plantar heel pain (PHP) can occurs as a resolute of a variety of soft tissue, neurological and osseous pathologies, Although plantar fasciitis is consider to be the most common Cause of PHP in adults [1,2] there are few other structures that may be involved in PHP, heel pad atrophy, Baxter nerve entrapment, calcaneal stress fracture, and tarsal tunnel syndrome can be a contributing factor in the chronic PHP.
Establishing an accurate diagnosis of the aggravated tissues, the fault biomechanics and the aggravating beaver is critical for choosing the right treatment but can be very challenging due to complex regional anatomy and the fact that in most cases of PHP patients start seeking treatment months or years after their first establish of pain approaching the clinic with a chronic multi-structural picture of over used heel.
Yi et al found in their study of 250 patients with PHP that plantar fasciitis was the most common diagnosis account for 53.2%, fat pad syndrome14.8%, Plantar fasciitis plus fat pad syndrome 9.2%, plantar fibromatosis 4.4%, plantar fascia rupture in 1.6% and neuropathy 0.8%(3).
lu et al found in their study of 200 patients with 266 heel pain (83 males and 117 females, mean age of 46 years) 67 heels with plantar fasciitis, 61 heels with calcaneal bursitis, 36 heels with plantar fat pad, 6 heels with calcaneus high pressure, 21 heels with nerve compression, 75 heels with mixed(4).
Chimutengwende-Gordon et al found in there magnetic resonance imaging (MRI) study of 112 patient with PHP who have atypical symptoms or who do not improve with appropriate management, 76% with plantar fasciitis, Patients with night pain were shown to have plantar fasciitis associated with calcaneal marrow edema,(71.4%) and acute pain was associated with plantar fascia tears in 4 out of 9(5).
Sabir et al found in a sonography study a strong correlation between plantar fascia and fat pad thickness measurements done by sonography (P < .001; r = 0.854) and MRI (P < .001; r= 0.798) (6).
To our opinion this results describing moderate picture due to very stiff diagnosis rolls and that in some degree of involvement the fat pad, the sub calcaneal burse and the calcaneus bone play greater role in chronic PHP.
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PHP is a common complain, approximately 1 in 10 people are predicted to develop chronic PHP during their lifetime . PHP is also estimated to account for approximately 8% of all running-related injuries [7,8] and that PHP occurs in two million Americans each year. The diagnosis and treatment of PHP accounts for over one million visits to physicians per year and over $284 million in medical costs in the US [10,11]
The AIM of this review is to establish a more complex approach to the chronic PHP based on the recent knowledge and our clinical experience, describing the chronic PHP as multi structural problem with the plantar fascia playing dominant roll but being only a part of a complex multi factorial problem
Plantar fasciitis described as a degenerative syndrome of the plantar fascia resulting from repetitive stretching trauma at its origin on the calcaneus [12,13 ]. Featuring pain and tenderness on the medial plantar prominence of the calcaneus. Patients usually complain on stabbing pain by bearing weight on the heel after long periods of rest, typically early in the morning, during their first steps after getting out of bed. Once the patient starts walking, the pain tends to recede . Plantar fasciitis is seen in the athlete population, but it's also prevalent in the general population, particularly in women ages 40-60, Bilateral symptoms can occur in 20-30% of those diagnosed with plantar fasciitis . Plantar fasciitis is usually a self-limiting condition typical resolves in 6-18 months and treated non-operatively . However, 10% to 20% develop chronic pain and may require surgery .
Most experts agree that early recognition and treatment of plantar fasciitis leads to a shorter course of treatment and greater probability of success with conservative therapies. Conservative treatment of plantar fasciitis should address the inflammatory component and the biomechanical factors that produce the disorder. Patient education is imperative. Patients must understand the etiology and the biomechanical factors that caused their problem. They should learn about recommended changes in daily activities, wear appropriate shoes and advised to relative rest until the plantar fasciitis resolves. The patient should apply foot and core muscle exercise, stretching of the plantar fascia and calf muscles , the patient should be subscribed to specific foot orthotic unloading aggravating factors by using high soft shock absorbing material beneath the fat pad and the plantar fascia insertion and full arc support, the orthotic technician should optimized the orthotic two and four weeks after it was subscribed, the patient should consider weight loss, and address the clinic for chosen physical therapy model including manual therapy, exercise, dry needling, ultra sound, laser therapy, if at least 6 months of conservative treatment is ineffective corticosteroid injections and extracorporeal shock-wave therapy can be considered .
