Companies:  Buy Activated Charcoal   Cabot   Calgon Carbon Corp  Chemviron

See also Water purification in the Purification section

Activated Carbon (AKA Activated Charcoal) is typically derived form charcoal or coal, although other raw materials including wood, sawdust, coconut shells, bamboo, peat, petroleum coke are also used. Charcoal is made by burning wood. But charcoal is not “activated charcoal”. Instead, it is one raw material for the manufacture of activated barbons. There are two basic activation processes (1) charcoal is once again heated to very hihg temperatures in the presence of oxidizing gases such as CO2, stea, or air or (2) charcoal is impregnated with chemicals such as acids like phosphoric acid or salts like zinc chloride and then exposred to high temperature. The activation process futher erode the charcoal’s internal surfaces which increases the adsorption capacity by creating an internal network of even smaller pores rendering it two to three times as effective a regular charcoal. 

Activated carbon is used as an emergency decontaminant in the gastrointestinal (GI) tract. It is used after a person swallows or absorbs almost any toxic drug or chemical. PULSORB®PGC is a powdered activated carbon fit for consumption in the treatmnet of ingested toxins. 

Activated carbon is also used in the purificaiton of pharmaceutical products such as proteins.

AC is also widely used as an adsorbent in the water and air treatment industries due to its exceptionally high surface area. 

Companies: Particle Measuring Systems 

Typical virus inactivation methods include low pH treatment (e.g., below pH 4.5, below 4.0 or even below 3.8, heat treatment, treatment with surfactants and radiation (e.g., ultraviolet light exposure).

Air Filters/cleaners:  Ultravation (has an interesting set of products which uses activated carbon and UV to sanitize the air). 

Oxidation: is used in industry with the production of cleaning products. Substances which have the ability to oxidize other substances are known as oxidative or referred to as oxidizing agents, oxidizers and oxidants. Oxidants remove electrons from other substances. Thus oxidants are themeselves reduced. Examples of oxidants include H2O2, CrO3 and have high oxidation numbers. They are highly electronegative that can gain one or two extra electrons by oxidizing a substance. For more information on oxidation click here.

UV Products:  Xenex  (pulsed UV disinfection robots)  UVivatec (Bayer)

Biosurfactants: are naturally occurring amphiphiles that are being actively pursued as alternative to syntehtic surfactants in cleaning, personal care, and cosmetic products. On the basis of their ability to mobilize and disperse hydrocarbons, biosurfactants are also involved in the bioremediation of oil spills. (Tsianou, “Rhamnolipid Micellizaiton and Adsorption Properites” Int J Mol Sci, 2022). 

–Rhamnolipids: are LMW glycolipid biosurfactants that consist of a mono or di-rhamnose head group and a hydrocarbon fatty acid chain. 

Definitions

Periodontal diseases: are bacterial associated inflammatory diseases of the supporting tissues of the teeth and range from the relatively mild form of gingivitis to the more aggressive forms which are characterised by the destruction of the tooth’s supporting structures. Periodontitis is associated with a subgingival infection of a consortium of specific Gram-negative bacteria that leads to the destruction of the periodontium and is a major public health problem. One bacterium of interest is Porphyromonas gingivalis.

Tooth loss is the ultimate determinetal effect of destructive periodontal disease.

Etiologic Agents:

Actinobacillus actinomycetemcomitans is the principal etiologic agent of early onset periodontitis but other select microorganisms also play a role. For example, Streptococcus mutans attaches to glucans deposited on the tooth surface. Such attachment is believed to enhance the ability of S. mutans to metabolize dietary sucrose to acid, which then can destroy tooth enamel and eventually result in a carious lesion. S. mutans and other oral streptococci use a surface protein called glucan-binding lectin (GBL) to attach to surface-bound glucan.

Porphyromonas gingivalis (P. gingivalis) is a black pigmented, anaerobic, proteolytic Gram-negative rod that obtains energy from the metaboism of specific amino acids. It has an absolute growth requirement for iron, preferentially in the form of heme or its Fe(III) oxidation product hemin. US 6,528,038 disclsoes antigens from P. gingivalis used for raising an immune response against P. gingivalis.

