**1. Introduction**

The empirical experience of surgeons operating patients with orthopedic infection shows that the mechanical properties of the bone (including strength) differ from physiological ones. The bone in or near the infected area tends to be more fragile and soft. Proper mechanical strength of the bone tissue is one of the key factors for completing successful osteosynthesis as the mechanical strength of the bone directly influences the stability of fixators, treatment of bone tissues in the surgery process, and other technical but pivotal aspects of the treatment.

Despite some empirical data, the change of mechanical properties of the bone in orthopedic infection remained practically unresearched for a long time. The change of the mechanical properties of the bone in inflamed areas had been connected to tissue destruction or lysis caused by bacterial pathogen. In other words, this change of the mechanical properties of the bone happening in the inflamed area was

viewed similarly as the complications in soft tissues in the purulent surgery, widely known for a long period of time.

Consequently, this falsely simplified view of the problem has led to a shortage of publications. For example, the search query in the PubMed database based on Mesh terms "Osteomyelitis" and "Bone mineral density" (latest access time: December 08, 2019, 0:01 UTC +3) has provided only 30 search results, the earliest of them is signed as published in February 1991. Most publications refer to dentistry and maxillofacial surgery but not to traumatology and/or orthopedics. Another search based on Mesh terms "Osteomyelitis" and "Metabolic disorders" (latest access time: December 08, 2019, 0:03 UTC +3) has provided 596 results, but most papers refer to other topics and problems: "combinations" of chronic osteomyelitis and diabetes mellitus [1, 2], chronic osteomyelitis and bisphosphonate-induced necrosis of the jaw [3, 4]; less papers refer to the problem of treating chronic osteomyelitis in patients with genetic, systemic, neuropathic, and oncological diseases [5–8]. In several papers, the accent is put on the clinical aspects of bone infection with particular pathogens only [9–11]. Some papers can be considered of a relatively good quality but the accent is put on clinical results themselves and not on the pathogenesis of metabolic bone tissue disorders in the presence of bone infection [12, 13].

Numerous clinical guidelines and publications on osteoporosis and related disorders have much to offer about the pathophysiology of these diseases, but have a rather serious common disadvantage: they do not describe or poorly describe the interaction of pathogen and bone tissue, although the infectious and purely osteoporotic metabolic processes have similar mechanisms.

Lack of understanding of the metabolic bone tissue disorders as a result of its interaction with bacterial pathogen during orthopedic infection practically eliminated the possibility of providing adequate etiological treatment; in most cases, the treatment methods were limited to surgical treatment (necrectomy, debridement, external fixation, and related methods) and antibiotic therapy. Despite being approved and reliable, these methods themselves are not enough to treat chronic osteomyelitis. The correction of the impaired bone tissue metabolism is also needed. For this purpose, a clinician should be familiar with the aspects of biochemistry, physiology, and pathophysiology of the bone affected by orthopedic infections.

At this moment, several fundamental papers in the domain of bone tissue and pathogen interaction are available [14, 15], which can be evaluated as a positive trend. These works can be useful to systematize the knowledge cumulated by the scientific community.

Within this chapter, we made an attempt to synergize the knowledge in pathophysiology of the disorders described, as well as illustrate the importance of correction of impaired bone tissue metabolism using the results of our own work published in 2019 [16].
