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- •Foreword
- •Preface
- •Contents
- •2.3 Diagnostic Modalities
- •2.4 Antibiotic Stewardship Principles
- •1.1 Historical Background
- •1.2 Epidemiology
- •1.4 Management
- •1.5 Conclusion
- •References
- •2.1 Introduction
- •2.5 Surgical Management
- •Bibliography
- •3.1 Introduction
- •3.2 Pharmacokinetics
- •3.3 Fluoroquinolones
- •3.6 Cephalosporins
- •3.7 Ceftobiprole
- •3.9 Linezolid
- •3.11 Daptomycin
- •3.12 Fosfomycin
- •3.15 Conclusion
- •References
- •4.1 Aetiology
- •4.1.2 Risk Factors
- •4.1.2.2 Bacteria
- •4.1.2.3 Other Causative Agents
- •4.2 Negative Pressure Wound Therapy
- •4.2.1 Summary
- •References
- •5: Bacterial Resistance
- •5.1 Introduction
- •5.3.1 Antibiotic Destruction
- •5.3.4 Target Replacement or Target Bypass
- •5.3.5 Target Site Alteration
- •References
- •6.1 Blood Chemistry Tests
- •References
- •7.1 Introduction
- •7.2 New Diagnostic Tools
- •7.2.1 Serological Tests
- •7.2.1.1 D-dimer
- •7.2.1.2 Fibrinogen
- •7.2.1.3 Neutrophil-to-Lymphocyte Ratio
- •7.2.1.4 Procalcitonin
- •7.2.2 Synovial Tests
- •7.2.2.1 Mass Spectrometry
- •7.2.2.2 Alpha Defensin
- •7.2.2.3 Synovial C-Reactive Protein
- •7.2.2.4 Synovial Interlukin-6
- •7.2.2.5 Calprotectin
- •7.2.3.1 Culture Sonication
- •7.3 Conclusion
- •References
- •8.1 Introduction
- •8.2 Etiology
- •8.4 Clinical Diagnosis
- •8.5 Laboratory Investigations
- •8.6 Biopsy
- •8.7 Radiological Investigations
- •8.8 Medical Management
- •8.8.1 Acute Osteomyelitis
- •8.8.2 Septic Arthritis
- •8.9 Pyomyositis
- •8.10 Surgical Management
- •8.11 Acute Osteomyelitis
- •8.12 Septic Arthritis
- •8.13 Complications
- •8.14 Chronic Osteomyelitis
- •8.15 Pathological Fractures
- •8.16 Post-infective Segmental Bone Loss
- •8.17 Post-infective Physeal Growth Arrest
- •8.18 Post-septic Hip Sequelae
- •8.19 Summary
- •References
- •9.2 Locations
- •Bibliography
- •10: Chronic Osteomyelitis
- •10.1 Introduction
- •10.2 Etiology
- •10.3 Epidemiology
- •10.4 Pathophysiology
- •10.7 Laboratory Test
- •10.8 Diagnostic Radiology
- •10.11 The Host
- •10.12 The Disease
- •10.13 Treatment
- •10.14 Systemic Antibiotic Therapy
- •10.15 Local Antibiotic Depots
- •10.16 Surgical Treatment
- •10.18 Soft Tissue Coverage
- •11.1.6 Imaging
- •11.2 Risk Factors
- •11.3 Common Species
- •10.20 Results
- •10.21 Summary
- •References
- •11.1 Diagnosis
- •11.1.2 Labs
- •11.1.3 Synovial Fluid
- •11.1.4 Culture
- •11.1.5 Histopathology
- •11.4.1 Soft Tissue
- •11.4.2 Bone
- •11.4.3 Joint
- •11.4.4 Periprosthetic
- •References
- •Further Readings
- •12.6 Conclusion
- •12.7 Biography
- •References
- •13.1 Vertebral Osteomyelitis
- •13.1.1 History
- •13.1.2 Epidemiology
- •13.1.3 Pathophysiology
- •13.1.4 Most Common Manifestations
- •13.1.5 Diagnosis
- •13.1.6 Imaging Studies
- •13.1.7 Treatment
- •13.2 Vertebral Tuberculosis
- •13.2.1 History
- •13.2.2 Epidemiology
- •13.2.3 Pathophysiology
- •13.2.4 Most Common Manifestations
- •13.2.5 Pediatric Spinal Tuberculosis
- •13.2.6 Diagnosis
- •13.2.7 Treatment
- •References
- •14.1 Introduction
- •14.2.2 Primary Injury
- •14.2.3 Early Versus Late Infection
- •14.2.5.1 Sequestrum
- •14.2.6 Patient Comorbid Factors
- •14.3 Treatment Options
- •14.3.3 Soft Tissue Coverage
- •14.3.4 External Fixation
- •14.3.5 Antibiotic Loaded Cement/Bioceramics
- •14.3.6 Membrane-Induced Osteogenesis (Masquelet Technique)
- •References
- •15.1 Introduction
- •15.1.1 Conservative Approach
- •15.1.2 Reconstructive Approach
- •15.2 Pedicled Flaps
- •15.2.1 Rectus Abdominis Musculocutaneous Flap
- •15.2.1.1 Surgical Technique
- •15.2.3 Gastrocnemius Flap
- •15.2.3.1 Surgical Technique
- •15.2.4 Soleus Flap
- •15.2.4.1 Surgical Technique
- •15.2.5 Vascularized Fibula Flap
- •15.2.5.1 Surgical Technique
- •15.2.6.1 Surgical Technique
- •15.2.7 Sural Flap
- •15.2.7.1 Surgical Technique
- •15.3 Microsurgical Flaps
- •15.3.1 Anterolateral Thigh Flap
