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Articular Cartilage Pathology and Therapies
Published in Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi, Articular Cartilage, 2017
Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi
Some notable examples of genetic defects that lead to osteoarthritis are described here: Alkaptonuria is an autosomal recessive genetic disorder resulting in abnormal phenylalanine and tyrosine metabolism, wherein the tyrosine metabolic byproduct is not cleared (homogentisic acid, or alkapton) and builds up in cartilage (ochronosis), heart valves, and the kidneys. Ochronosis leads to articular cartilage degeneration. The defect lies in the homogentisate 1,2-dioxygenase enzyme produced by the HGD gene on chromosome 3. This enzyme participates in tyrosine metabolism by converting homogentistic acid into 4-maleylacetoacetate (Figure 3.5).
Antioxidant and anti-tyrosinase activities of quercetin-loaded olive oil nanoemulsion as potential formulation for skin hyperpigmentation
Published in Journal of Dispersion Science and Technology, 2022
Cristiane C. Silva, Rogério B. Benati, Taís N. C. Massaro, Karina C. Pereira, Lorena R. Gaspar, Priscyla D. Marcato
Hyperpigmentation disorders, which include postinflammatory hyperpigmentation, solar lentigos and melasma, are characterized by dark spots on the skin.[1] Specifically, melasma is a chronic acquired condition of hypermelanosis characterized by homogeneous spots with irregular borders from light to dark brown, distributed on the epidermis, very frequent on the face.[2,3] The conventional treatment for this hyperpigmentation[2] consists of applying sunscreen and using 2-5% topical hydroquinone alone or in combination with retinoic acid (0.05-0.1%) since both interfere in melanogenesis and also retinoic acid, as a chemical peel, which acts on the desquamation of the epidermis.[2,4,5] Hydroquinone is a gold standard for skin hyperpigmentation as it prevents melanin synthesis with the inhibition of the tyrosinase enzyme. However, it can cause skin irritation, allergy, dermatitis and, in the case of chronic use, exogenous ochronosis, characterized as a rare bluish-black dermatosis.[6,7] There are other treatments, for example, kojic acid and azelaic acid as tyrosinase inhibitors, chemical peels, and laser therapy, in the place of the widely used hydroquinone. However, they also have limitations and undesirable effects. Kojic acid and azelaic acid have difficulty reaching the epidermis and they require long periods of treatment.[8] Furthermore, kojic acid, as a well-known ingredient for skin depigmentation, is unstable during the storage, has limited tyrosinase inhibitory activity, and may cause contact dermatitis and, over a long period, photodamaged skin.[9,10] Lastly, laser therapy and chemical peels have a high safety risk, with the possibility of inflammation, scarring, changes in skin color, or even rebound hyperpigmentation.[8,11]