The plantar fascia is a thick fibrous connective tissue composed from three components, lateral, medial, and central band. The central component originates from the medial tubercle on the undersurface of the calcaneus and fans distally, dividing into five digital bands that insert the plantar plate of the metatarsophalangeal joint and the base of the proximal phalanx. The term plantar fascia is actually a misnomer since this structure is not a facial layer, but a tendon's aponeurosis that shares histological and mechanical traits with tendons and ligaments , the plantar fascia lacks elasticity, exhibiting a maximal elongation of only 4% of its length and 1000N failure loud .
The plantar fascia has a continuous connection with the Achilles tendon, leading to tightening of the plantar fascia when tensile loads are applied to the tendon. The Stretch tension of the plantar fascia prevents the spreading of the calcaneus and the metatarsals and maintains the longitudinal arch [19,20].The plantar fascia takes an important role in absorbing shocks during weight- bearing activities, Its locks the foot and provide a rigid structure for propulsion, then passively contracts, converting the stored potential energy into kinetic energy aiding acceleration 
The windlass mechanism
The windlass mechanism is a term used to describe the role of the plantar fascia in dynamic function during gait, describing the foot and its ligaments as an arch-like triangular structure which vertical forces from body weight travel downward via the tibia and tend to flatten the longitudinal arch. Dorsi-flexion of the ankle and the hallux during the propulsive phase of gait winds the plantar fascia around the head of the metatarsals, shortening the plantar fascia and elevating the medial longitudinal arch .
Historically, plantar fasciitis was considered an inflammatory syndrome; however, recent studies have demonstrated that plantar fasciitis is actually due to histological changes of degenerative process rather than an inflammatory process. Microscopic examination of the plantar fascia often shows fiber fragmentation in association with myxoid degeneration, connective tissue calcium deposits, vascularization of the attached bone marrow, and disorganized collagen fibers [22,23].
Plantar fascia thickening  and loss of normal tissue elasticity  play an important role in the genesis of persistent plantar fasciitis. There is an increase of mechanical stiffness, which results in higher tissue hydrostatic pressure within the plantar tissues during loading consequently reduce the blood flow cross-section supply . The proximal plantar fascia is relatively hypo-vascular, as it is perfused by only a few vessels with none at its insertion onto the calcaneus. These events can cause tissue necrosis and replacement with undifferentiated scar tissue and is the presumed reason for lack of response to traditional nonsurgical therapies .
The etiology of plantar fasciitis combines extrinsic and intrinsic factors which contribute to the development of the syndrome.
Extrinsic factor: suggested in the literature include training errors such has training on unyielding surfaces, improper or excessively worn footwear and over training [28,29] and work related factors such as time spent standing and walking or floor surface characteristics .
Intrinsic factors suggested includes faulty biomechanics such as excessive pronation [31,32], plantar longitudinal arch configurations, leg length discrepancy, excessive lateral tibia-torsion, excessive femoral ante version[34,35], increased plantar load[36,37].
The tree major risk factors for planter fasciitis:
Decrease range of ankle dorsiflexion (below 10 degrees) due to tightness of either the Achilles tendon or the gastrocnemius muscle is probably one of the strong independent risk factors in the nonathletic population [2,35,38]
Obesity is present in up to 70% of patients with Plantar Fasciitis. According to the literatures, there is a strong association between increased body mass index and Plantar Fasciitis in a non-athletic population while there is no strong correlation in the athletic population [39,40,41].
Calcaneal heel spur have commonly been implicated as a risk factor for plantar fasciitis, studies demonstrate a highly significant association between calcaneal spur and plantar fasciitis [42,43]. Current studies found spurs radiographic evidence in about 11-27% of the population [41,44,45] and that plantar spur is more common in people whose lower limb tissues are under siege from age [46,41,47] , weight (40) and stress, and associated with general foot problems and pain [48,49].
Proximal contributes to plantar fasciitis
The tibialis posterior muscle provided the most significant dynamic arch support during the stance phase , eccentrically lengthens to control pronation and reduce the tension applied to the plantar fascia during weight acceptance, weakness of the tibialis posterior muscle can generate stress to the plantar fascia resulting plantar fasciitis. The combined effects of the flexor digitorum longus, flexor hallucis longus, peroneus longus, and Achilles tendons permit the supination needed to enhance the windlass mechanism . poor biomechanics of the coordinated muscles can results in plantar fasciitis. Proximal muscle weakness, the gluteus's, quadriceps muscles or the core muscles inhibits their ability to assist with the lower extremity load response, resulting with poor shock absorbing of the supporting foot  Furthermore, weakness of this muscles can accelerate lower extremity pronation, expose the plantar fascia to excessive traction.
