Keratosis Palmaris et Plantaris: Overview, Diffuse Hereditary PPK, Focal and Striate Hereditary PPK (2023)

Diffuse types without associated features

Epidermolytic PPK (Vorner PPK)

Synonyms for epidermolytic PPK (EPPK) include diffuse Vorner disease and PPK cum degeneratione granulosa. In some ethnic groups, this form is the most common type of hereditary PPK. For example, it has an estimated prevalence of at least 4.4 cases per 100,000 population in Northern Ireland. It is inherited in an autosomal dominant fashion. Onset occurs in the first few months of life, but the disease is usually well developed by age 3-4 years.

Clinical features are very similar to diffuse nonepidermolytic PPK (NEPPK). A well-demarcated, thick, yellow hyperkeratosis is present over the palms and soles. An erythematous band is frequently present at the periphery of the keratosis. The surface is often uneven and verrucous. Painful fissures and hyperhidrosis are common. Finally, it is usually nontransgredient, with a sharp demarcation of the lesions at the wrists.

Histologically, keratinocytes show epidermolysis, hyperkeratosis, acanthosis, and papillomatosis. Perinuclear vacuolization and large keratohyalin granules are seen. Cellular breakdown in the spinous and granular cell layers occurs rarely and can lead to blister formation. Several biopsy specimens may be required to confirm the changes, as they may be subtle and patchy.

This disorder is most frequently associated with mutations in keratin 9, although keratin 1 has been implicated in a small number of reported cases. Mutations in keratin 9 typically result in phenotypes confined to the palms and soles. In contrast, keratin 1 is expressed ubiquitously, thus these mutations can affect the entire body surface. [1]

Topical therapies that have proven useful for EPPK include salicylic acid, keratolytic agents (ie, lactic acid and urea), and 50% propylene glycol in water under plastic occlusion several nights per week. Mechanical debridement with a blade also may be useful. Oral retinoid therapy has had variable effects and may not benefit patients with certain genotype profiles, such as K1 mutations. Finally, gene editing via CRISPR/Cas9, [2] as well as RNA-interference-based therapy, [3] has shown benefit in mouse models of this disease and may represent a powerful therapeutic strategy in the future.

Nonepidermolytic PPK (Unna-Thost PPK and Bothnian-type PPK [1]

Synonyms include diffuse Unna-Thost disease and PPK diffusa circumscripta. Diffuse NEPPK is inherited in an autosomal dominant fashion. The condition may manifest in the first few months of life but is usually well developed by age 3-4 years. It is another common type of hereditary PPK. Bothnian-type PPK has a prevalence rate of 0.3-0.55% in Northern Sweden (near the Gulf of Bothnia).

Clinically, waxy, thick, well-demarcated hyperkeratosis is present over the palms and soles. A red band is frequently present at the periphery of the keratosis. It is usually nontransgredient, with a sharp demarcation of the lesions at the wrists. Aberrant keratotic lesions may appear in the dorsum of the hands, feet, knees, and elbows. The dorsa of the fingers may be involved with a scleroderma-like thickening of the distal digit. A cobblestone hyperkeratosis of the knuckles may be seen. Nails may be thickened. Bothnian-type PPK may be distinguishable by the spongy-white appearance of affected areas when exposed to water.

EPPK and NEPPK show considerable clinical overlap and may be indistinguishable without histologic evaluation; however, some clinical features may help differentiate the two entities. NEPPK may have a more waxy, even appearance, compared with that of EPPK. Hyperhidrosis and pitted keratolysis may be present with NEPPK. Finally, secondary dermatophyte infections are more common in NEPPK.

Histologic findings include orthokeratotic hyperkeratosis associated with hypergranulosis or hypogranulosis and moderate acanthosis. Changes are nonspecific and common to many varieties of keratoderma. An absence of epidermolysis differentiates it from EPPK.

