Why do Acne Scars Appear?

Before addressing acne scars and their treatment, it’s pertinent to point out that reddish acne marks that resemble scars are not actually scars because no permanent change has occurred. In other words they are not real scarring and disappear in time, however, while they are visible they can cause embarrassment.

Flat, red or reddish spots that appear at the final stage of most inflamed acne lesions are called Macules or “pseudo-scars”. After an inflamed acne lesion flattens, a macule may remain to “mark the spot” for up to 6 more months. When a macule eventually fades, no trace of it will remain, unlike a scar.

After the inflammation of an acne lesion has passed, skin pigmentation can become dark or discolorated. The lesion’s color varies from light brown to black. Under sunlight exposure (UV rays), lesions may become darker. It occurs more commonly in darker-skinned people, but can be occasionally seen in people with fair skin. Early application of a natural skin care product attenuates the occurrence of post-inflammatory pigmentation and also eliminates older marks. If untreated, post-inflammatory pigmentation can even persist for up to 18 months, specially with excessive sunlight exposure.

Acne Scars - How are they formed?

Acne scars appear after inflammation or improper healing of some spots. While for some people scarring seems to depend on genetic factors or skin color, precautions can be taken to avoid scars along with treatments, which significantly reduce a scarred skin’s appearance.

In the simplest terms, scars form at the site of damage and are the visible reminders of wound and tissue repair. In the case of acne, the lesion is caused by the body’s inflammatory reaction to sebum, microbes, and dead cells in the plugged sebaceous follicle. There are two types of true scars:

(1) Depressed areas, commonly associated with pitted acne scarring or ice-pick scars, and

(2) Raised thickened tissue such as keloids.

When tissue suffers a lesion, the body sends in its ‘repair kit’ to the wound site. The skin activitates all its defensive and repair systems, where elements such as leukocytes, inflammatory molecules, and reconstructive elements have the task of healing tissue and fighting infection. However, when their mission is done they can leave a somewhat messy repair patch in the form of fibrous scar tissue, or eroded tissue. But sometimes it’s different.

White blood cells and inflammatory molecules may remain at the site of an active acne lesion for days or even weeks. In people who are susceptible to scarring the result may be an acne scar. The occurrence and incidence of scarring is still not well understood, however. There is considerable variation in scarring between one person and another, indicating that some people are more susceptible to scarring than others (ex. genetic factors or skin color). Scarring usually results from severe inflammatory nodular cystic acne that occurs deep in the skin. But, scarring may also appear from more superficial inflamed lesions.

Clinical Presentation-Skin Disorders

Tinea capitis, or “ringworm” of the scalp, presents as one or more sharply marginated plaques of partial alopecia. Inflammation and scale are present, but often these two changes are quite minimal. The recognition of broken hairs (stubble and black dots at the follicular orifices) is the best clue to correct diagnosis. Nearly all cases occur in children, but the diagnosis should be considered in any adult presenting with evidence of localized alopecia . Kerion formation is a complication that occurs in about 10% of cases. This represents a sensitization phenomenon whereby the fungi induce a remarkably brisk inflammatory reaction with resulting pustulation, crusting, and edema formation. Wood’s lamp examination does not reveal fluorescence in the most common forms of tinea capitis or in kerion formation. Unfortunately, KOH preparations are difficult for the inexperienced to interpret. For this reason, any suspected diagnosis requires the plucking of infected hairs for fungal culture. Course and PrognosisTinea capitis and zoophilic tinea corporis usually resolve spontaneously after 6 to 12 months of activity. Tinea pedis, tinea cruris, and anthropophilic tinea corporis continue indefinitely. There are, however, periods of relative quiescence and exacerbation. All of these fungal diseases respond well to treatment, but with the exception of tinea capitis and zoophilic tinea corporis infections, recurrence following treatment is rather likely. PathogenesisTinea pedis, tinea cruris, and anthropophilic tinea corporis are most commonly caused by Trichophyton rulnum. Trichophyton interdigitate and Epidermophhyton floccoswn infections are also seen. Generally, one cannot predict the causative organism on the basis of clinical appearance. Zoophilic tinea corporis can be caused by Microsporum canis, Trichophyton mentagrophytes, and Trichophyton verrucosum. Tinea capitis is caused by Trichophyton tonsurans in 90% of cases. The likelihood of inoculation with any of these fungi is enhanced if cuts and scratches are present on the skin. Clinical evidence of infection following inoculation is enhanced by the presence of warmth and moisture, such as occurs in the groin and under footwear. Depression of cell-mediated immune responsiveness, as in atopic patients, is a major predisposing factor for the development of T. rubrum infection. TherapyTinea cruris and those cases of tinea pedis that involve only the web spaces can be treated with any of the topical antifungal agents. Other forms of tinea pedis usually require the use of griseofulvin. Mild cases of tinea corporis also respond well to topical agents. Extensive disease and those cases with a component of follicular involvement are best treated with griseofulvin. Tinea capitis requires the use of griseofulvin. Orally administered ketoconazole therapy is rarely appropriate for either tinea corporis or capitis. Kerion on nation, if present, can be treated with intralesional steroid injections or with a short burst of systemically administered steroids.