The diagnosis of plantar fasciitis is made with a reasonable level of certainty on the basis of history and physical examination alone [52,53].
• Patient will complain of sharp, localized pain under the anteromedial aspect of the plantar surface of the calcaneus.
• Pain worsen upon weight bearing after a period of non-weight bearing , typically early in the morning, during their first steps after getting out of bed, the pain start to recede after few minutes of weight bearing.
• Pain will tend to worsen toward the end of working day.
• The history usually indicates that there has been a recent change in activity, such as increased running distance, employment change that requires more time standing, or Weight gain.
• Dorsi-flexion at the ankle limited by 5 digress or more and Tightness of the Achilles tendon can be found in 70-80 percent of patients.
• Pain is usually unilateral, but up to 30% of cases have a bilateral presentation
• Palpation Reveal localized tenderness at the antero-medial aspect of the calcaneus.
• Pain often increases with stretching of the plantar fascia, which is achieved by passive dorsiflexion of the foot and toes
• Pain may be exacerbated having the patient stand on the tips of the toes.
Imaging is typically not necessary for the diagnosis of plantar fasciitis. Imaging would be useful to rule out other possible causes of heel pain or to establish a diagnosis of plantar fasciitis if the healthcare provider is in doubt. Imaging types used include ultrasonography and MRI for investigation of soft tissue structures (e.g. the plantar fascia) and x-rays for bone abnormalities.
Analysis of studies found that people with plantar fasciitis are likely to have a thickened plantar fascia with associated fluid collection, and that thickness values >4.0 mm are diagnostic of plantar fasciitis. Plantar fascia thickness values have also been used to measure the effect of treatments and there is a significant correlation between decreased plantar fascia thickness and improvement in symptoms [55,56] Additionally, sub-calcaneal spur formation is strongly associated with plantar fasciitis .
The compression theory
Kumai and Benjamin argued that calcaneal spurs develop in response to repetitive compression forces rather than traction, they suggest that calcaneal spurs are fibrocartilage nous outgrowths which form in response to vertical forces in an attempt to protect the calcaneus . Such an explanation is consistent with recent histological study which indicates that the bony trabeculae of spurs are vertically oriented, suggesting vertical forces are responsible for spur formation , Furthermore, studies have found that calcaneal spurs are more common in those who are overweight, older population, osteoarthritis, current or previous heel pain and in those who have decreased plantar heel fat pad elasticity, but are unrelated to radiographic measurements of foot posture . Studies have also found that most spurs are located deep to the plantar fascia, typically in the flexor digitorum brevis, quadratus plantae and abductor halluces muscle insertions [61,62] These findings support the theory that plantar calcaneal spurs may be an adaptive response to vertical compression of the heel.
Clinical facts supporting the compression theory:
1. Most plantar fasciitis patients complains of worsening symptoms by walking barefoot or walking with poor cushioning shoos while relive of pai walking whith soft shoes.
2. The main clinical sign for plantar fasciitis is pressing the medial tubercle of the undersurface of the calcaneus while stretching the plantar fascia or standing on tows is rarer sign.
3. The fact that dorsal flexion restriction is one of the dominant risk factor for plantar fasciitis can be explained by the fact that shortening of posterior components shift the body central mass backwards adding more pressure on the calcaneus while standing and walking.
4. Risk factors like time spent standing, working on stiff surface is more correlated with the compression theory.
heel fat pad syndrome
Plantar fat pad first described by Teitze in 1921, the plantar fat pad is a specialized adipose structure located beneath the calcaneus, protects the rear foot from shocks and stress generated during the heel-strike and the initial support phase. The impact load on the calcaneus was estimated up to 110% of one’s body weight when walking and 250% of body weight when running .
The plantar surface of the calcaneus is composed of three primary layers .
The superficial layer is rugged and protective outer skin layer, The deeper two layers compose the fat pad which is 18mm thick and has loaded surface area of between 9-19 cm\sq .
The superficial fat pad layer is dense microtubule layer which acts as a natural heel cup, located immediately inferior to the dermis, held together by separate walls of dense irregular collagen connective tissue, it is highly vascular, has a high degree of stiffness in response to loading and the separate walls are composed of predominately elastic fibers.
The deep layer is a macrotubule honeycomb configuration layer which contains large pockets of adipose tissue with no interconnection between the units, has an equal amounts of elastic and collagen fibers and respond with a proportionately larger degree of deformation and corresponds with overall heel pad stiffness [66,67]. The fibrous septa originate from the plantar aponeurosis or the calcaneus and extend toward the dermis.
