms. In active periods dull to severe pain,

limitation o jaw opening and/or myoacial pain, as well

as variable swelling, may be observed. In certain cases

Fig. .a,b. Patient with a squamous cell carcinoma

o the let lower jaw with concomitant secondary chronic

osteomyelitis. The patient was reerred to the maxilloa-

cial unit approximately 1 month ater surgical removal

o the lower let second molar with chronic local istula

ormation and pus discharge rom the extraction site. The

medical history, clinical appearance, and initial radiologi-

cal work-up (OPG; Fig. 2.19 and corresponding axial CT

scans in Fig. 2.20) were suspicious or secondary chronic

osteomyelitis; however, initial bone and sot tissue biop-

sies revealed an invasive squamous cell carcinoma with a

concomitant local bone inection

2

35




regional lymphadenopathy and reduced sensation o

the inerior alveolar nerve (Vincent’s symptom) are also

accompanying symptoms.

Primary chronic osteomyelitis o the jaws almost al-

ways targets the mandible. In our patient data all but

one case o primary chronic osteomyelitis involved

exclusively the lower jaw. In the remaining case, thezygoma demonstrated the clinical, radiological, and

histopathology ndings as the mandible, indicating a

possible spread o the pathological condition. Te nd-

ings in the literature are similar to our data. Flygare et

al. (1997) reported a case o primary chronic osteomy-

elitis with involvement o both jaws, which is consid-

ered to be a unique case.

2.6.4.2 Classification Problems of Primary

Chronic Osteomyelitis of the Jaws

As mentioned previously, the classication o osteomy-elitis o the jaws, and especially primary chronic osteo-

myelitis o the jaws, is somewhat conusing, mainly due

to the wide variety o terms used to describe this disease

entity. While diuse chronic sclerosing or chronic scle-

rosing osteomyelitis are the avorite used terms in the

Fig. .. (continued ) Histol-

ogy samples o the same pa-

tient shown in Figs. 2.19a and b.

Hematoxylin and eosin stains.

b Lamellar bone with preserved

osteocyte nuclei is present

besides signs o inlammation

ibrosis o marrow spaces (ar-

rows) and extensive iniltration

by inlammatory cells (arrow-

heads)

Fig. .. a A patient with a clinically extensive sec-

ondary chronic osteomyelitis o the rontal region with

multiple istula and abscess ormations. The patient was

treated with i.v. bisphosphonates or metastatic breast

cancer. (This case is described in detail in Chap. 12, case

report 10.) b A CT scan corresponding to a: The bone and

periosteal reaction is not as strong as would have been ex-

pected rom the clinical picture and compared with cases

o secondary osteomyelitis o the mandible with no un-

derlying bone pathology. (This case is described in detail

in Chap. 12, case report 10)

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