Wound Healing Process

In people and domestic animals, scarring left after a trauma, surgery, burn or sports injury is a major health problem, usually resulting in adverse aesthetics, loss of function, restriction of tissue elasticity and/or growth and adverse psychological effects.

Current treatments are empirical, unreliable and uncertain: there are no prescription drugs for the prevention or treatment of dermal scarring. Skin wounds on early mammalian embryos heal perfectly with no scars whereas wounds in adult mammals scar.

Specialists are investigating the cellular and molecular differences between perfect healing in embryonic and adult wounds. Important differences include the inflammatory reaction, which in embryonic wounds consists of lower quantities of less differentiated inflammatory cells. This, along with high levels of morphogenetic molecules implicated in skin growth and morphogenesis, means that the growth factor profile in a healing embryonic injury is very different from that in an adult injury.

These experiments result in scar-free injury healing in adults. Such experiments have allowed the recognition of therapeutic targets; a correct treatment markedly improves or completely avoids scarring during adult injury healing in experimental animals. Some of these new drugs have satisfyingly passed safety studies and others. This has allowed them to enter human clinical trials with approval from the appropriate regulatory authorities. Based on encouraging results obtained from these studies lead drugs have now entered human patient-based tests e.g. in skin graft donor sites.

The theory is that evolutionary factors have been exerted on intermediate sized, widespread, dirty wounds with high tissue destruction e.g. bites, bruises and contusions. Modern wounds (e.g. resulting from trauma or surgery) caused by sharp instruments and healing in a clean or sterile environment with close tissue apposition are new occurrences, not previously encountered in Nature and to which the evolutionary selected wound healing responses are somewhat useless. It has been shown that both healing with scarring and regeneration can occur within the same animal, including man, and of course within the same tissue, thereby implying that they share similar mechanisms and regulators.

Consequently, by subtly altering the proportion of growth factors present in adult wound healing, we can induce adult wounds to heal perfectly with no scars, with accelerated healing and with no adverse effects, e.g. on wound strength or wound infection rates. This means that scarring may no longer be an inevitable consequence of modem injury or surgery and that a completely new pharmaceutical approach to the prevention of human scarring is now possible. Scarring after injury occurs in many tissues in addition to the skin.

Thus scar-improving drugs could have widespread benefits and avoid complications in various tissues, e.g. prevention of blindness after scarring due to eye injury, support of neuronal reconnections in the peripheral and central nervous system by the avoidance of glial scarring, restitution of normal gut and reproductive function by avoiding strictures and adhesions after injury to the gastrointestinal or reproductive tracts, and restoration of locomotor function by avoiding scarring in tendons and ligaments.

Inflammatory Response and Acne Formation

The key trigger in acne during adolescence is hormonal, for at this phase androgens interact with terminals on the sebaceous glands and produce stimulation of the sebaceous gland to hypertrophy and hence form more sebaceous secretion of lipids and free fatty acids which damage the follicular canal. More specifically, there is evidence for increased peripheral metabolic transformation of the androgen testosterone to dihydrotestosterone at the level of the skin in people suffering from acne. It is further believed that receptors on the sebaceous gland for the active androgen dihydrotestosterone can show various degrees of sensitivity, and that an elevated sensitivity response may be partially or completely genetically inherited.

Basic lesion in acne is the comedone

The basic manifestation in acne is the comedo. On the contact with oxygen the comedone turns dark and forms what you call a blackhead. The comedo is created by retention of layers of devitalized skin called keratin in the wall of the follicles. In addition to hyperkeratosis (which is thickening or retained layers of keratin), there is an accumulation of sebum. The combination of the keratin and the sebum makes a blocking of the opening of the follicular canal, and papules are formed by inflammation around the comedones. Depending on the degree of inflammation, granulomatous reactions, pustules, nodules, cysts, scars, and keloids may develop.