Unna-Thost PPK and Bothnian-type PPK are both autosomal dominant, but they differ in their associated mutations. Unna-Thost PPK molecular biology features include linkage to type II keratin locus on band 12q11-13, corresponding to a keratin 1 gene mutation. Bothnian-Type PPK is marked by a monoallelic missense mutation in the aquaporin 5 gene. Aquaporin 5 is expressed in eccrine sweat glands. [4]

Topical treatment options for NEPPK are similar to those for EPPK. These include salicylic acid, keratolytic agents (ie, lactic acid and urea), and 50% propylene glycol in water under plastic occlusion. Mechanical debridement with a blade may also be useful. Oral retinoid therapy has had variable effects. Treatment with an antifungal agent is beneficial if dermatophyte infection coexists with the NEPPK.

Mal de Meleda [5]

(Video) Palmoplantar Keratoderma | Plantar Keratoderma | Punctate Keratoderma | PPK Skin Disease

A synonym is keratosis extremitatum hereditaria trangrediens et progrediens. Mal de Meleda is an autosomal recessive disease. Onset occurs in early infancy, but the condition is rare. The prevalence is 1 case per 100,000 population. Initially, it was described in inhabitants of the Adriatic Island of Meleda (now called Mljet). [1]

Clinical features of mal de Meleda include a diffuse, thick keratoderma with prominent erythematous borders. Lesions are transgradient with spreading onto the dorsa of the hands and the feet. Constricting bands are present around the digits and can result in spontaneous amputation. Well-circumscribed psoriasislike plaques or lichenoid patches may be present on the knees and the elbows. Patients may have severe hyperhidrosis, possibly accompanied by malodor. Secondary bacterial and fungal infections are common. Perioral erythema; periorbital erythema and hyperkeratosis; nail changes (eg, koilonychia, subungual hyperkeratosis); and lingua plicata, syndactyly, hair on the palms and the soles, high-arched palate, and left-handedness are other clinical features.

Histologic findings include orthokeratosis, normogranulosis, and a pronounced stratum lucidum without epidermolysis. There is a prominent perivascular lymphohistiocytic infiltration.

Molecular biology features include mutations in the gene encoding SLURP-1 found on band 8q24.3. Proteins of the SLURP family have been implicated in transmembrane signal transduction, cell activation, and cell adhesion.

Treatment is with oral retinoids and topical keratolytic agents.

Nagashima-type PPK [6]

This condition is inherited in an autosomal recessive fashion. Onset of disease occurs between birth and age 3 years with stable disease severity over time. To date, the approximately 30 reported cases have occurred in Japan and China.

Clinically, the disease was initially described as a milder form of mal de Meleda. Some classify this keratosis as its own distinct entity, with common involvement of other sites, including the elbows and knees. Hyperhidrosis and tinea pedis infection are associated features. Case reports have described an increased prevalence of malignant melanoma in the hyperkeratotic lesions of Japanese patients with Nagashima-type PPK. [7] This may be due to the lack of epidermal Langerhans cells as seen on histopathology of hyperkeratotic skin. [8]

Treatment options include emollients and keratolytic agents.

Whole-exome sequencing has identified the molecular basis of Nagashima-type PPK as a defect in the SERPINB7 gene. The serpin superfamily of proteins is diverse and contributes to inflammation, immunology, and metastasis. [9]

Progressive PPK (Greither disease)

A synonym is transgrediens et progrediens PPK. This is inherited in an autosomal dominant fashion. Onset occurs in early infancy but may occur later in childhood.

Clinically, Greither disease is a transgradient PPK with extension of plaques onto the dorsa of the hands and the feet. There is characteristic involvement of the Achilles tendon. Scaly plaques may be found on the elbows, knees, and flexural areas. Hyperhidrosis and intrafamilial phenotypic variation are common. Pseudoainhum formation with amputation of the digits has been described.

Histologic features include epidermolysis of the granular cell layer. Lipid-laden corneocytes may be seen.

(Video) Lecture-58: Syndromic Keratoderma and miscellaneous keratotic disorders

Molecular biology features include mutations in the gene encoding keratin 1. [10]

Treatment includes emollients, topical retinoids, keratolytics, and topical steroids.

Diffuse types with associated features

Mutilating PPK (Vohwinkel or Camisa syndrome)

Synonyms include PPK mutilans, loricrin keratoderma, and keratoderma hereditaria mutilans. Mutilating PPK is inherited in an autosomal dominant fashion. Onset occurs in infancy.