- •15.3.1.1 Surgical Technique
- •15.3.2 Latissimus Dorsi Muscle Flap
- •15.3.2.1 Surgical Technique
- •15.3.3 Gracilis Free-Flap
- •15.3.3.1 Surgical Technique
- •References
- •16: Diabetic Foot Osteomyelitis (DFO)
- •16.1 Introduction
- •16.3.3 Radiographic Examinations
- •16.3.3.1 X-ray
- •16.3.3.2 MRI
- •16.3.3.3 PET-CT
- •16.3.4 Biopsy
- •16.4.1 Antibiotics Therapy
- •16.4.2 Conservative Surgery
- •16.4.3 Aggressive Surgery
- •References
- •17.1.1 Osteoradionecrosis (ORN)
- •17.1.1.1 Prevalence
- •17.1.1.3 Management
- •17.1.2 Risk Prediction
- •17.1.2.1 Conclusion
- •17.1.3.1 Medications
- •17.1.3.3 Patients At-Risk
- •17.2 Pathophysiology
- •17.2.1 Bone Remodeling Inhibition
- •17.2.3 Angiogenesis Inhibition
- •17.2.4 Acquired Immune Dysfunction
- •17.3.2 Local Factors
- •17.3.2.1 Dentoalveolar Procedures
- •17.3.2.2 Anatomic Factors
- •17.3.2.3 Concomitant Oral Disease
- •17.3.2.4 Treatment Goals
- •17.3.3 MRONJ Prevention Strategies
- •17.3.4 Treatment Strategies
- •17.3.4.1 Nonoperative Therapy
- •17.3.5 Operative Therapy
- •17.3.6.1 Pulpitis
- •17.3.6.2 Acute Apical Periodontitis (Periapical Abscess)
- •17.3.6.3 Periapical Granuloma
- •17.3.6.4 Periapical Cyst
- •17.3.7.3 Garre’s Sclerosing Osteomyelitis
- •References
- •18.1 Introduction
- •18.2 Risk Factors
- •18.3 Evidence-Based Preventive Measures
- •18.3.1 Preoperative Measures
- •18.3.1.1 Surgical Hand Preparation
- •18.3.1.5 Preoperative Bathing or Showering
- •18.3.1.6 Preoperative Skin Preparation
- •18.3.1.7 Hair Removal
- •18.3.1.8 Glycemic Control
- •18.3.2 Intraoperative Measures
- •18.3.2.2 Second Dose Antibiotic
- •18.3.2.3 Incisional Wound Irrigation
- •18.3.2.4 Perioperative Oxygenation
- •18.3.2.8 Behavioral Aspects
- •18.3.3 Postoperative Measures
- •18.3.3.1 Postsurgical Wound Care
- •18.3.3.2 Postoperative Antibiotics
- •References
- •19: Periprosthetic Joint Infection: General Aspects
- •19.2 “Local” Patient Risk Factors
- •19.4.1 Presurgical
- •19.4.2 Intraoperative
- •19.4.3 Post-operative
- •19.4.3.1 “Mechanical” Thromboembolic Prophylaxis [101, 102]
- •References
- •20: Low-Grade Periprosthetic Infections
- •20.1 Diagnosis
- •20.3 Outcomes
- •20.4 Conclusion
- •References
- •21.1 Introduction
- •21.5.1 Multidisciplinary Approach
- •21.5.2 Surgical Strategies
- •21.5.3 Other Therapeutic Strategies
- •References
- •22.1.1 Introduction
- •22.2 PJI After Shoulder Arthroplasty
- •22.2.1 Epidemiology
- •22.2.2 Risk Factors
- •22.2.3.2 Diagnostic Criteria
- •22.2.3.3 Clinical Presentation
- •22.2.3.4 Radiology
- •22.2.3.6 Synovial Aspirate
- •22.2.4 Management
- •22.2.4.1 Prevention
- •22.2.4.2 Treatment
- •Implant Retention
- •One-Stage Revision Arthroplasty
- •Two-Stage Revision Arthroplasty
- •Antibiotic Spacer
- •Resection Arthroplasty
- •22.3 PJI after Elbow Arthroplasty
- •22.3.2 Risk Factors
- •22.3.3 Diagnosis
- •22.3.4 Treatment
- •22.3.4.1 Implant Retention
- •22.3.4.2 One-Stage Revision Arthroplasty
- •22.3.4.3 Two-Stage Revision Arthroplasty
- •22.3.4.4 Salvage Procedures
- •References
- •23.1 Introduction
- •23.2 Epidemiology
- •23.3 Pathophysiology
- •23.4 Etiology
- •23.6 Diagnosis
- •23.6.1 Lab Test
- •23.6.2 Imaging
- •23.6.3 Cultures
- •23.7 Risk Factors
- •23.8 Surgical Treatment
- •23.8.2 One-Stage Revision Surgery
- •23.8.3 Two-Stage Revision Surgery
- •23.9 Conclusions
- •References
- •24.1 Introduction
- •24.2 Knee
- •24.2.1 Overview
- •24.2.3 Static Spacers
- •24.2.4 Static Versus Articulating Spacers
- •24.2.5 Distal Femoral or Proximal Tibial Replacement Infection
- •24.2.6 Stage 1 Arthrodesis Spacers
- •24.2.7 Articulating DFR/PTR Spacers
- •24.3 Hip
- •24.3.1 Static Spacers
- •24.3.2 Articulating Spacers
- •References
- •25: Native Hip Joint Infection
- •25.1 Introduction
- •25.2.1 Epidemiology
- •25.2.2 Etiology
- •25.2.3 Clinical Presentation
- •25.2.4 Diagnosis
- •25.2.6 Treatment
- •25.3 Infection Following Hip Preservation Surgery