Inflammatory Response

Airborne contamination and other harmful materials further exacerbate the inflammatory reaction. As bacteria begin to grow inside the clogged pore your defensive system reacts by releasing granulocytes and macrophages, which are groups of white blood cells that eliminate the bacteria. The inflammation process is necessary to eliminate the continuing effects of excess bacteria and signal the body to heal the damage to tissues. Often times the defensive response system can’t stop the reproduction of acne bacteria due to lack of white blood cells or an impaired system.

Activity of the Sebaceous Gland

When a comedone is clogging the outlet of the sebum ducts, the sebaceous glands continue to produce sebum, which accumulates in the sebum canal augmenting the comedone in size. The expansion in size results in pressure and leads to a further intense inflammation response in the nearby skin and produces swelling, redness, unpleasantness, and a mass (pimple, redhead, acne papule). Frequently your immune response system cannot act on the acne papule thus furthering the phase of growth and infection.

Growth of Acne Bacteria

The mentioned conditions promote the growth of bacteria and result in infection inside the canal, the sebaceous gland, and nearby tissue. The commencement of the infection makes more inflammatory changes, therefore starting a cycle of accentuated blockage of the outflow of sebum which produces even more pressure, inflammation, and progressing infection causing cysts and pustules to occur. The effect on skin tissues caused by these infections is highly damaging and the healing process usually results in a scar.

Pimple Formation and Treatment

Pimples are an inflammatory skin ailment characterized by superficial skin eruptions that are caused by sudden and strong outflow of sebum.This damages the cells lining the sebum conducts inside the skin follicles, or by blocking of the skin pores.

When the sebum glands are hyperactive or when they first become active during adolescence and produce large quantities of oil (sebum) the sudden outflow of large quantities of such sebum either ends up damaging the cells that line the sebum conduct or the sebum blocks the opening of the follicles (usually called pores).

If the cells lining the sebum canals get damaged the body triggers an inflammatory reaction to eliminate the problem and if the inflammatory reaction is uncontrolled as it usually is you get pus, pain and destruction by your own body not only of the sebum but also some of the surrounding cells. If sebum (oil) which usually drains to the exterior gets clogged it becomes a rich feeding environment for the growth of bacteria, and here a good pimple treatment comes in handy.

How To Treat Pimples

Different types of acne start the same way. Pimples start out as a microcomedone. Microcomedones become non-inflamed skin lesions named comedones - either a whitehead or a blackhead: When the clogged sebum and bacteria stay below the skin surface, a whitehead is created. Whiteheads may show up as small white spots, or they may be so small that they are imperceptible to the naked eye. A blackhead occurs when the clogged sebum and bacteria partially open to the surface and turn dark due to melanin, the skin’s pigment. It is not dirt and can’t be washed away. Blackheads can stay for a long time because the contents very slowly drain to the surface.

A blackhead or whitehead can expel its contents to the exterior and heal. Or, the cells lining the follicle wall can become injured and inflammatory acne can ensue. These lesions can be initiated by random occurrence or by picking at or touching the skin. Once a pimple has formed it is highly possible that you be left with some degree of acne scarring.

Papules: A papule occurs when there is a lesion in the follicular wall. Leukocytes rush in and the pore becomes inflamed.

Pustules: A pustule forms several days later when white blood cells make their way to the surface of the skin. This is what people usually refer to as a zit or a pimple. An inflamed lesion can often completely collapse or explode, strongly inflaming the surrounding skin, and usually destroying surrounding follicles. These lesions are named nodules or cysts and may require a special acne treatment:

Nodule: When a follicle breaks along the bottom, total collapse can occur, resulting in a large, inflamed bump that can be sore to the touch.

Cyst: Sometimes a severe inflammatory reaction can produce a very large pus filled lesions or cyst. This kind of acne must be treated by a specialist.

Different Solution To Different Acne

To find the best treatment you have to remember that every solution is individual, so you need to find what is best for you. Start with something mild first until you find out what works.

Acne Cysts

Comedones are formed by the accumulation of sebum at the external orifice of the sebaceous gland conduct and/or the hair follicle. A comedone can become modified chemically, as well as physically, thus turning a material which is foreign to the organism.

This condition of “foreignness” promotes a further inflammatory response, including immune reactions and other responses of several defense systems, specially those related with granulocytes and macrophages. If the inflammatory response and the immune and other defense reactions are effective in destroying or stopping the repercussions of the comedone, further advancement of acne manifestations do not occur. Frequently, however, the immune and other defense reactions are not effective in terminating the acne process at this stage and the process advances partly or wholly as described below.