Both macro and micro-chambers contain a combination of different fatty acids with a greater ratio in order that viscosity is maintained in temperatures lower than body heat .
Overuse, cumulative micro trauma or acute traumatic injury may damage the architecture of the heel pad, increased tissue thickness and modification of the tissue bio-mechanical properties, such as stiffening, lower strain threshold and change of the compressibility tissue index [69,70]. Morphologically the adipose chambers get smaller, fibrous septa get thicker, fibrous components become disorganized because of breaking of collagen bundles and fragmentation of elastin [71,66]. Consequently, decrease the fat pad ability to cushion and protect the musculoskeletal system, causing the foot to be more vulnerable to mechanically related complications such as heel pad inflammation, plantar fasciitis and calcaneal stress fracture .
Heel fat pad pain is typically more diffuse, usually in the middle of the heel, and can be reproduced with firm palpation. Walking barefoot or on hard surfaces exacerbates the pain. In contrast to pain caused by plantar fasciitis, heel pad pain tends not to radiate anteriorly, dorsi flexion of the toes does not increase the pain, night pain and bilateral pain is more prevalent with less first-step after rest pain phenomena .
Plantar fascia rapture
Since the first report (1978)of plantar fascia rapture in athletes it has been considered as an acute injury related to a high velocity sport injury particularly in athletes engaged in sports that require running and jumping such as distance running, basketball, football, and tennis [73,74,75].
Since the early 90's spontaneous plantar fascia ruptures have been reported related to continued overuse when plantar fasciitis is present  and related to steroid injections .
Patients with an acute rupture will classically complain of acute pain accompanied by a snapping noise  and marked associated swelling. However, patients with preexisting plantar fasciitis often suffer from a spontaneous rupture, not aware of the event and the diagnosis of plantar fascia rupture is often missed, The patient often subscribe a gradual relief of the original heel pain, which had been replaced by a variety of new foot problems, including dorsal and lateral midfoot pain, swelling, foot weakness, metatarsal pain and flattening of the involved arch. 
Most cases of plantar fascia rupture involve the proximal portion of the fascia near its calcaneal insertion, although more anterior tears have also been described (75,80). Physical examination may reveal a palpable deficit in the plantar fascia or a small enlarged area at the distal aspect of the plantar fascia rupture.
Yi et al found in their study 1.6% with misdiagnosed plantar fascia rapture in PHP patient(3), Tsai et al found 1% with misdiagnosed plantar fascia rapture(81), Sutera et al found 16%fascia partial tear in php patient.(82) and Mukai et al found in their study of 112 PHP patients, 5 plantar fascia partial tear, in their study 9 patient where considered to have acute unset, Four of the 9 patients were found to have a tear of the plantar fascia(83).
Plantar fibromatosis, or Ledderhose disease, is a rare hyperproliferative disorder of the plantar aponeurosis first described in 1894 by Dr. Georg Ledderhose. Its etiology is unknown. Plantar fibromatosis is characterized by fibrous proliferation of the plantar fascia and can be associated with other superficial fibromatosis, mainly with palmar fibromatosis (Dupuytren's contracture) . It has been found that the incidence may be as high as 25% in the middle-aged and elderly population and that the condition affects men approximately 10 times more often than women and accurse more in males. Plantar fibromtosis found more commonly on the central component of the plantar fascia. On examination, fibrous nodules can be palpated, these nodules are painless or cause only vague to moderate pain. They are frequently multiple and bilateral, which can be helpful diagnostically.
Yi et al found in their study 4.4% with plantar fibromatosis in PHP patient (3)
Flexor digitorum brevis and the Quadratus plantae
Flexor digitorum brevis and quadrates plantae are strong internal flexors of the foot which arise from the concave surface of the calcaneus just inter-medial and deep to the plantar fasciitis pain site. These intrinsic muscles play an important dynamic role in weight bearing tasks working with the plantar fascia dynamically to prevent deflection of the arch during mid stance and assisting with the heel elevation during the late portion of stance.
Late studies show that the heel spur more often located at the insertion site of these muscles indicates they may be exposed to over load injuries and MRI researches found some involvement of these muscles in plantar fascia rupture.
I didn’t found any research trying to assess the involvement of the intrinsic muscles as pain generators in the PHP syndrome or trying to assess the part of these muscles weakness in the progression of plantar fasciitis, but screening most of the treatment strategies offered in the literature, most of them include intrinsic flexors exercise as significant part for treating plantar fasciitis.