- •25.3.1 Hip Arthroscopy
- •25.3.1.1 Epidemiology
- •25.3.1.2 Diagnosis
- •25.3.1.4 Treatment
- •25.3.2 Periacetabular Osteotomy
- •25.3.2.1 Epidemiology
- •25.3.2.2 Diagnosis
- •25.3.2.4 Treatment
- •25.3.3 Surgical Hip Dislocation
- •25.3.3.1 Epidemiology
- •25.4.1 Epidemiology
- •25.4.2 Diagnosis
- •25.4.3 Treatment
- •References
- •26: Infective Complications After Trauma Surgeries
- •26.1 Introduction
- •26.3 Epidemiology
- •26.4 Risk Factors
- •26.5 Pathogenesis
- •26.8 Treatment
- •26.8.1 Radical Debridement
- •26.8.2 Implant Handling
- •26.9 Local Antimicrobial Therapy
- •26.9.1.1 Ilizarov Technique
- •26.9.1.2 The Masquelet Technique
- •26.9.1.4 3D Printing
- •26.12.1 Pre-operative Measures
- •26.12.1.1 Skin Preparation Solutions
- •26.12.1.2 Skin Hair Management
- •26.12.2 Peri-operative Management
- •26.12.2.1 Drapes
- •26.12.2.2 Double Gloving
- •26.12.2.3 Antibiotics Coated Implants
- •References
- •27: Infective Complications After Open Fractures
- •27.1 Introduction
- •27.2 Epidemiology
- •27.3 Pathophysiology
- •27.4 Risk Factors
- •27.5.1 Laboratory Examination
- •27.5.2 Imaging Procedures
- •27.6 Nuclear Imaging
- •27.7 Microbiology
- •27.8 Molecular Technologies
- •27.9 Histopathology
- •Irrigation
- •27.10.1.2 Appropriate Intravenous Antibiotics
- •Timing
- •Local Antibiotics
- •27.10.1.3 Meticulous Injury Zone Excision (Debridement)
- •Irrigation
- •27.10.1.4 Fracture Stabilization
- •27.10.1.5 Second Look
- •27.10.1.6 Soft Tissue Closure
- •27.10.2.1 Advantages
- •References
- •28.1 Introduction
- •References
- •29: Infective Complications After Spinal Instrumentation
- •29.1 Introduction
- •29.4 Diagnosis
- •29.5 Treatment
- •29.7 Conclusions
- •References

Contents
xi
26 Infective Complications After Trauma Surgeries . . . . . . . . . . . . 383
Khaled M. Emara, Ahmed K. Emara,
and Mohamed O. Eissa
27 Infective Complications After Open Fractures . . . . . . . . . . . . . . 393
Khaled M. Emara, Ramy A. Diab,
and Mohamed O. Eissa
28 Infections in Orthopedic Oncology . . . . . . . . . . . . . . . . . . . . . . . . 403
Alberto Crimì, Elisa Pala, Giulia Trovarelli,
Andrea Angelini, and Pietro Ruggieri
29 Infective Complications After Spinal Instrumentation . . . . . . . . 415
Andrea Angelini, Giovanni Baldin, Ron Batash,
and Pietro Ruggieri

Bone andJoint Infections:
Introduction andEpidemiology
AndreaAngelini andPietroRuggieri
1
1.1 Historical Background
Osteomyelitis, the infection and inammation of
long bones or bone marrow, has been documented
in medical literature throughout history, from
ancient Egypt and Greece to modern times.
Various terms have been used to describe this
condition, such as “cold of bones,” “necrosis,”
“typhus,” “carbuncle of the bone,” “osteitis,”
“periostitis,” “osteoperiostitis,” and “periosteomyelitis.” These terms all convey the notion of an
inammatory process affecting the bone [1]. The
historical understanding of osteomyelitis has
evolved signicantly from ancient times, as evidenced by the descriptions found in early human
remains and medical texts from Europe, Asia,
and Northern Africa. Ancient Egyptian papyri,
such as the Edwin Smith Surgical Papyrus,
detailed bone involvement in open fractures with
pus formation. Hippocrates later described osteomyelitis of the skull and long bones following
wounds, noting that sequestra could depress scar
tissue and underlying bone. Roman physicians
Celsus and Galen emphasized the importance of
suppuration for healing postfracture infections
[2]. In the Medieval period, injuries sustained in
A. Angelini · P. Ruggieri (*)
Department of Orthopedics and Orthopedic
Oncology, University of Padova, Padova, Italy
e-mail: andrea.angelini@unipd.it;
pietro.ruggieri@unipd.it
battles and accidents were common causes of
infections, often leading to chronic osteomyelitis.
Moreover, poor sanitation and lack of aseptic surgical techniques contributed to the high incidence
of infections.