While the comedone is obstructing the outlet of the conduct, the sebaceous glands can keep to produce sebum, which accumulates in the duct and in the glands, distending both. The distension and the resulting pressure produce further intensification of the inflammatory reaction in the adjacent skin and subcutaneous tissues and produce additional swelling (edema), redness (erythema), unpleasantness, and a mass, which includes the blocked and therefore encysted sebaceous gland (”redhead”, “pimple”, or acne papule). Frequently, the defense systems are not adequate to terminate this process promptly at the acne papule phase and it continues to progress as outlined below.

The above conditions favor the proliferation of bacteria, and the resultant infections involve the duct, the sebaceous glands and the nearby tissues, commonly in that order. The onset of the infection makes further inflammatory changes, thereby initiating a vicious cycle making continued and/or elevated obstruction of the passage of the sebum, which in turn leads to more pressure, more inflammation and continued or progressive infection.

This leads to the formation of the acne pustule. The immune and other defense systems having been useless to avoid these conditions from appearing, frequently fail to stop or reverse the process early in the acne pustule phase and it persists or progresses further.

Nodules and cysts

Obstruction with or without infection leads to the formation of cysts. Infection of a cyst produces the formation of an abscess which leads to local tissue destruction. If this destruction of tissue has involved the connective tissue elements of the skin or subcutaneous tissues to an enough degree, healing is frequently accompanied and/or followed by scar formation.

The scars in acne can vary from minimal to extensive and highly disfiguring conditions which are permanent consequences of acne. While the process by which acne appears and lasts for an indefinite time may and frequently does come to a halt as a result of therapy or spontaneously, the scars persist for life unless they are removed.

An inflamed lesion can sometimes completely collapse or explode, severely inflaming the nearby skin, and sometimes destroying neighboring follicles. These lesions are called known nodules or cysts.

Natural Ingredients - Powerful Ally for Acne Treatments

Acne is an inflammatory reaction to damaged cells within the sebum canals caused by excessive sebum output. If bacteria grows within the obstructed pores infection will appear.

Natural Solutions for Acne and Pimples

Finding the right acne treatment isn’t easy, but here are a couple of ingredients you should look for.

* Willow bark extract is capable of unclogging pores by reducing keratin and keeping bacteria under control. It is a natural salicylic acid that works as a biological medicine that causes no irritating secondary effects.

* Licorice extract is capable of restraining inflammation, irritation and the secretion of antimicrobials, antioxidants and sebum.

* Snail secretion has recently been discovered to repair and regenerate damaged skin cells. It is a fluid of biological origin reinforced with protein enzymes that unblocks pores. It has renovating skin agents that heal blemishes, antimicrobials to resist bacteria, antioxidants that get rid of free radicals, communication cells that can discriminate healthy cells from damaged ones and strengthen the immune system in its attempt to resist foreign elements and bacteria. This scientifically proven ingredient also supplies water molecules that retain hydration keeping the skin permanently hydrated.

A badly treated acne breakout will surely cause scarring and result in added stress and anxiety. Because stress stimulates the production of cortisone creating more sebum it is highly important to control stress to avoid falling into a vicious cycle. If for some reason you find yourself in this cycle your best choice is to find an effective scar removal treatment.

Acne’s Origins come from the Protective Actions of our Body

Acne is the consequence of the immune system efforts to defend the body from foreign elements and bacteria using inflammation. When inflammation settles down toxic substances from the white blood cells enter the blood stream and tissues to liberate the body from foreign elements. These chemicals augment the blood flow which results in redness and warmth. If there is a leak into the tissues swelling will result.

During inflammation phagocytes are the first immune agents to arrive to the infected area reenforced with lysosome that allows them to digest bacteria, debris and dying cells. A complicated side effect of inflammation is the production of hydrogen peroxide, which is excellent in the elimination of bacteria but leaves notorious acne scars on the skin.

Hope for Acne Treatment found in Natural Products

Actually, there are products created with natural components that come together to form an effective scar cream. These products are based on a mixture of natural ingredients and snail secretion. The combination of these ingredients and the regenerating capacity of snail’s secretion can rebuild damaged cells and regenerate body tissues. Snails and humans share similar skin components thus the secretion that rebuilds the snail’s shell can also regenerate damaged cells in humans skin. This amazing ability is capable of erasing scars and rebuilding a new skin.

Natural acne treatments offer a safe and effective renewal of damaged and depleted skin tissue. However it’s critical that you make sure that the product you chose contains the ingredients that are best for your skin’s recovery. Many products that call themselves natural are anything but that. Skin recovery and acne prevention are only attributable to certain natural ingredients so chose wisely.