Clinically, this condition manifests in infants as a honeycomblike keratosis of the palms and the soles. It becomes transgredient during childhood. Later, constricting, fibrous bands appear on the digits and can lead to progressive strangulation and autoamputation. Starfish-shaped keratoses may occur on the knuckles of the fingers and toes, which is a characteristic feature of this disorder. Alopecia, hearing loss, spastic paraplegia, myopathy, ichthyosiform dermatosis, and nail abnormalities are associated findings. Cases of epithelioma cuniculatum have been reported.

Histologic findings include hyperkeratosis, acanthosis, and a thickened granular cell layer with retained nuclei in the stratum corneum.

Molecular biological studies have confirmed that the most common mutation found in Vohwinkel syndrome involves the gene GJB2, which encodes the gap junction protein connexin 26. [11] This subtype is associated with hearing loss. In contrast, a mutation in the gene for loricrin, involved in epidermal differentiation, is associated with mutilating keratoderma and ichthyosis, but not deafness.

Treatment includes oral retinoids. Reconstructive plastic surgery may be necessary for treatment of digital autoamputation. [12]

Also see Vohwinkel Syndrome.

Bart-Pumphrey syndrome [13]

A synonym is PPK with knuckle pads, leukonychia, and deafness. It is inherited in an autosomal dominant fashion. Onset occurs in infancy.

Clinically, all neonates are hearing impaired from birth and develop diffuse PPK in childhood. Leukonychia and hyperkeratoses over the joints of the hand also appear.

Molecular biological studies describe a new mutation in the GJB2 gene encoding connexin 26, which explains the clinical overlap with Vohwinkel syndrome.

Diffuse NEPPK and sensorineural deafness

(Video) Aquagenic keratoderma | Wikipedia audio article

This condition is inherited in an autosomal dominant fashion. [14]

Clinical features include diffuse palmoplantar hyperkeratosis in mid childhood preceded by slowly progressive, high-frequency hearing loss in early childhood.

Molecular biology features include a connexin 26 mutation. This mutation occurs on a distinct domain from that found in Vohwinkel syndrome. A mitochondrial point mutation has also been demonstrated as the cause of this phenotype, making this the only type of keratoderma associated with a mutation in mitochondrial DNA (serine tRNA). [11]

PPK with sclerodactyly (Huriez syndrome) [15]

PPK with sclerodactyly is inherited in an autosomal dominant fashion. Onset occurs in infancy.

Clinical features include red, atrophic skin on the dorsal hands and feet at birth. Diffuse, mild keratoderma is more marked on the palms than the soles. Other clinical features include sclerodactyly and nail abnormalities (hypoplasia, fissuring, ridging, koilonychia). PPK with sclerodactyly is also associated with marked atrophy and aggressive squamous cell carcinoma in areas of atrophic skin.

Histologic findings include acanthosis, accentuation of the granular layer, and orthokeratosis; Langerhans cells are almost completely absent in the affected skin. Under electron microscopy, dermoepidermal junctions and desmosomes are normal; however, dense bundles of tonofilaments are seen in the epidermal layer. The granular layer shows large, coarse, clumped keratohyalin.

Molecular biologic findings include a mutation in the gene mapped to 4q23.

Owing to the increased risk of skin cancer, close monitoring of patients is recommended. Other treatments include emollients, keratolytics, and topical and oral retinoids.

Hidrotic ectodermal dysplasia (Clouston syndrome)

This syndrome is an autosomal dominant disorder.

Clinical features include diffuse papillomatous PPK (especially over pressure points of the palms and soles), dystrophic nails, and hypotrichosis. Thickened, hyperpigmented skin may also appear over the small and large joints, including the knuckles, elbows, and knees. Thickened, severely dystrophic nails develop, but they may be normal at birth. Universal sparsity of hair affects the scalp, eyebrows, eyelashes, and axillary and genital regions. Sensorineural deafness, polydactyly, syndactyly, clubbing of fingers, mental retardation, dwarfism, photophobia, and strabismus are associated features.