Calcaneal marrow edema
plantar fasciitis with calcaneal enthesophathy as a result of a repetitive trauma can produce plantar calcaneal bone marrow edema on the insertion site of the plantar fascia, but bone marrow edema of the medial portion of the calcaneus can be also develop as a response to poor calcaneal fat-pad athropy, over pronated foot, improper worn footwear and working long hours standing on stiff surfaces. Calcaneal marrow edema or calcaneal brows can produce a PHP and mimic plantar fasciitis symptoms.
Muaki at el found in his MRI research of 112 patient with PHP who have atypical symptoms or who do not improve with appropriate management 16 patients with calcaneal marrow edema. 71% of the patient how suffer from night pain had a calcaneal marrow edema.
Calcaneal Stress Fracture
Stress fractures of the foot and ankle are a common problem encountered by athletes of all levels and ages and elderly patients with osteopenia, the highest rate of calcaneal stress fracture accurse in military recruits and long-distance runners  Stress fractures occur due to repetitive sub maximal loading of the calcaneus and the inability of bone formation to match resumption. Pure cautioning shoes, fatigue muscles, small amount of sleeping hours, fault training program are probably major contributing factor leading to micro fractures. The calcaneus is the second most frequent location of stress fractures of the foot second only to the metatarsals. Patients typically complain of diffuse heel pain and tenderness over the medial and lateral aspects of the heel  Pain is exacerbated by activity and weight bearing, and it may progress to become persistent even at rest . A positive calcaneal compression test with some amount of swelling is usually present. Radiographic findings are usually normal in the early stages , and follow-up radiography discloses diagnostic features in only 50% of cases .
PHP of neural origin
PHP may have a neural origin, with a lesion or dysfunction of the sciatic, tibial, and plantar or calcaneal nerves. Nerve dysfunction can lead to Hyperalgesia, allodynia or radicular pain off the plantar heel lesion, but neural dysfunction can also reduce the proprioceptive impute and muscles strength around the heel leading to poor coordination, muscle imbalance and local injury.
Nerve dysfunction can be of some levels; in the overt level the patient may complain on weakness, pain, tingling or numbness, the diagnosis will be clear and simple by neurological tests.
When the nerve dysfunction is covert or hidden the patient do not complain on neural symptoms the nerve dysfunction is in a low level just beneath the radar or in other cases the nerve entrapment may happened under specific provocation such as walking with working boots for few hours. In this scenario diagnosis will become hard and misdiagnosis is a common.
Patients with PHP of neural origin, will complain on pain characterized as sharp, shooting, electric, localized or radiating pain that is worse during or after weight-bearing activities and improves with rest(90). Patient with PHP of neural origin will also complain of pain when first standing after long periods of rest, typically in the first steps in the morning (91).
Tarsal tunnel syndrome
The tarsal tunnel is a continuation of the deep posterior compartment of the leg, located distal and posterior to the medial malleoli, with an osseous floor formed by the medial talar surface, the sustentaculum tali, and the medial calcaneal wall and Its roof formed by the flexor retinaculum. The posterior tibial nerve, posterior tibial artery, and tendons of the tibialis posterior, flexor digitorum longus, and flexor hallucis longus muscles travel in a bundle through the tarsal tunnel. Inside the tarsal tunnel, the posterior tibial nerve splits into his three different segments the medial calcaneal branch and the medial and lateral plantar branches.
Tarsal tunnel syndrome is a compressive neuropathy of the tibial nerve or its branches in the tarsal tunnel. Various causes of this condition have been described and classified into trauma, space-occupying lesion and foot deformities .
The tarsal tunnel syndromes often occur as a result of pes planus involving hind foot inversion and for foot abduction causing more tension on the tibial nerve and on the tendons passing through the tarsal tunnel (93) or hind foot eversion with pronated forefoot causing shortening of the abductor hallucis muscle decreased the cross-sectional area of the tarsal tunnel.
Baxter Nerve Entrapment
The Lateral Plantar Nerve supplies most of the foot muscles and the skin of the lateral one-third of the plantar aspect of the foot and the fourth and fifth toes, the first branch of the lateral plantar nerve, Baxter nerve, innervates the flexor digitorum brevis, quadratus plantae and abductor digiti minimi muscles and provide sensation to calcaneal periosteum(94).
Entrapment of Baxter nerve can occur at 3 different sites: at the sharp edge of the deep fascia of the abductor hallucis, at the medial edge of the calcaneus, particularly in the presence of a calcaneal spur or plantar fasciitis and between the abductor hallucis and the medial head of quadratus plantae muscle(95).
