**7. Summary of scheme review**

*Clinical Implementation of Bone Regeneration and Maintenance*

using the immunoassay method [36].

tion, but also of a MMP action.

**6. Background factors**

function [21–23].

D-insufficiency [37].

secreted amounts.

that can be "found out" using markers, occur [38–40]:

• "Mobilization" of calcium and phosphates from the bones.

The matrix destruction leads to increase in following resorption markers: B-cross-laps (С-terminal telopeptide) and desoxypyridinoline/creatinine ratio.

• B-cross-laps: This marker is a product of collagen destruction that is a basis of bone tissue matrix. B-cross-laps have two octapeptide fragments in structure, which are linked with a transverse molecular bond. Its level can be evaluated

• Increase in the desoxypyridinoline/creatinine ratio: Desoxypyridinoline is a molecular basis for transverse bonds between collagen I type molecules in bone tissue matrix. Its level increases while the matrix is destroyed. It is important to note that this factor can be increased as a result of not only osteoclast activa-

A clinician should note that the destruction of the matrix is combined with lowering of its synthesis by osteoblasts. Therefore, both processes act in a synergic way and occur at the same time, which negatively influences the treatment (**Figure 4**).

The main background factors that can exacerbate bone tissue metabolism impairment at the site of bone infection are: generalized osteoporosis, D-deficit, D-insufficiency, and secondary hyperparathyreosis. These factors exacerbate also the condition of patients with bone infection, lowering the regenerative potential of

• The lack of D hormone leads to lowered absorption of calcium in the intestine, lowered mineralization of the bone, and consequent decrease of the osteoblast

D-insufficiency and is actually a compensative reaction. It has rather complex pathogenetic action mechanism [37]. It is shown that during short-term increase in PTH level, its influence on bone tissue is anabolic, while during a long-term constant increase, its effect becomes catabolic with bone loss as a result, for example, at the condition of chronic hormone D-deficit or hormone

Thus, because of the excessive PTH action on bone tissue, two major effects,

• Increase in calcium and phosphate levels in the urine because of relatively high

As a result, calcium and phosphates are being literally "washed out" of the bone in amounts more than physiological. After that, they are secreted out of the organism through urine. A bright example is an increase in vertebral bodies fractures risk in patients with primary hyperparathyreosis. Even simple densitometry can help to diagnose the lowered bone density and trabecular thinning.

• Secondary hyperparathyreosis: This condition is a result of D-deficit or

bone tissue. On the scheme, these factors are marked as yellow blocks.

**144**

In this part of the chapter, the etiopathogenetic mechanisms of bone tissue metabolism impairment are discussed, as well as reasons for change of laboratorymeasured bone metabolism markers and their levels.

The mentioned markers have a direct link with metabolic impairments of a certain type. Such impairments can be found in different diseases, especially in patients with chronic osteomyelitis and other forms of bone infection.

The therapy of metabolic bone tissue impairments due to bone (orthopedic) infection should combine etiopathogenetic and compensating approaches. For example, bisphosphonates can be recommended for use in addition to antibiotic therapy and surgery, as well as calcium, D hormone, and other drugs because of the bisphosphonates' ability to decrease the osteoclasts' activity.