Clouston syndrome is mapped to 13q11. One form is caused by a mutation in the gene encoding connexin 30. Ultrastructural studies of the hair of these patients demonstrate disorganization of hair fibrils with loss of the cuticular cortex. Evidence reported in 2016 suggests that patients may be immunodeficient, with reduced phagocytic activity of granulocytes and monocytes. [16]

Mutilating PPK with periorificial keratotic plaques (Olmsted syndrome)

(Video) Pictures of PPK ✨ porokeratosis ✨ TS ✨ Nerofibromatosis

This type can be autosomal dominant, autosomal recessive, or X-linked recessive depending on the affected genes. Onset occurs in the first year of life.

Clinically, Olmsted syndrome begins focally in infancy and subsequently becomes diffuse. Later findings include flexion deformities and constriction of the digits, sometimes leading to spontaneous amputation. Progressive, well-defined perioral, perianal, and perineal hyperkeratotic plaques are present, as is onychodystrophy. Alopecia, deafness, nail dystrophy, and dental loss may be associated. Squamous cell carcinoma and malignant melanoma have developed in the areas of keratoderma. [17]

Histologic findings include hyperkeratosis without parakeratosis and mild acanthosis. Positive Ki-67 immunostaining of suprabasal keratinocytes suggests that hyperproliferation of the epidermis is a feature of this disease. [18]

Autosomal dominant and recessive forms have been associated with a gain-of-function mutation on the transient receptor potential vanilloid-3 (TRPV3) gene. X-linked recessive forms have been associated with mutations in the membrane-bound transcription factor protease, site 2 gene. [19]

Treatment includes oral and topical retinoids. Full-thickness excision and skin grafting has also been reported to result in clinical improvement. The development of a TRPV3 antagonist would provide the opportunity for targeted therapy.

PPK with periodontitis (Papillon-Lefèvre syndrome)

This condition is inherited in an autosomal recessive fashion. The prevalence of PPK with periodontitis is 4 cases per million. A variant, Haim-Munk syndrome, features, in addition to PPK and periodontitis, arachnodactyly, acroosteolysis, and onychogryphosis.

Clinically, diffuse transgredient PPK may be observed, typically developing within the first 3 years of life. Punctiform accentuation, particularly along the palmoplantar creases, may be seen. Unless treated, periodontosis results in severe gingivitis and loss of teeth by age 5 years. No significant correlation has been demonstrated between the level of periodontal infection and the severity of skin affections, which supports the concept that these major components of this syndrome are unrelated to each other. Patients exhibit increased susceptibility to cutaneous and systemic infections owing to neutrophil dysfunction. Scaly, psoriasiform lesions are often observed over the knees, elbows, and interphalangeal joints. Finally, patients may have malodorous hyperhidrosis. Reports from 2008 indicate a high prevalence of malignant melanoma in Japanese patients with Papillon-Lefèvre syndrome. [20]

Histologic findings include hyperkeratosis with irregular parakeratosis and moderate perivascular infiltration. Electron microscopic features include lipidlike vacuoles in corneocytes and granulocytes, a reduction in tonofilaments, and irregular keratohyalin granules.

Molecular biology findings include mutations in the CTSC gene. This gene codes for cathepsin C and mutations have been mapped to 11q14-q21. [21] Cathepsin C is a lysosomal protease known to activate enzymes that are vital to the body's defenses. Reports of multiple distinct mutations on the CTSC gene have been reported from consanguineous families in Turkey. [22]

Treatment includes oral retinoids for the PPK. Elective extraction of involved teeth may prevent excess bone resorption. Appropriate antibiotic therapy may be required for periodontitis and recurrent cutaneous and systemic infections. Early treatment with acitretin in childhood may allow patients to have normal adult dentition. Finally, in a 2018 in vitro study, introduction of recombinant cathepsin C partially restored some of the downstream immunologic functions of mutant cells and could represent an attractive therapeutic option in the future. [23]

Diffuse NEPPK with woolly hair and arrhythmogenic cardiomyopathy (Naxos disease) [24]

This condition is inherited in an autosomal recessive fashion.

