Abstract: Methods and systems for diagnosing a bone disease or other condition related to collagen in a subject are provided. These include providing a bone sample from the subject and determining a quantitative collagen morphology value of the bone sample. A reference value is provided from a non-affected control subject where the reference value is a quantitative collagen morphology value from the same type of bone sample obtained from a population of non-affected control subjects. The quantitative collagen morphology value of the subject's bone sample is compared to the reference value. If the collagen morphology value is altered versus the reference value, the subject is diagnosed as having a collagen related bone disease. The collagen morphology value can include mean fibril spacings and distributions of the fibril spacings taken from a subject's bone sample.

Abstract: Methods and systems for diagnosing a bone disease or other condition related to collagen in a subject are provided. These include providing a bone sample from the subject and determining a quantitative collagen morphology value of the bone sample. A reference value is provided from a non-affected control subject where the reference value is a quantitative collagen morphology value from the same type of bone sample obtained from a population of non-affected control subjects. The quantitative collagen morphology value of the subject's bone sample is compared to the reference value. If the collagen morphology value is altered versus the reference value, the subject is diagnosed as having a collagen related bone disease. The collagen morphology value can include mean fibril spacings and distributions of the fibril spacings taken from a subject's bone sample.

Abstract: Methods are provided for ascertaining and measuring RPTP-? activity in response to insults such as UV irradiation and with respect to administration of a treatment and/or composition. Attenuation of EGFR activity by RPTP-? affects aspects of photoaging, including damage to the skin, suppression of the immune system, DNA damage, and connective tissue degradation. Intervention with respect to the effects of photoaging can include protection of RPTP-? from oxidation. The methods can be used for discovery of anti-aging treatments, adjuncts, or other preventative treatments, such as sunscreens.

Abstract: Methods are provided for ascertaining and measuring RPTP-? activity in response to insults such as UV irradiation and with respect to administration of a treatment and/or composition. Attenuation of EGFR activity by RPTP-? affects aspects of photoaging, including damage to the skin, suppression of the immune system, DNA damage, and connective tissue degradation. Intervention with respect to the effects of photoaging can include protection of RPTP-? from oxidation. The methods can be used for discovery of anti-aging treatments, adjuncts, or other preventative treatments, such as sunscreens.

Abstract: Rosacea is treated with a composition comprising an antimicrobial and at least one of an anti-inflammatory and a non-retinoid inhibitor of at least one of NF-KB, AP-1, MMPs, adhesion molecules, TLRs, and CD14. The composition may further comprise a retinoid.

Abstract: Methods and compositions to prevent scarring of the skin include a matrix metalloproteinase inhibitor and a vehicle suitable for topical application. Scarring and damage to the epidermis and extracellular matrix may be reduced and/or prevented. Following skin damage, application of the matrix metalloproteinase inhibitor reduces expansion of the extracellular matrix portion of the skin compared to untreated skin.

Abstract: Methods are provided for ascertaining and measuring RPTP-? activity in response to insults such as UV irradiation and with respect to administration of a treatment and/or composition. Attenuation of EGFR activity by RPTP-? affects aspects of photoaging, including damage to the skin, suppression of the immune system, DNA damage, and connective tissue degradation. Intervention with respect to the effects of photoaging can include protection of RPTP-? from oxidation. The methods can be used for discovery of anti-aging treatments, adjuncts, or other preventative treatments, such as sunscreens.

Abstract: Acne-affected skin has been found to be accompanied by the presence of matrix-degrading enzymes such as MMPs and neutrophil elastase, induction of neutrophils, and a reduction in procollagen biosynthesis. This invention treats scarring and inflammation accompanying acne by administering, topically or systemically, at least one of (i) an inhibitor of the matrix degrading enzymes and (ii) a cytokine inhibitor that alleviates inflammation and thus also alleviate neutrophil infiltration. Alleviating the matrix degradation and renormalizing procollagen biosynthesis allows for reduced inflammation and better natural repair of acne-affected skin. Inhibiting cytokines alleviates induction of MMPs in resident skin cells, and also alleviates inflammation with its concommitant induction of neutrophils from the blood stream bringing MMPs and elastase into the acne lesion.