In normal individual, primarily gram positive flora. Upon infection or disease, shift to gram negative organisms. Majority of pathogology due to P. gingivalis (gram negative).

P. gingivalis infection stimulates TLR2 epxression on mouse macrophages but not TLR4. TLR2 is Required for P. gingivalis Mediated Oral Bone Loss. TLR2-deficient mouse macrophages fail to stimulate P. gingivalis mediated artheroscloerosis.

The oral cavity provides a habitat for about 700 microbial speceis forming complex and dynamic multispecies biofilams, asl referred to as “dental plaque”. The oral Gram-negative anaerobic bacteria P. gingivalis is typically a late colonizer of subgingival biofilms and has been correlated with several destructive periodontal dsieases, including periodontitis and peri-implantitis. P. gingivalis pathogenicity is reflected in an arsenal of virulence factors involved in tissue colonization and destruction, and interference with host defense systems. Bioflm development is a complex, multi-stage process. Initially, bacteria adhere to abiotic or biotic surfaces by production of surface appendages. Next, biofilms mature by the development of a three-diemnsional structure containing microcolonies in which different species can itneract with each other (biofilm maturation). In the last phase, cell disperse form the biofilm, allowing the formaiton of new fiofilms (biofilm dispersal) About 18% of the P. gingivalis genome is differentially expressed when the bacteria is grown as a biofilm, demonstrating the complexity of biofilm development. Given the side vareity of substrates to which P. gingivalis can attach in the oral cavity (e.g., oral soft tissues, implant materials, and other bacteria), many extracellular structures play a role in mediating specific and stable substrate attachment. Examples include fimbriae, LPS and capsules. Quorum sensing is a bacterial communicaton mechanisms in which the expression of genes is coordinated through the accumualtion of specific signaling molecules. This quarum sensing system has been shwon to play a role in interspecies communicaiton of P. gingivalis. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

P. gingivalis is one of the most prevalent bacteria in preiodontitis, a chronic inflammatory disease of the oral cavity. The disease is characterized by destruction of the supporting structures of the teeth (ie., the gingiva, the periodontal ligament and the alveolar bone) and can eventually lead to loss of teeth. Furthermore, periodontitis has recently been associated with an increased risk for delivery of premature labor and low birth weight infants. P. gingivalis is also recognized as a kestone pathogen in perio-implantitis, a periodontal disease characterized by inflammation of the hard and soft tissues surrounding dental implants. When oft untreated, peri-implantitis can result in loss of the dental implant. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Treatment Strategies:

Treatment procedures of P. gingivalis-mediated diseases such as periodontitis and peri-implantitis focuse on the eradication of oral pathogens at the site of infection, usually by surface debredement procedures followed by adjunctive therapies, including the use of antiseptics or/and antbiotics. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Chlorhexidine: is an antiseptic that has been widely used in dental practice becasue of its broad specturm ani-microbial activity. Local applicaotn of chlorhexidine can be done in the form of gels, chips, mothwashes or films. Despite its wiedspread use, some limtiations include brown discoloration of the teeth, supraginigival calculus formation and more rarely oral mucosal erosion and parotid swelling. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Antibiotiocs: Several antibiotic classes have also been suggested for the treatment of P. gingivalis related infections including tetracyclines (tetracycline hydrochloride, minocycline, doxycycline), macrolides (erythromycin), lincosamides (clindamycin), beta-lactams (ampicillin, amoxicillin) and nitroimidazoles (methronidazole). These antibiotics can be administered by either local or systemic routes. Local adminsitraiton has the advantage that higher therapeutic concentraiton of antibiotics can be delivered inside the pocket, avoidng some of the side effects of systemic adminsitration. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Quorum sensing inhibitors: have been presented as promising alternative for the treatment of biofilm-related infections, as they do not affect grwoth and thus have a low potential for resistance development. In this respect, quorum sensing inhbitors have been shown to reduct both P. gingivalis monospecies and F. nucleatum and P. gingivalis mixed-species biofilm development. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Antimicrobial peptides: are widely proposed as a new source of future antibiotics, as they often ahve braod spectrum activity and a low tendency for resistance devleopment. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Plant-dervived antibacterial agents: The non-dialyzable material fraction of cranberry uice rich in proanthocyanidins and A-type cranberry proanthocyanidins extracted form cranberry juice concentraiton were shown to exhibit activity against P. gigivalis. A number of prenylated flavonoids isoalted from Epimedium species were reproted to inhibit biofilm formation by P. gingivalis. Licinatrin dervied form Citrus fuiits and tea catechin dervied form Cameilia sinesis have been desmonstrated to inhibit biofilm formation of P. gingivalis biofilms and to desorb pre-formed biofilms. Extracted oils obtained from plants also posses activity against P. gingivalis biofilms. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Screening of compound libraries has resulted in the identification of new antibacterial agents that show activity agaisnt P. gingivalis. For example, a screen from a compound library in search for new molecules that exhibit activity agaisnt the opportunistic pathogen Pseudomonas aeruginosa identified a dichlorocarbazol derivative as a new antibacterial agent with road spectrum activity, including activity agaisnt P. gingivalis biofilms. In another study, a library of small molecuels based on 2-aminoimidazole and 2-aminobenzimidazole scaffolds were screened with the aim of identifying compounds that could inhibit co-colonizaiton of P. gingivalis and S. gordonii. In this screening, three small molecuels derived from oridin and cotnaining 2-aminoimidazole or 2 aminobenzimidazole moieties were identifed. These compounds inhibt co-colonization by reducing expression of both mfa1 and fimA fimbrial genes in P. gingivalis. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Products

Toobrushes: Water Pik Sonic-fusion (toothbrush and waterpik at same time)

Dental Associations: Oregon Dental Association 

Companies working in the Oral Care Industry: Oragenics  fertin Pharma (chewing gum for oral care)

Dental Cavities

I. Etiological agents and Pathological Mechanisms:

1. Bacteria:

–Streptococcus mutans (S. mutans): is the main etiological agent of dental caries (US 6,024,958). Strains of S. mutans are divided serologically into 8 types, a to h. Among these serotypes, serotype c strains are most frequently isolated form human dental plaque. S. mutans produces both water soluble and water insoluble polysaccharides from sucrose by the action of multiple forms of glucosyltransferase (GTase) and fructosyltransferase (FTase). The enzyme, glucosyltransferase decomposes sugars in foods, and generates water insoluble polysaccaride glucan. The glucan combines with the bacteria S. mutans and forms plaque (dental plaque) that adheres to the surface of the teeth. In the plaque, S. mutans metabolizes the sugar and generates acids such as lactic acid. The acid dissovles calcium from enamel of the surface of the teeth, resulting in dental caries (US 2009/0041782). Mutants of S. mutans lacking the ftf gene, have been shown to be less cariogenic than the native strains.

2. Dental plaque: is a biofilm coating tooth surfaces and is composed of bacteria, cells, proteins, enzymes, and their byproducts. One of the major virulence factors of cariogenic bacteria is their ability to produce extracellular polysaccharides, which facilitate their adhesion to tooth surfaces and act as a reservoir of nutrition for the bacteria.

–ß-D-Fructosyltransferases are among the cell free enzymes found in the oral cavity. FTF products fructans (polyfructoses) from sucrose, and these play a role in the pathogenicity and formation of the dental bioflim. The origin of these extracellular enzymes are several sepcies of oral bacteria included Streptococcus mutans, Streptoococcus salivarius, Streptococcus sanguis, and Actinomyces viscosus. Degradation of fructans by fructanase to fermentable sugars serves as a source for acid production by oral bacteria, thus inducing the cariogenic challenge in the oral cavity. Fructans may also serve as binding sites for oral bacterial in the dental plaque biofilm.