Clinically, a diffuse, nontransgredient keratoderma with an erythematous border appears during the first year of life. Woolly (dense, rough, and bristly) scalp hair is present at birth. Cardiac disease, manifested by arrhythmias, heart failure, or sudden death, becomes evident during and after late puberty. Other cutaneous manifestations include acanthosis nigricans, xerosis, follicular hyperkeratosis over the zygoma, and hyperhidrosis.

(Video) Heriditary skin diseases Part 1

Histologic findings include hyperkeratosis, hypergranulosis, and acanthosis.

Molecular biology findings include a mutation in the plakoglobin gene, mapping to 17q21, which is responsible for Naxos disease. Cardiomyopathy with alopecia and palmoplantar keratoderma (CAPK) is a subtype of Naxos disease described in a family with alopecia and right ventricular arrhythmogenic cardiomyopathy. CAPK has been linked to a mutation in the JUP gene coding for plakoglobin. [25] Plakoglobin is an important component of cell-to-cell and cell-to-matrix adhesion complexes of many tissues, including the skin and cardiac junctions. It also plays a role in signaling in the formation of desmosomal junctions. Mutations in the plakoglobin gene may lead to detachment of the cardiac myocytes, resulting in myocyte death. Plakoglobin mutations may also lead to desmosomal junction fragility in hair shafts, explaining the clinical phenotype of woolly hair.

Normalization of plakoglobin levels has been shown to restore cardiac function in mice and may be a viable therapeutic approach for improving the cardiac, and other, manifestations of this disease. [26]


What is keratosis palmaris et plantaris? ›

Keratosis palmaris et plantaris (KPP), also referred to as tylosis and by many other synonyms,* is a heredofamilial ectodermal defect characterized by hyperkeratosis of the palms and soles.

What is the treatment for PPK? ›

The PPK can be treated with topical emollients, keratolytics, and oral retinoids. Genetic counseling may be offered to families once a diagnosis is established. Synonyms include tyrosinemia type II. Oculocutaneous tyrosinemia is inherited in an autosomal recessive fashion.

What is the difference between focal and diffuse PPK? ›

Classification of keratodermas depends on whether it is inherited or acquired, and the clinical features. Diffuse keratodermas affect most of the palms and soles. Focal keratodermas mainly affect pressure areas. Punctate-type keratoderma results in tiny bumps on the palms and soles.

What is PPK disease? ›

Palmoplantar keratoderma (PPK) is a heterogeneous group of inherited or acquired disorders characterized by excessive epidermal thickening of the palms and soles.

Is there a cure for keratosis? ›

Treatment cannot cure keratosis pilaris, so you'll need to treat your skin to keep the bumps under control. Your maintenance plan may be as simple as using the medicine twice a week instead of every day. Another option may be to switch to a non-prescription moisturizing cream.

Is keratosis a tumor? ›

Skin growths like seborrheic keratoses are sometimes also called epidermal tumors. That doesn't mean they're cancer, though. Technically, moles and warts are also epidermal tumors. That just means they are clusters of extra cells on the epiderma, the outer layer of the skin.

How do you get rid of keratoderma? ›

Treatment options include regular use of saltwater soaks, emollients, topical keratolytic such as urea or salicylic acid, antifungal tablets or creams if indicated, topical retinoids, Calcipotriol, systemic retinoids, skin grafting, and topical steroids.

Is palmoplantar keratoderma a disability? ›

Hypohidrosis-enamel hypoplasia-palmoplantar keratoderma-intellectual disability syndrome is a rare, genetic, syndromic intellectual disability disorder characterized by severe intellectual disability with significant speech and language impairment, hypohydrosis (often resulting in hyperthermia) with normal sweat gland ...

Is palmoplantar keratoderma an autoimmune disease? ›

1 Palmoplantar keratodermas (PPKs) are characterized by hyperkeratosis of the skin on the palms and soles. 2 Multiple cases have been reported associating PPK with autoimmune thyroiditis.

Which Palmoplantar Keratoderma PPK is associated with esophageal carcinoma? ›

Definition. Tylosis with oesophageal cancer is characterised by thickening of the skin of the hands and feet (focal, non-epidermolytic form of palmoplantar keratoderma) associated with a very high lifetime risk of developing squamous cell carcinoma of the oesophagus (OSCC).