By the late eighteenth and early nineteenth
centuries, Hunter and Dorsey elucidated the
mechanisms of sequestrum formation and bone
necrosis, advocating for early incision to maintain periosteal blood supply and prevent
abscesses. The discovery of microorganisms
causing osteomyelitis by Pasteur in 1860 and
Koch’s isolation of the tubercle bacillus in 1882
marked signicant advancements in understanding the disease’s etiology [3]. At the same time,
the introduction of antiseptic techniques by
Joseph Lister signicantly reduced postsurgical
infections [4].
Throughout the 19th and 20th centuries, further insights were gained into osteomyelitis’
pathophysiology and clinical manifestations, and
in the past decades, new concepts were introduced, which include the immune system activation by osteocytes, cortical bone involvement,
and Staphylococcus aureus is to be the main
pathogen responsible for osteomyelitis [5]. The
discovery of penicillin and the subsequent development of other antibiotics revolutionized the
treatment of BJIs, dramatically reducing
morbidity and mortality [6]. With the advent of
advanced imaging techniques, including scintig-
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
P. Ruggieri et al. (eds.), Bone and Joint Infections, https://doi.org/10.1007/978-3-031-96383-4_1
1

2
A. Angelini and P. Ruggieri
raphy, ultrasonography, CT, MRI, and PET-FDG,
the diagnosis and understanding of the early
phases of osteomyelitis have markedly improved
[7]. These modalities enable precise detection
and detailed characterization of the infection,
allowing for earlier and more accurate diagnosis
and thereby enhancing the effectiveness of subsequent management strategies [8].
1.2 Epidemiology
The overall incidence of osteomyelitis in adults is
21.8 cases per 100,000 persons annually in the
United States, with approximately 20% of these
cases attributed to hematogenous spread [9]. The
condition shows a higher prevalence in males and
increases with age, although the reasons for this
gender disparity remain unclear. In pediatric populations, the incidence of osteomyelitis varies,
often inuenced by different etiological factors
compared to adults. Staphylococcus aureus is the
most common pathogen implicated in both acute
and chronic osteomyelitis, along with coagulasenegative staphylococci, aerobic gram-negative
bacilli, Enterococcus, and various Streptococcal
species [5]. The clinical presentation of osteomyelitis is heterogeneous, affecting individuals
across all age groups and patient types (Table1.1).
High-risk and life-threatening conditions that
predispose individuals to osteomyelitis and systemic infections include immunosuppression,
diabetes with peripheral neuropathy, sickle cell
anaemia, microangiopathies such as cardiovascular disorders and smoking, and intravenous drug
use. These conditions signicantly increase the
risk of severe systemic infections. In immunocompromised patients, a broader spectrum of
pathogens is observed, including Mycobacterium
tuberculosis and Bacillus Calmette-Guérin in
patients with bladder carcinoma, and fungal
pathogens such as Candida species, Blastomyces,
Cryptococcus, and Aspergillus. Bartonella
henselae is associated with HIV-positive patients,
and Pseudomonas and Enterococcal infections
are frequently seen in intravenous drug users,
whereas Eikenella corrodens and Pasteurella
Table 1.1 Pathogens and correlated population and
conditions
Pathogen Population
Staphylococcus aureus Children and adults,
Bacile calmatte-Guerin Bladder carcinoma patients
Streptococcal species,
Kingella kingae
Blastomyces Immune-suppressed
Eikenella corrodens,
Pasteurella multocida
Salmonella Children with Sickle Cell
Pseudomonas,
Enterococcus
Bartonella henselae HIV patients
Fungal species:
Blastomyces,
Cryptococcus,
Aspergillus
Mycobacterium
Tuberculosis
including posttrauma or
prosthetic joint infections.
In children and newborns.
patients
Dog bite/human bite
Anemia
IV drug users
Immune suppressed
patients, long-term IV
medications, parenteral
nutrition patients
Pott’s disease after TB
manifestation
multocida are common following dog or human
bites, respectively [10–13].
On the other hand, with the advent of joint
replacement surgeries, prosthetic joint infections
became a signicant clinical issue in the modern
age [14, 15]. The other two elds of interest on
BJIs are the Healthcare-Associated Infections
due to the increased use of invasive procedures
and devices in hospitals led to a rise in nosocomial infections, and the emergence of antibioticresistant bacteria, such as methicillin-resistant
Staphylococcus aureus (MRSA), that has complicated the management [16–18].
1.3 Classication, Pathogenesis,
andBiolm
Osteomyelitis is classied based on timing, staging, mechanism, and host status. Acute osteomyelitis occurs within the rst 2 weeks of onset,
subacute between one and several months, and
chronic when the condition persists for months
to years [19]. The Cierny-Mader classication
system is a widely used method for classifying

1 Bone andJoint Infections: Introduction andEpidemiology
3
osteomyelitis based on the anatomic involvement (I: medullary, II: supercial, III: localized,
IV: diffused), the involved bone, and host status
(A host: normal, B host: systemic or local compromise, C host: where therapy is worse than the
disease itself) (Figs. 1.1 and 1.2) [20].
Osteomyelitis can be divided into primary and
secondary types: primary osteomyelitis results
from a distant source of infection with hematogenous spread of microorganisms to the long
bones, predominantly affecting children, while
in adults, it primarily affects the vertebrae [21].
