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The most common complication observed was wound healing deficiency and infection (n = 21 (61.7%)).
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Wound healing can be problematic in several clinical settings because of massive tissue injury (burns), wound healing deficiencies (chronic wounds), or congenital conditions and diseases.
Further, as Grimer et al. [ 9] reported we have also made promising experiences using vacuum-assisted closure devices in wound-healing deficiencies.
The bilateral tendency and delayed progress in healing suggest intrinsic deficiencies of the bone tissue beyond local stress factors.
In conclusion, the reported clinical experiences and the parallel experimental data support the hypothesis that FXIII deficiency may impair healing in patients with MI while replacement therapy may alleviate complications.
The crucial role of zinc is well documented and zinc deficiency delays wound healing [ 21].
Impaired blood flow at the wound surface can result in oxygen and nutrient deficiency, limiting nutrient access for healing.
It is not clear why vitamin D enhances healing of rickets in children with calcium-deficiency rickets, even in those with adequate vitamin D status, as we have previously shown excellent intestinal calcium absorption without D supplementation.
These results suggested a significant increase of TNF- α following macrophage PPAR γ deficiency, which may account for the delayed wound healing.
Symptoms of deficiency include dry skin, hair loss, and impaired wound healing.
To address this demand, the present case reports raised the question if vitamin D deficiency influences implant survival in the early stages of healing.
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