What is the treatment for palmoplantar keratosis? ›

Topical (emollients, keratolytics, retinoids, steroids) and systemic treatments (mostly different retinoids), often combined, are used to relieve symptoms. Oral retinoids appear to be the most efficient treatment, but not in all PPK forms, and with variable tolerance.

What are the acquired causes of PPK? ›

The causes of acquired PPK vary, and include exposure to certain chemicals (e.g., arsenic, chlorinated hydrocarbon fluids) 4, ; side effects of certain drugs (e.g., beta-glucan, lithium, chemotherapy agents) and metabolic disorders (gravidity, menopause, hypothyroidism, myxedema) are other possible causes 2.

How does keratoderma start? ›

MEDNIK syndrome results from mutations in AP1S1, encoding a subunit (1A) of an adaptor protein complex (AP-1) that is involved in the organization and transport of proteins during skin and spinal cord development.

Should I worry about keratosis? ›

If your doctor says your skin growth is a seborrheic keratosis, you usually don't need to worry about it. But if it is growing fast, looks unusual, or is bleeding or causing pain, see your doctor. You may be referred to a dermatologist.

Can keratosis become cancerous? ›

Some actinic keratoses can turn into squamous cell skin cancer. Because of this, the lesions are often called precancer. They are not life-threatening. But if they are found and treated early, they do not have the chance to develop into skin cancer.

When should I worry about keratosis? ›

See your doctor if the appearance of the growth bothers you or if it gets irritated or bleeds when your clothing rubs against it. Also see your doctor if you notice suspicious changes in your skin, such as sores or growths that grow rapidly, bleed and don't heal. These could be signs of skin cancer.

Is keratosis caused by HPV? ›

Genital seborrheic keratoses are human papillomavirus-related lesions.

Should keratosis be removed? ›

A seborrheic keratosis typically doesn't go away on its own, but treatment isn't needed. You might choose to have it removed if it becomes irritated or bleeds, or if you don't like how it looks or feels.

What does a cancerous keratosis look like? ›

What do actinic keratoses look like? AKs often appear as small dry, scaly or crusty patches of skin. They may be red, light or dark tan, white, pink, flesh-toned or a combination of colors and are sometimes raised. Because of their rough texture, actinic keratoses are often easier to feel than see.

How do you stop keratosis growth? ›

There is no way to completely prevent the development of seborrheic keratoses. However, if you know you're at risk or you frequently develop these growths, working with a dermatologist means you can limit the impact this skin condition has on your life.

How do you get rid of keratosis naturally? ›

How to treat keratosis pilaris at home
  1. Keep baths and showers short. ...
  2. Use a mild, fragrance-free cleanser. ...
  3. Gently exfoliate skin with keratosis pilaris once a week. ...
  4. Moisturize your skin. ...
  5. Avoid shaving or waxing skin with keratosis pilaris.
Jun 24, 2021

Can you get rid of keratosis at home? ›

Actinic keratosis is a skin condition caused by prolonged exposure to the sun. While no home remedies can treat this condition, a doctor might prescribe at-home topical medications to reduce its appearance.

What foot problems qualify for Social Security disability? ›

If you have osteoarthritis in your feet and can no longer work, you may be eligible for financial assistance through the Social Security Disability program.

What causes palmoplantar keratoderma? ›

There are many possible causes for acquired palmoplantar keratodermas including drugs, menopause, chemicals (e.g. arsenic), mechanical stimulation, malnutrition, systemic conditions (e.g. thyroid disease, circulatory disorders), malignancies (e.g. lung cancer, colon cancer, lymphomas), skin conditions (e.g. psoriasis, ...

Is palmoplantar keratoderma painful? ›

Pain is a prominent symptom in hereditary palmoplantar keratodermas (PPKs). Pain in patients with PPK can be difficult to treat. Pain mechanisms in PPKs are poorly understood.