Secondary osteomyelitis arises due to trauma,
surgery, oncologic conditions, or sepsis of various etiologies [22]. This form is often contiguous, occurring in young adults, whereas in older
patients, it typically manifests with pressure
ulcers [5, 23]. Biolm formation, a crucial factor
in osteomyelitis, begins when bacteria in the
planktonic phase attach to a surface such as
bone, implants, plates, polyethylene, or polymethylmethacrylate (PMMA) cement. Following
adhesion, the bacteria enter a silent phase characterized by the formation of an extracellular
polymeric substance (EPS) matrix that surrounds
them. This matrix renders the bacteria more
resistant to antibiotics due to the difculty in
penetrating the biolm [24].
Osteomyelitis, due it its diverse etiologies,
presents a diagnostic challenge requiring a high
index of suspicion [25]. Acute osteomyelitis
may manifest with localized symptoms such as
swelling, erythema, warmth at the infection
site, dull pain, fever, and potentially septic
arthritis if the metaphysis is intracapsular.
Special attention is warranted for new-onset
back or neck pain accompanied by fever, bacteremia, endocarditis, and elevated C-reactive
protein (CRP) and erythrocyte sedimentation
rate (ESR) to diagnose vertebral osteomyelitis.
Chronic osteomyelitis presents similarly but
with symptoms persisting over a prolonged
period, often with less pronounced fever [26]
(Figs.1.3 and 1.4).
Fig. 1.1 Stage 4
(diffuse osteomyelitis):
an infection that
involves the entire
thickness of the bone
and may result in
structural instability. A
58-year-old woman with
a history of a compound
fracture of the femur. (a)
Radiograph and (b)
coronal and sagittal CT
scans show a diffuse
infection compromising
the structural integrity of
the bone
ab

4
A. Angelini and P. Ruggieri
Fig. 1.2 Same patient. MRI (STIR and T2-weighted FAT-SAT) clearly shows the involvement of soft tissues by the
infectious process
Fig. 1.3 Chronic Osteomyelitis in a 21-year-old man
with persistent pain in the thigh, swelling, and intermittent
drainage from a sinus tract. Radiographs show periosteal
reaction, cortical irregularities, and possible sequestrum
(dead bone fragment)

1 Bone andJoint Infections: Introduction andEpidemiology
5
Fig. 1.4 PET/CT Findings in chronic osteomyelitis. The
midshaft of the femur shows signicantly increased FDG
uptake, indicating active infection and inammation. The
hot spots correlate with the areas of sinus tract extending
from the bone to the surrounding soft tissue. The corre-
1.4 Management
Before the discovery of penicillin, osteomyelitis
management was primarily surgical, involving
debridement, saucerization, and wound packing
to facilitate secondary healing. This approach
carried a high mortality rate due to sepsis. The
introduction of antibiotics is considered a “gamechanger” as they signicantly reduced the mortality from staphylococcal osteomyelitis.
However, with the emergence of antibioticresistant strains such as methicillin-resistant
Staphylococcus aureus (MRSA), which account
for approximately one-third of all staphylococcal
infections [27], put the dealing physicians are
faced with less effective treatments that necessitate more aggressive approaches [28]. Recent
studies have validated a multidisciplinary treatment approach involving orthopedic surgeons,
infectious disease specialists, radiologists,
nurses, pediatricians, and social workers [29–31].
Evidence-based guidelines emphasize tailoring
antibiotic regimens to the specic microorganism
sponding CT images reveal cortical irregularities and
destruction, indicative of chronic osteomyelitis. Sequestra
(white arrow) are visible as dense, sclerotic bone fragments within the medullary canal
and patient host factors, along with various surgical interventions—such as curettage, Masquelet
technique, osteotomy, Ilizarov bone handling, or
negative pressure wound therapy—to address
biolm production and enhance recovery [6, 32,
33]. The management of BJIs has changed over
time in relation to the evolution of epidemiological aspects. Improved sanitation, advances in
trauma care and orthopedic surgery, and public
health measures have reduced the overall incidence of infections, including BJIs. Moreover,
vaccination programs (such as those against
tuberculosis and other infectious diseases) have
decreased the incidence of related bone and joint
infections.
1.5 Conclusion
In summary, osteomyelitis is a complex condition to treat due to multiple factors and heterogeneity of the disease, requiring consideration of
microorganisms, host factors, infection site, and

6
A. Angelini and P. Ruggieri
clinical presentation. Clinicians must maintain a
high level of suspicion and carefully tailor the
best treatment to prevent severe complications
such as sepsis, pathologic fractures, neurologic
decits, and even malignant transformation in
long-standing infections. The epidemiology of
BJIs reects broader trends in medical and public
health advancements, with signicant improvements in prevention, diagnosis, and treatment
over time. However, challenges remain, particularly with antibiotic resistance and healthcareassociated infections.
Author Contributions Conceptualization, project administration: AA, PR; data curation and
formal analysis: AA, PR; supervision: PR;
writing- original draft: AA; writing-review and
editing: AA, PR; All authors have read and agreed
to the published version of the manuscript.
Institutional Review Board Statement Not
applicable.
Informed Consent Statement Written
informed consent was obtained from patients at
the time of admission to our Institute. However,
all pictures have been reported anonymized.
Consent for Publication (Include Appropriate
Statements) We conrm that this chapter,
including related data, gures and tables, has not
been published previously, it is not under consideration for publication elsewhere, and, if
accepted, it will not be published elsewhere in the
same form, in English or in any other language,
without the written consent of the publisher.
Conicts of Interest/Competing Interests
(Include Appropriate Disclosures)
Ruggieri P
is a consultant for Stryker and Exactech (not relevant to the present manuscript). The other
Authors declare that there are no relationships/
conditions/circumstances that present a potential
conict of interest with the present manuscript.