Cavity Protection/Treatment:

Dental caries is characterized by dissolution of the mineral portion of the tooth, which can result in pain and loss of viability of the tooth, necessitating costly report or extraction of the tooth. Various methods have been developed to prevent dental caries including the addition of sodium fluoride, sodium silicofluorideand hydrofluosilicic acid to drinking water and sodium fluoride or tin fluoride to topical preparations including mouth rinses. Coating teeth with polymeric materials or sealants has also been used although these techniques are costly, can require etching of the teeth with phosphoric acid and can be effective only in young children who have not yet developed caries.

–Antibacterial agents which kill microorganisms that are responsible for producing acid in the mouth has also been used. But antibiotics are not selective in the killing of oral bacteria and also kill benefiical bacterial present in the oral cavity.

—-Chlorhexidine (CHX) is one of the most potent antibacterial and antiplaque drug used in dentistry. It has been shown that CHX inhibits production of fructan synthesis by cell free FTF.exhelping to reduce swelling and redness of the gums and bleeding when you brush. idine is used along with regular tooth brushing/flossing to treat gingivitis a gum disease that causes red, swollen and easily bleeding gums. It works be creasing the amount of bacteria in the mouth.

Chlorhexidine (0.12% rinse) is used along with regular tooth brushing/flossing to treat gingivits, a gum disease that causes red, swollen and easily bleeding gums. Chlorhexidine belongs to a class of drugs called antimicroials. Chlorhexidine is also used to clean skin before surgery. 

–Vacination: Lehner (US 6,024,958) discloses peptide subunits of S mutans antigen I/II which are useful to prevent and treat dental caries either by eliciting an immunological response or by preventing adhesion of S mutans to the tooth.

Tooth Whitening

tooth whitening (i.e., the removal of stains from teeth) is a multibillion dollar indsutry. Numerous approaches have been tried to whiten teeth, some of which are described below.

–use of abrasives: such as diatomaceous earth, silica and baking soda have been used to whiten teach. Abrasives are a major element of most toothpastes and prophylaxis pastes are used by dentists.

–Chemical whitening additives: are applied to the teeth to allow the active ingredient to whiten the teach. A common chemical whitening agent is peroxide. Often, strips and trays are used to apply peroxide for contact times beyond that achievable with typical tooth brushing. US 5,891,453 and 5,8i7,691 describe a whitening product comprising a peroxide composition. However, peroxides can cause soft tissue irritation.

–actinidin: Bergeron: (US 2007/0110682A1) discloses the active ingredient “actinidin” which is produced from kiwifruit for whitening teeth.

–strawberries and apples contain malic acid, a natural stain remover.

–The citric acid in limons can also brighten teeth.

–chewing on raw fruits and vetables, 

–sugarless gum,  See also fertin Pharma which has chewing gum products for oral care. 

–avoid coffee, red wine and dark soft drinks or use a straw to reduce the liquid’s contact with teeth,

–brush with baking soda twice a month.

Tooth Brushes

Sonic Toothbrushes: In a 4 week clinical trial, the Sonicare sonic toothbrush was demonstrated to be superior to manual toothbrushes in improving periodontal health in patients with gingivitis (Ho, J. Clin. Dent., 1987, 8, 15-9).  

Haemostasis (control of bleeding)

Haemostasis is initaited by the formation of a complex between tissue factor (TF) being exposed to the circulating blood following an injury to the vessel wall, and FVIIa which is present in the circulation in an amount corresponding to about 1 of the total FVII protein mass. This complex is anchored to the TF-bearing cell and activates FX into FXa and FIX into FIXa on the cell surface. FXa activates prothrombin to thrombin which activates FVIII, FV, FXI and FXIII. In addition, the limited amount of thrombin formed in this initial step of haemostasis also activates the platelets. Following the action of thrombin on the platelets, the platlets change shape and expose charged phospholipids on their surface which form the template for the further FX activation and the full thrombin generation. Further FX activation on the activated platelet surface occurs via a FIXa-FVIIIa complex formed on the surface of the activated platelet, and FXa then converts prothrombin into thrombin while still on the surface. Thrombin then converts fibrinogen into fibrin which is insoluble and which stabilizes the initial platelet plug. This process is compartimentalized (i.e., localised to the site of TF expression or exposure, thereby minimizing the risk of a systemic activaiton of the coagulation system. The insoluble fibrin forming the plug is also stabilised by FXIII-catalysed cross linking of the fibrin fibers. 