Bexter nerve entrapment considered to be the most common cause of plantar heel pain of neural origin and represent 15–20% of the patients with chronic plantar heel pain (96).
Medial calcaneal nerve entrapment
MCN is the second most commonly reported nerve that has been related to plantar heel pain of neural origin, It emerges from the posterior aspect of the posterior tibial nerve provides sensory innervations to the heel fat pad and to the to the anterior-medial plantar surface of the calcaneus.
entrapment of the MCN may not be a very prevalent condition as Most branches of the MCN lie superficially to the foot flexors but can be irritated entrapped between the calcaneus and the ground following atrophy of the heel fat pad(97).
Heel pain may occur in patients with various systemic conditions, including rheumatoid arthritis, ankylosing spondylitis, Reiter's syndrome, gout and systemic lupus erythematosus [98,99,100], Most patients with systemic disease present with multiple joints pain in other areas of the body. Carful history examination can help diagnose the systemic disorder. The number of patients whose heel pain is caused by systemic arthritic diseases is small but these arthritic diseases must be ruled out.
PHP is a common disorder usually involves the plantar fascia attachment to the calcaneus. However, various other problems may play a significant role in the development of PHP and should not be overlooked.
The aim of this paper was to highlight some of the difficulties establishing clear diagnosis when we approaching the PHP syndrome and to emphasize the possibility that PHP and specially the chronic PHP is not a simple inflammatory process of the plantar fascia but a collection of problem's led by plantar fasciitis that may occur in the overload heel.
References:1. Singh D, Angel J, Bentley G, Trevino SG. Fortnightly review. Plantar fasciitis. BMJ. 1997;315:172–5.2. Cole C, Seto C, Gazewood J. Plantar fasciitis: evidence-based review of diagnosis and therapy. Am Fam Physician. 2005;72:2237–42.3. Yi TI1, Lee GE, Seo IS, Huh WS, Yoon TH, Kim BR. Clinical characteristics of the causes of plantar heel pain. Ann Rehabil Med. 2011 Aug;35(4):507-13. doi: 10.5535/arm.2011.35.4.5074. Lu D1, Xu WX, Ma GP, Guo QF. Small needle-knife for the treatment of heel pain according to its classification. Zhongguo Gu Shang. 2010 Aug;23(8):616-5. Magnetic Resonance Imaging in Plantar Heel Pain Mukai Chimutengwende-Gordon, Paul O'Donnell, and Dishan Singh.Foot Ankle Int, October 2010; vol. 31, 10: pp. 865-870.6. Sabir N, Demirlenk S, Yagci B, Karabulut N, Cubukcu ,Clinical utility of sonography in diagnosing plantar fasciitis. J Ultrasound Med 2005;24:1041–1048.7. Riddle DL, Pulisic M, Pidcoe P, Johnson RE. Risk factors for plantar fasciitis: a matched case-control study. J Bone Joint Surg Am. 2003;85-A:872–7.8. Taunton JE, Ryan MB, Clement DB, McKenzie DC, Lloyd-Smith DR, Zumbo BD: A retrospective case-control analysis of 2002 running injuries. Br J Sports Med 2002, 36:95-101.9. Lysholm J, Wiklander J: Injuries in runners. Am J Sports Med 1987, 15(2):168-171.10. Riddle DL, Schappert SM. Volume of ambulatory care visits and patterns of care for patients diagnosed with plantar fasciitis: a national study of medical doctors. Foot Ankle Int 2004; 25: 303–310.11. Tong KB, Furia J. Economic burden of plantar fasciitis treatment in the United States. Am J Orthop (Belle Mead NJ) 2010;39(5):227–23.12. . Cornwall MW. McPoil TG. Plantar fasciitis: etiology and trciitnient. J Orthop Sports Pins Tlicr l999;29:756-76.13. . Lemont H, Ammirati KM, Usen N. Plantar fasciitis: a degenerative process (fasciosis) without inflammation. J Am Podiatr Med Assoc. 2003;93:234–7.14. Charles LM. Plantar fasciitis. Lippincotts Prim Care Pract. 1999;3:404-407.15. Atkins D, Crawford F, Edwards J, Lambert M. A systematic review of treatments for the painful heel.Rheumatology (Oxford). 