Abstract: UVB radiation of about 300-310 nm wavelength and UVA radiation of about 380-390 nm wavelength, each of which exists in solar light, induces MMPs (matrix metalloproteinases) in human skin that degrade the collagen of the dermal matrix. This degradation contributes to photoaging of human skin, which can be prevented by blocking these wavelengths of solar radiation. In contrast, diseases that result in the overproduction of collagen can be treated by exposing the affected with to radiation having wavelengths in those regions, for these wavelengths not only induce MMPs but also inhibit collagen biosynthesis. For lighter skinned people so affected, the UVA wavelengths are preferred because of the reduced amount of erythema, whereas dark skinned people can be treated with the UVB radiation because they generally do not suffer from erythema.

Abstract: Exposure of human skin to ultraviolet (UV) radiation from the sun not only induces the production of enzymes (matrix metalloproteinases) that degrade collagen, but also inhibits the synthesis of new collagen by inhibiting the synthesis of procollagen. This UV-induced inhibition of the synthesis of collagen can be prevented by the topical application of a retinoid or c-JUN inhibitor to the skin prior to exposure to UV radiation.

Abstract: Rosacea is treated with a composition comprising an antimicrobial and at least one of an anti-inflammatory and a non-retinoid inhibitor of at least one of NF-??, AP-1, MMPs, adhesion molecules, TLRs, and CD14. The composition may further comprise a retinoid.

Abstract: Compositions and methods are provided for ameliorating various effects of UVA and UVB radiation from the sun. The compositions include an ingredient that prevents photoaging from MED and subMED radiation, namely a direct acting MMP (matrix metalloproteinase) inhibitor. The compositions can include another, indirect MMP inhibitor, such as a retinoid, certain other compounds (such as N-acetylcysteine, 2-furildioxime, and vitamin C), tetracyclines, and if a retinoid is used then in addition optional compounds that inhibit the CYP-26 (chytochrome P-450) mediated metabolism of retinoids such as ketoconazole and other azole compounds. In the method, the composition is applied prior to exposure to the sun; for direct acting MMP inhibitors, application should be just prior to exposure, and if indirect inhibitors such as retinoids are used in addition, then application of the indirect inhibitor should be at least about seven hours prior to exposure.

Abstract: Chronological aging of human skin can be delayed with the topical application of an MMP inhibitor, preferably a retinoid (an indirect MMP inhbitor); retinoids also normalize procollagen biosynthesis. Chronological aging, or natural aging, is evidenced in elderly (80+ years old) skin by increased MMP levels and decreased procollagen levels when compared with younger individuals. Prophylactic treatment of not yet chronologically-aged skin with a retinoid both inhibits degradation of dermal collagen and restores procollagen synthesis. Biopsied sections from elderly skin show that a single treatment of chronologically-aged skin with a retinoid can increase epidermal thickness, improve the dermal collagen density, and promote the formation of rete pegs and dermal papillae. Such benefits are helpful in preventing bruising, tearing, and ulceration of elderly skin. Accordingly, prophylactic treatment begun much earlier in life with an MMP inhibitor and/or a retinoid delays the onset of such symptoms.

Abstract: Acne-affected skin has been found to be accompanied by the presence of matrix-degrading enzymes such as MMPs and neutrophil elastase, induction of neutrophils, and a reduction in procollagen biosynthesis. This invention treats scarring and inflammation accompanying acne by administering, topically or systemically, at least one of (i) an inhibitor of the matrix degrading enzymes and (ii) a cytokine inhibitor that alleviates inflammation and thus also alleviate neutrophil infiltration. Alleviating the matrix degradation and renormalizing procollagen biosynthesis allows for reduced inflammation and better natural repair of acne-affected skin. Inhibiting cytokines alleviates induction of MMPs in resident skin cells, and also alleviates inflammation with its concommitant induction of neutrophils from the blood stream bringing MMPs and elastase into the acne lesion.

