Bruno Silvestrini

By Bruno Silvestrini, Chuen Yan Cheng and Matteo Innocenti

This chapter discusses the physiologic, metabolic, and clinical aspects of collagen, including the role of nutritional factors in a new nosographic entity, called “extended collagen carential disease.” Except water and possibly fats, carbohydrates, and other structural proteins, perhaps there is more collagen in the mammalian body than anything else. Moreover, collagen participates in almost all of the body functions, adjusting its structure constantly in response to changes in environment, development, growth, and external clues. Collagens found in bones and nails are different from collagens found in body fluids and other biological structures, such as basement membrane, skin, tendons, muscles, and hair. The ubiquity of collagen functions accounts for its phylogenetic ubiquity, involving any tissue, organ, and apparatus. This is shown by the so-called “collagen carential disease,” involving nails, hair, osteoarticular and gastrointestinal systems. For instance, the Ehlers-Danlos syndrome describes another group of genetic collagen disorders, affecting the collagen processing and structure. Some of them are inherited in an autosomal dominant manner, while others emerge in the absence of essential nutritional factors. It is the case of Vitamin C, which plays a critical role in the maintenance of a normal mature collagen network. Hence, the idea of an “extended collagen carential disease,” applicable to the absence of essential nutritional factors.

Part of the book: Collagen Biomaterials

By Bruno Silvestrini and Mauro Silvestrini

This story deals with the role of protein denaturation in inflammation. The starting point was the description of the necrotizing action of inflammatory proteins, followed by the discovery of the antidenaturant action of NSAIDs (nonsteroidal anti-inflammatory drugs). Hence, the idea is that the antidenaturant action accounted for the action of NSAIDs. This hypothesis was dropped following the discovery of the antiprostaglandin action of NSAIDs, which shifted the focus to the arachidonic acid cascade. It was revived by assuming that protein denaturation is a process in its own, suitable for separate medical treatment. This approach led to bendazac and bindarit, the first selective antidenaturant drugs. This experience shows that protein denaturation has two main pathological sequelae. The first concerns the so-called primary (innate) inflammation. The second sequela concerns the so-called secondary (acquired) inflammation. Natural antidenaturant agents represent a promising alternative to the synthetics bendazac and bindarit. Within this framework, tendinitis finds a separate but significant place.

Part of the book: Tendons