Diseases of Haemostasis

Haemophilia: is a group of hereditary disorders which impairs the control of bleeding.

–treatment: 

(i) FVIIa: Commerical preparations of recombinant human FVIIa are sold as NovoSeven® for treatment of bleeding episodes in haemophilia A and B patients.

(ii) Plasminogen Activator Inhibitor (PAI-1): is also referred to as endothelial type plasminogen activator inhibitor (c-PAI) and inhibits urokinase type plasminogen activator (u-PA) and tissue type plasminogen activator (t-PA). Rojkjaer (US 2006/0030531) discloses use of PAI-1 for treating bleeding episodes due to surgery, traumaand other forms of tissue damage. The bleedings can occur in organs such as the liver, lung, gastrointestinal tract. Jian-Dong (US 12/670,778) also disclose a method for treatment of a hemorrhagic lung condition by administering PAI-1.

Wound Healing: (Process)

Would healing is a complex biological process involving extracellular matrix, blood cells, parenchymal cells and mediators such as cytokines. After the wound reaches hemostasis, the point where bleeding stops, the healing process begins. It occurs in 3 stages: (1) inflammation, (2) tissue formation (proliferation), and (3) tissue regeneration. 

(1) Within 4-6 hours after injury, inflammation begins. During inflammation, neutrophils, monocytes and macrophages infiltrate the wound. These phagocytic cells release growth factors for the proliferative phase, enzymatic mediators (proteases) that degrade proteins, and phagocytose bacteria, dead and dying cells thus debriding the wound.

(2-3) In the proliferation phase, collagen is deposited, forming scar tissue. Fibroblasts produce proteoglycans, which bind the collagen fibers together. Over time, the collagen is degraded by proteases adn remodeled into a stronger scar structure.

Wound Healing Products 

Surgical wound closure is currently acheived by sutures and staples that facilitate healing by pulling tissues together.

QuikClot: mineral zeolite cyrstals cause adsorption of the water molecules in the blood, thus concentrating the clotting factors and accelerating blood clotting. The water adsorption mechanism of mineral zeolite cannot occur without the rlease of a large amount of heat. As such, application results in high termperatures and severe burns at the injury site, making later medical care more complicated.

HemCon bandage: contains a chitosan mixture which has a positive charge and attracts red blood cells which have a negative charge. The red blood cells are drawn into the dressing, forming a seal over the wound and stabilizing the wound surface. However, the chitosan network can be saturated with blood and fail quickly when faced with brisk flow. The HemCon bandage patch is available only as a stiff patch that cannot fit easily into irregular wounds.

Gelatin:Preiss-Bloom (WO2008076407)  discloses a cross linikable protein and a non-toxic material which induces crooss linking of the cross linkable protein. Preferably, the cross linkable protein includes gelative and the non-toxic material is transglutaminase. When actied upon by a translutaminase, gelatin, which is a denatured form of the protein collagen, undergoes rapid crosslinking to form a virant gel. The gelation process that takes place is extremely similar to the nature late stage clotting cascade that frigin underoges when it comes into contact with Factor XII and calcium.

Italdermol® Triticum vulare: is a creme used for wound healing whcih includes Tricum vulare (see natural products below) and the antimicrobiotic 2-Fenoxietanol. Pehnooxyethanol is a germicidal aromatic alcohol often used with quaternary ammonium compounds. 

Natural Products for Wound Healing

Tumeric: reportedly augments the healing process of both chronic and acute wounds (see US Patent No. 5,401,504).