Availability of Data and Material (Data
Transparency) Manuscript data are embedded
in the text and fully available on specic request.
Funding There was no external funding source
in support of this study.
References
1. Gross SD.The anatomy, physiology, and diseases of
the bones and joints. John Grigg; 1830.
2. Broughton G 2nd, Janis JE, Attinger CE.A brief history of wound care. Plast Reconstr Surg. 2006;117(7
Suppl):6S–11S. https://doi.org/10.1097/01.
prs.0000225429.76355.dd.
3. Breasted JH.The Edwin-Smith surgical papyrus. The
Chicago University Press; 1930.
4. Toledo-Pereyra LH. Joseph Lister’s surgical revolution. J Investig Surg. 2010;23(5):241–3. https://doi.
org/10.3109/08941939.2010.520574.
5. Hofstee MI, Muthukrishnan G, Atkins GJ, Riool
M, Thompson K, Morgenstern M, Stoddart MJ,
Richards RG, Zaat SAJ, Moriarty TF. Current concepts of osteomyelitis: from pathologic mechanisms to advanced research methods. Am J Pathol.
2020;190(6):1151–63. https://doi.org/10.1016/j.
ajpath.2020.02.007.
6. Cortés-Peneld NW, Kulkarni PA. The history of
antibiotic treatment of osteomyelitis. Open Forum
Infect Dis. 2019;6(5):ofz181. https://doi.org/10.1093/
od/ofz181.
7. Hatzenbuehler J, Pulling TJ. Diagnosis and management of osteomyelitis. Am Fam Physician.
2011;84(9):1027–33.
8. Andre L, Clark MD, Accardo SI.Nuclear medicine
musculoskeletal assessment, protocols, and interpretation, in StatPearls. Treasure Island: StatPearls
PublishingCopyright © 2024, StatPearls Publishing
LLC; 2024.
9. Kremers HM, Nwojo ME, Ransom JE, Wood-Wentz
CM, Melton LJ 3rd, Huddleston PM 3rd. Trends in
the epidemiology of osteomyelitis: a populationbased study, 1969 to 2009. J Bone Joint Surg Am.
2015;97(10):837–45. https://doi.org/10.2106/
JBJS.N.01350.
10. Burnett MW, Bass JW, Cook BA.Etiology of osteomyelitis complicating sickle cell disease. Pediatrics.
1998;101(2):296–7. https://doi.org/10.1542/
peds.101.2.296.
11. Holt RIG, Cockram CS, Ma RCW, Luk AOY.Diabetes
and infection: review of the epidemiology, mechanisms and principles of treatment. Diabetologia.
2024;67(7):1168–80.
024- 06102- x. Epub 2024 Feb 20.
12. Rehman S, Arif S, Ushakumari LG, Amreen J, Nagelli
A, Moonnumackel SJ, Nair A.Assessment of bacterial infections and antibiotic regimens in intravenous
drug users. Cureus. 2023;15(9):e45716. https://doi.
org/10.7759/cureus.45716.
13. Secamilli EN, Drummond MR, Serrano JYM, Stelini
RF, Cintra ML, Velho PENF.Is Bartonella sp. infec-
https://doi.org/10.1007/s00125-

1 Bone andJoint Infections: Introduction andEpidemiology
7
tion relevant in hematological malignancies in HIVnegative patients? A literature review. Leuk Res
Rep. 2023;21:100402. https://doi.org/10.1016/j.
lrr.2023.100402.
14. Anis HK, Ramanathan D, Sodhi N, Klika AK,
Piuzzi NS, Mont MA, Higuera CA, Molloy
RM. Postoperative infection in cementless and
cemented total knee arthroplasty: a propensity score
matched analysis. J Knee Surg. 2019;32(11):1058–62.
https://doi.org/10.1055/s- 0039- 1678678.
15. Lemaignen A, Bernard L, Marmor S, Ferry T,
Grammatico-Guillon L, Astagneau P. Scientic
Committee for Complex Bone and Joint Infections
Reference Centers (CRIOAc), on behalf of
the CRIOAc network. Epidemiology of complex bone and joint infections in France using a
national registry: the CRIOAc network. J Infect.
2021;82(2):199–206. https://doi.org/10.1016/j.
jinf.2020.12.010.
16. Tsantes AG, Altsitzioglou P, Papadopoulos DV,
Lorenzo D, Romanò CL, Benzakour T, Tsukamoto
S, Errani C, Angelini A, Mavrogenis AF.Infections
of tumor prostheses: an updated review on risk factors, microbiology, diagnosis, and treatment strategies. Biology (Basel). 2023;12(2):314. https://doi.
org/10.3390/biology12020314.
17. Turner NA, Sharma-Kuinkel BK, Maskarinec SA,
Eichenberger EM, Shah PP, Carugati M, Holland TL,
Fowler VG Jr. Methicillin-resistant Staphylococcus
aureus: an overview of basic and clinical research.
Nat Rev Microbiol. 2019;17(4):203–18. https://doi.
org/10.1038/s41579- 018- 0147- 4.
18. Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin
SK, Gorwitz RJ, Kaplan SL, Karchmer AW, Levine
DP, Murray BE, Rybak JM, Talan DA, Chambers
HF, Infectious Diseases Society of America. Clinical
practice guidelines by the infectious diseases society
of america for the treatment of methicillin-resistant
Staphylococcus aureus infections in adults and children. Clin Infect Dis. 2011;52(3):e18–55. https://doi.
org/10.1093/cid/ciq146.