1999;38:968–973. doi: 10.1093/rheumatology/38.10.968.16. Rompe JD. Plantar fasciopathy. Sports Med Arthrosc. 2009;17:100–104. doi: 10.1097/JSA.0b013e3181a3d60e.17. goff j.d, and Crawford r.:diagnosis and treatment of plantar fasciitis. Am fam physician 2011;84:pp. 676-682.18. Wright DG, Rennels DC: A study of the elastic properties of plantar fascia. J Bone Joint Surg Am 1964;46(3):482–492.19. . Viel E, Esnault M. The effect of increased tension in the plantar fascia: a biomechanical analysis.Physiother Pract. 1989;5:69–73.20. Fuller EA. The windlass mechanism of the foot: a mechanical model to explain pathology. J Am Podiatr Med Assoc. 2000;90:35–46.21. Bolgla LA, Malone TR. Plantar fasciitis and the windlass mechanism: a biomechanical link to clinical practice. J Athl Train. 2004;39:77–82.22. Puttaswamaiah R, Chandran P. Degenerative plantar fasciitis: A review of current concepts. Foot.2007;17 :3–9.23. GRASEL RP, SCHWEITZER ME, KOVALOVICH AM, ET AL: MR imaging of plantar fasciitis: edema, tears, and occult marrow abnormalities correlated with outcome. AJR Am J Roentgenol 173: 699, 1999.24. Mahowald S, Legge BS, Grady JF. The correlation between plantar fascia thickness and symptoms of plantar fasciitis. J Am Podiatr Med Assoc. 2011;101:385–9.25. Sahin N, Ozturk A, Atici T. Foot mobility and plantar fascia elasticity in patients with plantar fasciitis.Acta Orthop Traumatol Turc. 2010;44:385–91.26. Mithraratne K, Ho H, Hunter PJ, Fernandez JW. Mechanics of the foot Part 2: A coupled solid-fluid model to investigate blood transport in the pathologic foot. Int J Numer Method Biomed Eng27. Peacock EE., Jr Fundamental aspects of wound healing relating to the restoration of gliding function after tendon repair. Surg Gynecol Obstet. 1964;119:241–5028. Knobloch K, Yoon U, Vogt PM. Acute and overuse injuries correlated to hours of training in master running athletes. Foot Ankle Int. 2008;29(7):671–67629. Scher DL, Belmont PJ, Jr., Bear R, et al. The incidence of plantar fasciitis in the United States military. J Bone Joint Surg Am. 2009;91(12):2867–287230. Werner RA, Gell N, Hartigan A, Wiggerman N, Keyserling WM. Risk factors for plantar fasciitis among assembly plant workers. PM R. 2010;2(2):110–11631. Chandler TJ, Kibler WB. A biomechanical approach to the prevention, treatment and rehabilitation of plantar fasciitis. Sports Med. 1993;15:344–352.32. Kwong PK, Kay D, Voner PT, White MW. Plantar fasciitis: mechanics and pathomechanics of treatment.Clin Sports Med. 1988;7:119–12633. Pohl M, Hamil J, Davis I. Biomechanical and anatomic factors associated with a history of plantar fasciitis in female runners. Clin J Sport Med. 2009;19:372–6. 10.1097/JSM.0b013e3181b8c270.34. Messier SP, Pittala KA. Etiologie faetors associated with selected runnine injuries. Med Sei Sporls Excrc 1988:2O:5Ol-.5O5. 1535. Warren BL. Anatomical factors assoeiated with predicting plantar fasciitis in distance runners36. Bedi HS, Love BR. Differences in impulse distribution in patients with plantar fasciitis. Foot Ankle Int.1998;19:153–637. Wearing SC, Smeathers JE, Urry SR. The effect of plantar fasciitis on vertical foot-ground reaction force.Clin38. Kibler WB, Goldberg C, Chandler TJ. Functional biomechanical deficits in running athletes with plantar fasciitis. Am J Sports Med. 1991;19:66–71. 10.1177/03635465910190011139. Hill JJ, Cutting PI. Heel pain and body weight. Foot Ankle. 1989;9:254-256.40. Sadat-Ali M. Plantar fasciitis/calcaneal spur among security forces personel. Mil Med. 1998;163:56-57.41. Shama SS, Kominsky SJ, Lemont H. Prevalence of nonpainful heel spur and its relation to postural foot position. J Am Podiatr Med Assoc. 1983;73:122-123.42. . Irving DB, Cook JL, Menz HB. Factors associated with chronic plantar heel pain: a systematic review. J Sci Med Sport. 