Information on Linear Porokeratosis

Linear Porokeratosis is a rare type of porokeratosis and characterized by chronic, unilateral extremities lesions. Linear porokeratosis generally develops in childhood or can grow in adult life. Lesion has abnormal keratinization characterized by a healed or atrophic center surrounded by keratin limits, with histopathologic changes that include compact column of parakeratotic cells in small epidermal invaginations, constituting the cornoid lamella. Occasionally there is a family history of linear porokeratosis or another kind of porokeratosis such as disseminated superficial actinic porokeratosis (DSAP), suggesting a genetic predisposition. Linear porokeratosis affect men twice as often as women. Many risk factors for the progress of porokeratosis have been identified; these factors comprise genetic inheritance, ultraviolet radiation, and immunosuppressant. Immunosuppressant related with porokeratosis may be secondary to a disease process such as HIV infection or lymphoma or an iatrogenic suppression such as with immune-modulating drugs used to prevent organ transplant rejection or to treat autoimmune diseases. Symptoms of linear porokeratosis can develop within a linear porokeratosis patch. Linear Porokeratosis may be also a basal or squamous cell carcinoma, and is more expected to arise in older adults. If a lump or sore appears within a porokeratosis lesion, arrange for it to be reviewed by your dermatologist. It may need a biopsy or cutting out. There is no cure for linear porokeratosis and treatment is normally disappointing. Topical 5-fluorouracil can induce remission in all forms of porokeratosis. Treatment must be continued until a brisk inflammatory reaction is obtained. Calcipotriol and tacalcitol have been shown to be helpful treatment of linear porokeratosis. Sun protection is very important as exposure to ultraviolet radiation may result in the development of skin cancer lesions within the linear porokeratosis. Cryotherapy is also used in Linear porokeratosis heal. Cryotherapy refers to a treatment in which surface skin lesions are frozen. It is a minimally invasive way of inducing resolution for huge numbers of lesions. Cryotherapy stings and may be painful, at the time and for a variable period afterwards. There may be instant swelling and redness. Surgical treatment is essential for porokeratosis lesions that have undergone malignant transformation.

Tinea capitis, or “ringworm” of the scalp, presents as one or more sharply marginated plaques of partial alopecia. Inflammation and scale are present, but often these two changes are quite minimal. The recognition of broken hairs (stubble and black dots at the follicular orifices) is the best clue to correct diagnosis. Nearly all cases occur in children, but the diagnosis should be considered in any adult presenting with evidence of localized alopecia . Kerion formation is a complication that occurs in about 10% of cases. This represents a sensitization phenomenon whereby the fungi induce a remarkably brisk inflammatory reaction with resulting pustulation, crusting, and edema formation. Wood’s lamp examination does not reveal fluorescence in the most common forms of tinea capitis or in kerion formation. Unfortunately, KOH preparations are difficult for the inexperienced to interpret. For this reason, any suspected diagnosis requires the plucking of infected hairs for fungal culture.
Course and Prognosis

Tinea capitis and zoophilic tinea corporis usually resolve spontaneously after 6 to 12 months of activity. Tinea pedis, tinea cruris, and anthropophilic tinea corporis continue indefinitely. There are, however, periods of relative quiescence and exacerbation. All of these fungal diseases respond well to treatment, but with the exception of tinea capitis and zoophilic tinea corporis infections, recurrence following treatment is rather likely.
Pathogenesis

Tinea pedis, tinea cruris, and anthropophilic tinea corporis are most commonly caused by Trichophyton rulnum. Trichophyton interdigitate and Epidermophhyton floccoswn infections are also seen. Generally, one cannot predict the causative organism on the basis of clinical appearance. Zoophilic tinea corporis can be caused by Microsporum canis, Trichophyton mentagrophytes, and Trichophyton verrucosum. Tinea capitis is caused by Trichophyton tonsurans in 90% of cases.

The likelihood of inoculation with any of these fungi is enhanced if cuts and scratches are present on the skin. Clinical evidence of infection following inoculation is enhanced by the presence of warmth and moisture, such as occurs in the groin and under footwear. Depression of cell-mediated immune responsiveness, as in atopic patients, is a major predisposing factor for the development of T. rubrum infection.
Therapy

Tinea cruris and those cases of tinea pedis that involve only the web spaces can be treated with any of the topical antifungal agents. Other forms of tinea pedis usually require the use of griseofulvin. Mild cases of tinea corporis also respond well to topical agents. Extensive disease and those cases with a component of follicular involvement are best treated with griseofulvin. Tinea capitis requires the use of griseofulvin. Orally administered ketoconazole therapy is rarely appropriate for either tinea corporis or capitis. Kerion on nation, if present, can be treated with intralesional steroid injections or with a short burst of systemically administered steroids.

For more info about clinial dermatology and skin care advice have a look at authors site.