19. He M, Arthur Vithran DT, Pan L, Zeng H, Yang G,
Lu B, Zhang F.An update on recent progress of the
epidemiology, etiology, diagnosis, and treatment
of acute septic arthritis: a review. Front Cell Infect
Microbiol. 2023;13:1193645. https://doi.org/10.3389/
fcimb.2023.1193645.
20. Conway JD, Hambardzumyan V, Patel NG, Giacobbe
SD, Gesheff MG. Immunological evaluation of
patients with orthopedic infections: taking the
Cierny-Mader classication to the next level. J Bone
Jt Infect. 2021;6(9):433–41. https://doi.org/10.5194/
jbji- 6- 433- 2021.
21. Tsantes AG, Papadopoulos DV, Vrioni G, Sioutis S,
Sapkas G, Benzakour A, Benzakour T, Angelini A,
Ruggieri P, Mavrogenis AF.World association against
infection in orthopedics and trauma W A I O T study
group on bone and joint infection denitions. Spinal
infections: an update. Microorganisms. 2020;8(4):476.
https://doi.org/10.3390/microorganisms8040476.
22. Trovarelli G, Angelini A, Pala E, Cappellari A, Breda
A, Ruggieri P.Infection in orthopaedic oncology: crucial problem in modern reconstructive techniques. Eur
Rev Med Pharmacol Sci. 2019;23(2 Suppl):271–8.
https://doi.org/10.26355/eurrev_201904_17501.
23. Bettale C, Chisari E, Parvizi J. 8.1 Osteomyelitis 8.1.
1 highlights (table 8.1) denition—infection of the
bone or bone marrow epidemiology. In: Textbook of
musculoskeletal disorders. Springer; 2023. p.67.
24. Rather MA, Gupta K, Mandal M.Microbial biolm:
formation, architecture, antibiotic resistance, and control strategies. Braz J Microbiol. 2021;52(4):1701–18.
https://doi.org/10.1007/s42770- 021- 00624- x. Epub
2021 Sep 23.
25. Forsberg JA, Potter BK, Cierny G 3rd, Webb
L. Diagnosis and management of chronic infection.
J Am Acad Orthop Surg. 2011;19(Suppl 1):S8–S19.
https://doi.org/10.5435/00124635- 201102001- 00003.
26. Schmitt SK. Osteomyelitis. Infect Dis Clin N Am.
2017;31(2):325–38.
27. Al-Nammari SS, Bobak P, Venkatesh R.Methicillin
resistant Staphylococcus aureus versus methicillin sensitive Staphylococcus aureus adult haematogenous septic arthritis. Arch Orthop Trauma
Surg. 2007;127(7):537–42. https://doi.org/10.1007/
s00402- 007- 0285- z.
28. Wang J, Wang L. Novel therapeutic interventions
towards improved management of septic arthritis.
BMC Musculoskelet Disord. 2021;22(1):530. https://
doi.org/10.1186/s12891- 021- 04383- 6.
29. Angelini A, Tiengo C, Sonda R, Berizzi A, Bassetto
F, Ruggieri P. One-stage soft tissue reconstruction following sarcoma excision: a personalized
multidisciplinary approach called “Orthoplasty”. J
Pers Med. 2020;10(4):278. https://doi.org/10.3390/
jpm10040278.
30. Muller Q, Gerber F, Papadimitriou Olivgeris
M, Di Summa P, Boillat Blanco N, Steinmetz
S. Prise en charge multidisciplinaire des infections de fracture [Multidisciplinary approach
to fracture-related infection]. Rev Med Suisse.
2022;18(808):2363–70. French. https://doi.
org/10.53738/REVMED.2022.18.808.2363.
31. Trimaille A, Kerfant N, Henry AS, Ta P,
Rouanet M, Le Nen D, Stindel E, Ansart S, Hu
W.Multidisciplinary management of the bone and
joint infection complicating treatment of an open
fracture of the lower limb. Ann Chir Plast Esthet.
2020;65(5–6):380–93. https://doi.org/10.1016/j.
anplas.2020.05.012.
32. Panteli M, Giannoudis PV. Chronic osteomyelitis: what the surgeon needs to know. EFORT
Open Rev. 2017;1(5):128–35. https://doi.
org/10.1302/2058- 5241.1.000017.
33. Copley LA, Kinsler MA, Gheen T, Shar A, Sun D,
Browne R. The impact of evidence-based clinical
practice guidelines applied by a multidisciplinary
team for the care of children with osteomyelitis. J
Bone Joint Surg Am. 2013;95(8):686–93. https://doi.
org/10.2106/JBJS.L.00037.

Antibiotic Stewardship
inOrthopedic Surgery
KhaledM.Emara, RamyA.Diab,
andKyrillosRashid
2
2.1 Introduction
Addressing different types of musculoskeletal
infections necessitates a skilled hand from an
orthopedic surgeon. These infections originate
from surgical interventions, blood ow dispersal,
immediate trauma, and other sources. Timely care
is necessary to forestall catastrophic outcomes,
including bone infection, joint inammation, and
implant failure. The strategic application of antibiotics, guided by scientic research, is critical to
achieving optimal patient outcomes while counteracting the growing threat of drug resistance [1].