What triggers palmoplantar psoriasis? ›

[2][3][4] Environmental triggers include smoking, irritants, friction, and manual or repetitive trauma. Paradoxically, anti-tumor necrosis factor-alpha agents have been shown to induce palmoplantar eruptions. The majority of patients with palmoplantar pustulosis are current or former smokers.

What age does palmoplantar Keratoderma occur? ›

3) Progressive Palmoplantar Keratoderma

Onset of clinical features usually appears between ages 8 and 10.

What are the symptoms of palmoplantar Keratoderma? ›

Disease at a Glance

Palmoplantar keratoderma (PPK) is a group of skin conditions characterized by thickening of the skin on the palms of the hands and soles of the feet. PPK can also be a feature of various underlying syndromes. In rare forms of PPK, organs other than the skin may also be affected.

What is the treatment for palmoplantar keratoderma? ›

Topical (emollients, keratolytics, retinoids, steroids) and systemic treatments (mostly different retinoids), often combined, are used to relieve symptoms. Oral retinoids appear to be the most efficient treatment, but not in all PPK forms, and with variable tolerance.

How do you get rid of plantaris? ›

Lifestyle and home remedies
  1. Maintain a healthy weight. Extra weight can put extra stress on your plantar fascia.
  2. Choose supportive shoes. Buy shoes with a low to moderate heel, thick soles, good arch support and extra cushioning. ...
  3. Don't wear worn-out athletic shoes. ...
  4. Change your sport. ...
  5. Apply ice. ...
  6. Stretch your arches.
Jan 20, 2022

What causes plantar hyperkeratosis? ›

Plantar hyperkeratosis typically occurs when areas of the sole are put under too much pressure (for example, if ill-fitting shoes rub and pinch your feet). Excessive pressure triggers excessive keratin production, which results in the excessive thickening of the skin.

What causes keratosis to grow? ›

Experts don't completely understand what causes a seborrheic keratosis. This type of skin growth does tend to run in families, so there is likely an inherited tendency. If you've had one seborrheic keratosis, you're at risk of developing others. A seborrheic keratosis isn't contagious or cancerous.

Is Palmoplantar a disability? ›

Palmoplantar pustulosis, or pustular palmoplantar psoriasis, is a possibly related dermatosis characterized by small, sterile pustules that may be a type of palmoplantar psoriasis or a distinct entity. [1] Both conditions are chronic in nature and produce significant functional disability.

What does plantaris pain feel like? ›

Symptoms of Plantaris Strains and Tears

Sudden pain in the back of the calf. A swelling or bunching of the calf muscle. Swelling and bruising in the back of the leg. Cramping and spasm sensations of the calf muscle.

What causes plantaris? ›

Plantar fasciitis can be caused by a number of factors, including type of shoes, foot structure, overuse and types of walking surfaces. The main symptom of plantar fasciitis is heel pain. Treatment for plantar fasciitis usually does not require surgery.

How long does it take for a plantaris muscle to heal? ›

The diseases of the aging athlete are not fun. The good news is, recovery from a plantaris tendon rupture only takes about two weeks. I just might get to wear those cute shoes after all. medial head of the gastrocnemius tears from its bony origin or from the musculotendinous junction.

Can hyperkeratosis be cancerous? ›

Follicular hyperkeratosis: Also known as inverted follicular hyperkeratosis, this condition presents as a single bump, often on the face, of middle-aged or older adults. These growths are benign (noncancerous), but they often look like cancerous lesions.

What are the symptoms of plantar keratosis? ›

This condition often presents as painful cracking and fissuring of the plantar heel as well as the palms. Clinicians often see this condition spread from the plantar heel to the sides of the foot. This condition mainly affects postmenopausal females and can be painful.

What is the best treatment for plantar hyperkeratosis? ›

There are several treatment methods for plantar hyperkeratosis, such as salicylic acid plaster, scalpel debridement, intralesional bleomycin injection,1 and conservative modalities. In general, salicylic acid plaster and scalpel debridement are the most common treatments.

Is keratosis a serious condition? ›

Complications. If treated early, actinic keratosis can be cleared up or removed. If left untreated, some of these spots might progress to squamous cell carcinoma. This is a type of cancer that usually isn't life-threatening if detected and treated early.

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