Triticum vulare: is the commonly known weat plant and is well-known for accelerating tissue repair. A specific aqueous extract of Triticum vulgare (TVE-DAMOR) manufactured by Farmaceutici DAMOR (Naples, Italy) is currently an active component in the manufacture of certain pharmaceutical products already marketed in Italy and abroad under the brand name Fitostimoline®, in the formulation of cream and medicated gauze and is commonly used for the treatment of decubitus ulcers, burns, scarring delays, dystrophic diseases, and in conditions in which it is necessary to stimulate re-epithelialization or tissue regeneration processes. 

Varicose veins (primary or secondary varicosis) form on account of a mechanical impediment in the venous flowback of blood and the peripheral venous pressure increased thereby, surfaces varices and deep varices with congestion phenomena forming.

The cause may be a slowed circulation (e.g., in case of longer confinement to bed), constiutionally caused as a consequence of a congenital connective tissue weakness or as a consequence of other vein diseases.

For local treatment, in most instances creams, ointments, gels and the like are used which contain heparin. Haparin has an antighrombotic effect due to its function as a catlyst, by inhibiting the serine proteases in the coagulation cascade. Thereby, a series of blood coagulation factors are inactivated. But in case ofa tendency to bleeding and in case of thrombocytopenias, heparin must not be used. Furthremore, it should not get into contact with open wounds, the eys or the mucous membranes.

Genital Warts

Treatment:

–Condylox Gel (0.5%) Podofilox): is a solution or gl that is applied to the affectied area for several weeks. It has shown to clear about 45-90% of wars, although the warts may reemerge in 30-60% of cases.

–Polyphenon E MediGene AG: has been approved by the FDA for the treatment fof genital and perianal warts. Polyphenon E oitment contains a concentrate of catechines extracted from green tea leaves. It is manufactured by MediGene under the trademark Verigene.

–Thuja occidentalis (White Cedar tree) (Skinhale): is a non-presecription cream that has been succesffully used in the treatment of warts not responding to cyrotherapy and radiosurgery. (Inidan J Nephrol. 2013 Sep-Oct; 23(5) 362-364

–Imiguimod: has been approved for the treatment of genital warts caused by infection of human papillomavirus. TLR7 deficient mice do not respond to synthetic imidazoquinolines.

–Dermatend (natural herbal rememdy advertised to safely remove moles, warts and skin tags).

Suncreens

It is important to just sunscreen every day. In fact, incidental sun exposure can account for more of our lifetime exposure to ultraviolet rays than at the beach. Make sure you are covered with at least SPF15.

Potentially Dangerous Ingredients in suncreens:

How to Choose a good Suncreen:

The sunscreen should contain the minerals zinc or titanium, which help reduce UVA exposures. Also important is to avoid sunscreen chemicals considered to be a potentially harmful such as oxybenzone or Vitamin A.

Sunscreen typically contain chemical agents such as certain benzophenones, dibenzylmethanes or substituted paraaminobenzoates (i.e., compounds absorbing ultraviolet radiation, so that it cannot penetrate the skin). Some of the ocmpounds used for this purpose have shown to lack sufficient light stability and may even become toxic over long term application. In addition, they must stay continuously on the surface of the skin at the time of exposure to be effective.

Don’t Use Harsh Cleanser Detergents: Avoid detergents which contain lauryl sulfate and other harsh detergents (those that often leave a lot of suds) which can strip your skin of vital lipids. Instead, look for cleansers that contain fatty acids and fortify your skin, like Dove’s ProAge products or even simple cold cream.

Use Retinols: Retinol, a form of vitamin A, is the only topical ingredient proven not only to prevent wrinkles but to minimize the one you already have. Over the counter creams that contain retinol include Roc Retinol Correxion Deep Wrinkle Night Cream, Neutrogena Healthy Skin Night Cream and SkinCeuticals Retinol 1.0. Dermatologists can prescribe higher concentration prescription retinoid like Retin-A, Differin or Tazorac.

However, a  form of vitamin A known as retinyl palmitate may be connected to skin disease and cancer. Although the FDA is still investigating this, it may be wise to stay away from suncreens that contain retinyl palmitate until more is known. This chemical may be found in 41% of today’s sunscreens! Another potentially dangerous chemical is oxybenzone, which can be found in some sunscreens. It is a hormone-disrupting compound which penetrates the skin and enters the bloodstream.