Additionally, controlling infections is a vital component of orthopedic surgery since, if neglected,
they may have disastrous effects. In orthopedic
procedures, antibiotics are essential for preventing and treating infections, and new developments
in antibiotic regimes have completely changed
how these infections are handled. This chapter
investigates the current understanding and suggestions for effectively treating bone and joint
infections, stressing the essential role of antibiotic
sensitivity in orthopedic medical procedures.
Moreover, it highlights their signicance in assuring the best possible patient outcomes and the
new procedures for antibiotic usage in various
orthopedic surgery instances.
K. M. Emara · R. A. Diab · K. Rashid (*)
Department of Orthopedic Surgery, Ain Shams
University, Cairo, Egypt
2.2 Pathogenesis
andMicrobiology ofBone
andJoint Infections
Effective treatment techniques are based on
understanding the pathophysiology and microbiological origin of bone and joint infections,
which is crucial [5]. Staphylococcus aureus holds
the leading role in these instances, signicantly
affecting the unfolding of the related ailments.
The struggle with methicillin-resistant strains
originates from their innate defense systems [2].
It is essential to recognize that multiple factors
contribute to these diseases. Various possible
pathogens, including Streptococcus species,
gram-negative bacilli, and anaerobes, contribute
to the complex ecology of bone and joint diseases. Recent scientic research has shown that
biolm development on implant surfaces is crucial in encouraging persistent infections [9]. This
discovery has broad repercussions since biolms
allow pathogens to resist host immune responses
and common antibiotic treatments.
The formation of biolms protects the microbial population from immune monitoring and
forms a barrier that hinders the effectiveness of
antimicrobial drugs [1]. This complex interaction
between infections and biolms highlights the
urgent need for precisely planned treatment
approaches that may successfully penetrate these
biolm barriers [4]. The conclusions drawn from
these disclosures push for substituting precision-
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
P. Ruggieri et al. (eds.), Bone and Joint Infections, https://doi.org/10.1007/978-3-031-96383-4_2
9

10
K. M. Emara et al.
guided interventions for broad-spectrum empirical therapies [2]. Identifying the microorganisms
implicated and the distinctive features of their
biolm forms signicantly impacts the effectiveness of antibiotic regimens [7]. In order to
improve patient outcomes in orthopedic surgery,
the next frontier in the therapy of bone and joint
infections depends on focused, therapeutic methods that negotiate the complexity of microbial
etiology and biolm dynamics.
2.3 Diagnostic Modalities
Effective therapy of bone and joint infections
depends heavily on accurate and prompt diagnosis, which directs the choice of suitable treatment
approaches. We are now able to quickly and precisely detect these illnesses because of considerable improvements in diagnostic techniques.
Modern imaging methods have become essential
components of the diagnostic toolkit [6]. With its
unmatched soft tissue contrast and multiplanar
capabilities, magnetic resonance imaging (MRI)
has completely changed how bone and joint
infections may be seen. MRI enables the early
diagnosis of infections even before radiographic
abnormalities become obvious because it makes
it easier to see small changes in the bone marrow
and nearby soft tissues [17]. Nuclear scintigraphy, such as Technetium-99m bone scans and
Gallium-67 scans, also provides extraordinary
sensitivity in identifying infection spots that are
actively spreading, helping to localize the regions
that need more research and treatment.
Molecular diagnostic equipment has become
more popular in the age of individualized treatment. Microorganisms that cause disease may
now be quickly and precisely identied thanks to
polymerase chain reaction (PCR), which amplies certain DNA sequences. It includes slowmoving or picky diseases that may be uncommon
in traditional civilizations [7]. Additionally, the
capability of PCR to provide proles of antibiotic
susceptibility enables doctors to customize medication early in the course of treatment, thereby
improving patient outcomes [12]. In the diagnostic landscape, integration is crucial [9]. The infec-
tion’s breadth, severity, and etiology may all be
fully understood by integrating clinical, radiographic, and molecular results [8]. Orthopedic
surgeons may create specialized treatment plans
that focus on the distinctive traits of each illness,
thanks to this multidimensional approach, which
also improves diagnostic accuracy.
2.4 Antibiotic Stewardship Principles
Personalized Treatment: Antibiotic therapy’s paradigm is changing from a one-size-ts-all strategy to customized treatment programs that
consider unique patient traits, microbiological
information, and bone and joint infection severity
[9]. With this change, it is acknowledged that
patient responses to medicines might vary and
that different infecting bacteria have different
susceptibilities [17]. Clinicians may maximize
therapeutic results while lowering the risk of
needless antibiotic usage by customizing therapy
to unique patient characteristics, such as age,
comorbidities, and prior antibiotic exposure. By
preventing indiscriminate medication exposure,
this strategy not only lowers the chance of negative effects but also prevents the development of
antibiotic resistance [10]. Additionally, by using
cutting-edge diagnostic technologies like molecular methods and genomic sequencing, doctors
may quickly and correctly identify the causal
organisms, allowing tailored antibiotic selection.
With targeted and evidence-based therapy techniques, personalized treatment ushers in a new
age of precision medicine in orthopedic surgery.
De-escalation and Duration: De-escalation
tactics are critical in the therapy of bone and joint
infections, according to recent recommendations.
Clinicians should switch from broad-spectrum
empiric antibiotics to narrower, more focused
medications once microbiological culture data
are available [11]. Since narrower-spectrum
medicines successfully target the specic pathogen while sparing nonpathogenic bacteria, this
method is consistent with optimizing antibiotic
usage [11]. Additionally, shorter antibiotic
courses may reduce side effects such as drug-
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