Abstract: Exposure of human skin to ultraviolet (UV) radiation from the sun not only induces the production of enzymes (matrix metalloproteinases) that degrade collagen, but also inhibits the synthesis of new collagen by inhibiting the synthesis of procollagen. This UV-induced inhibition of the synthesis of collagen can be prevented by the topical application of a retinoid or c-JUN inhibitor to the skin prior to exposure to UV radiation.

Abstract: Chronological aging of human skin can be delayed with the topical application of an MMP inhibitor, preferably a retinoid (an indirect MMP inhbitor); retinoids also normalize procollagen biosynthesis. Chronological aging, or natural aging, is evidenced in elderly (80+ years old) skin by increased MMP levels and decreased procollagen levels when compared with younger individuals. Prophylactic treatment of not yet chronologically-aged skin with a retinoid both inhibits degradation of dermal collagen and restores procollagen synthesis. Biopsied sections from elderly skin show that a single treatment of chronologically-aged skin with a retinoid can increase epidermal thickness, improve the dermal collagen density, and promote the formation of rete pegs and dermal papillae. Such benefits are helpful in preventing bruising, tearing, and ulceration of elderly skin. Accordingly, prophylactic treatment begun much earlier in life with an MMP inhibitor and/or a retinoid delays the onset of such symptoms.

Abstract: People's hands undergo daily exposure to hot, cold, and chemicals (such as cleansers). These exposures can cause dermatitis due to activation of the Epidermal Growth Factor Receptor (EGFR). One effect of activation of the EGFR is hyperproliferation of skin cells, which presents as rough, dry, and/or peeling hands, generally known as dermatitis. The use of a natural EGFR inhibitor, such as genistein or quercetin, can help to treat or prevent these kinds of dermatitis.

Abstract: Exposure of human skin to ultraviolet (UV) radiation from the sun not only induces the production of enzymes (matrix metalloproteinases) that degrade collagen, but also inhibits the synthesis of new collagen by inhibiting the synthesis of procollagen. This UV-induced inhibition of the synthesis of collagen can be prevented by the topical application of a retinoid or c-JUN inhibitor to the skin prior to its exposure to UV radiation.

Abstract: Many human conditions, often skin conditions, are treated topically or orally with a retinoid such as retinoic acid or acetretin, which treatment often has the side effect of dry, irritated, and/or peeling skin. The use of soaps, detergents, chemical irritants, and such can also cause these same side effects. These side effects can be reduced or eliminated by the topical administration of an inhibitor, especially a natural inhibitor, of the epidermal growth factor receptor (EGFR), administered concomitantly with the retinoid, separately from the retinoid (such as on an as needed basis), or both. Administration of the two together is facilitated by a composition suitable for topical application and comprising both the retinoid and a natural EGFR inhibitor. Preferred natural inhibitors are genistein and other isoflavones extracted from natural occurring substances, or simple derivatives of such substances.

Abstract: The deleterious effects of the passage of time on human skin (i.e., chronological aging of human skin) can be prevented and treated with the topical application of a retinoid, preferably retinol. We have found that some of the same pathways (namely the stress-activated pathways, SAPs) activated in photoaging of human skin (i.e., sun-induced premature skin aging) are similarly elevated in the skin of elderly people. We have also found that other pathways (namely the mitogen-activated ERK pathway) is depressed in the same skin. Treatment of chronologically-aged skin with a non-retinoid MMP inhibitor and optionally a retinoid both inhibits degradation of dermal collagen and promotes procollagen synthesis. Biopsied sections from skin of elderly (80+ years old) show that a single treatment can increase epidermal thickness, improve the dermal collagen density, and promote the formation of rete pegs and dermal papillae (see FIG.