Companies working in the psoriasis area: Leo Pharma

Treatment: 

TNF-alpha inhibitors:

Humira (adalimumab) demonstrated that in patients with moderate to severe chronic plaque psoriasis, adalimuamb acheived statically significant results after 12 weeks.

Vitamin D and corticosteroid: has been used for the treatment of psoriasis. Leo Pharma (6,753,013) discloses a composition comprising at least one vitamin D or vitamin D analogus and at least one corticosteroid for topical application which is storage stable sold under the brand name Taclonex® which is FDA approved

PDE4 Inhibitors:

Otezla® is a phosphodiesterase-4 (“PDE4”) inhibitor marked by Amgen which is used for treating psoriasis and related conditions. 

Anti-oxidants: Antioxidants play an important role that protects skin against ROS-induced injury. Such antioxidants include Ascorbic acid, ?-tocopherol, ?-carotene, selenium, butylated hydroxytoluene and dietary antioxidants

A growing body of evidence suggets that reactive oxygen species (ROS) are generated by UV radiation, resulting in oxidative damage to cellular components such as mitochondria as well as nuclear DNA damages, which in turn accelerates aging and contributes to skin cancers. The term ROS includes free radicals such as the superoxide anion (O2-) and the hydroxyl radical (OH), as well as nonradical intermediates wuch as hydrogen peroxide (H2O2) and singlet oxygen (1O2). There is growing evidence that UVA irradiation induces the generation of superoxide anion both in mitochondra and extramitochondrial sites. The O2- is very toxic to tissue and may also result in the generation of ROS of other types

Vitamins and natural compounds

EGCG, a constituent of green tea, has been reported to be a powerful antioxidant protecting skin cells against photodamage.

Vitamin A: has been used as an antagonist to decreased cell growth and elevated collage-degrading matrix metalloproteases while concurrently stimulating collagen accumulation in naturally aged human skin.

Vitamin B3 (nicotinamide): has been shown to reduce the risk the risk of skin cancer as well as pre-cancerous lesions called actinic keratosis. 

Foods which contain good vitamins for the skin

Watermellon: contains vitamins A, B6 and C. Mix 1 tablesppon of watermellon juice with with the same amount of greek yogurt for a great soothing lotion for the skin. Spread over your face and leave on for 10 minutes. Rinse and pat dry. 

Patents and Skin Compounds

3DG Inhibitors: 3-deoxyglucosone (3DG) and other alpha-dicarbonyl sugars associated diseases and disorders are present and produced in the skin. US Patent Application Publication 20050159383 discloses inhibitors agaisnt 3DG. Dynamis Therapeutics is engaged in products for such inhibitors.  

Amiline derivatives: A means to prevent skin deterioration or ageing is to provide compounds scavenging free radicals. EP 0 761 214 for example discloses singlet oxygen quenchers comprising aniline derivative and difufuyl amine derivative, which are reported to reduce the oxidative stress to the skin.

Ascorbic acid: or analogues thereof are disclosed to increase the synthesis of tenascin and/or collagen VII for reinforcing the cohesion at the DEJ (US 2004/0005342).

D-xylene: or esters thereof or oligosaccharides containing D-xylose are disclosed to stimulate the synthesis and/or secretion of proteoglycans and/or glycosaminoglycans by the keratinocytes (US 6495147)

Magnesium aspartate/chloride: is disclosed to promote the adhesion of keratinocytes in the epidermal basal layer in the dermal-epidermal junction (US 6471972).

Meroterpene or meroterpene extract is disclosed to help reduct fine lines and/or wrinkles of skin (US 20090036545A1).

Saponins or sapogenols: particularly those extracted from plants such as soya or Medicago are disclosed for treating the skin in order to increase the amount of collagen IV in the dermanl-epidermal junction.

Ursolic acid and/or oleanolic acid: WO 2002/015869

Yeast: extracts are disclosed to retard the degradation of the dermal-epidermal junction to improve the surface condtiion of the skin (^S 6531132).