2006;9:11–22.43. Johal KS, Milner SA. Plantar fasciitis and the calcaneal spur: Fact or fiction? Foot Ankle Surgery.2012;18:39–4144. Rubin, G., Witten, M. (1963). Plantar calcaneal spurs. American Journal of Orthopaedics, 5: 38-4145. McCarthy, D.J., Gorecki, G.E. (1979). Anatomical basis of inferior calcaneal lesions: a cryomicrotomy study. Journal of the American Podiatric Medical Association, 69: 527-53646. Bassiouni M: Incidence of calcaneal spurs in osteo-arthrosis and rheumatoid arthritis, and in control patients. Ann Rheum Dis 1965, 24:490-49347. Banadda BM, Gona O, Vas R, Ndlovu DM: Calcaneal spurs in a Black African population.Foot Ankle 1992, 13(6):352-35448. Moroney PJ, O'Neill BJ, Khan-Bhambro K, O'Flanagan SJ, Keogh P, Kenny PJ. The Conundrum of Calcaneal Spurs: Do They Matter? Foot Ankle Spec. 2014 Apr;7(2):95–10149. Prichasuk S, Subhadrabandhu T: The relationship of pes planus and calcaneal spur to plantar heel pain.Clin Orthop Relat Res 1994, 306:192-196.50. Thordarson DB, Schmotzer H, Chon J, Peters J. Dynamic support of the human longitudinal arch: a biomechanical evaluation. Clin Orthop. 1995;316:165–17251. Sahrmann SA. Diagnosis and Treatment of Movement Impairment Syndromes. St Louis, MO: Mosby; 2002. Movement impairment syndromes at the hip; pp. 121–19352. Alvarez-Nemegyei J, Canoso JJ. Heel pain: diagnosis and treatment, step by step. Cleve Clin J Med. 2006;73:465-471.53. Barrett SJ, O’Malley R. Plantar fasciitis and other causes of heel pain. Am Fam Physician. 1999;59:2200-2206.54. Roxas M. Plantar fasciitis: Diagnosis and therapeutic considerations. Altern Med Rev. 2005;10:83–93.55. Saber N, Diab H, Nassar W, Razaak HA. Ultrasound guided local steroid injection versus extracorporeal shockwave therapy in the treatment of plantar fasciitis. Alexandria J Med. 2011;48:35–42.56. Wearing SC, Smeathers JE, Sullivan PM, Yates B, Urry SR, Dubois P. Plantar fasciitis: Are pain and fascial thickness associated with arch shape and loading? Phys Ther. 2007;87:1002–857. McMillan AM, Landorf KB, Barrett JT, Menz HB, Bird AR. Diagnostic imaging for chronic plantar heel pain: a systematic review and meta-analysis. J Foot Ankle Res. 2009;2:32. doi: 10.1186/1757-1146-2-3258. Kumai T, Benjamin M. Heel spur formation and the subcalcaneal enthesis of the plantar fascia. J Rheumatol. 2002;29:1957–196459. Li J, Muehleman C. Anatomic relationship of heel spur to surrounding soft tissues: greater variability than previously reported. Clin Anat. 2007;20:950–955. doi: 10.1002/ca.20548.60. Ozdemir H, Soyuncu Y, Ozgorgen M, Dabak K. Effects of changes in heel fat pad thickness and elasticity on heel pain. J Am Podiatr Med Assoc. 2004;94:47–52.61. Smith S, Tinley P, Gilheany M, Grills B, Kingsford A. The inferior calcaneal spur - anatomical and histological considerations. Foot. 2007;17:25–31. doi: 10.1016/j.foot.2006.10.002.62. Barrett SL, Day SV, Pignetti TT, Egly BR. Endoscopic heel anatomy: analysis of 200 fresh frozen specimens. J Foot Ankle Surg. 1995;34:51–55.63. Perryj: anatomy and biomechanics of the hindfoot. Clin orthopedic relat res 1983, undefined :pp .9-1564. Blechschmidt E. The structure of the calcaneal padding. Foot Ankle 2: 260–283, 198265. Bojsen-Møller,F.,Jørgensen U. (1991) The Plantar Soft Tissues: Functional Anatomy and Clinical Applications. Chapter in Jahss M.H. (1991) Disorders of the Foot and Ankle-Medical and Surgical Management 2nd Ed. W.B.Saunders, Philadelphia66. Jahss M.H., Michelson J.D., Desai P., Kaye R., Kummer F., Buschman W., Watkins F., Reich S. (1992) Investigations into the Fat Pads of the Sole of the Foot: Anatomy and Histology. Foot and Ankle Vol.13 No.5 p.233-24267. Hsu C.C., Tsai W.C., Wang C.L., Pao S.H., Shau Y.W., Chuan Y.S. (2007) Microchambers and macrochambers in heel pads: are they functionally different? J. Appl. Physiology 102: 2227-223168. Buschmann WR, Hudgins LC, Kummer F, Desai P, Jahss MH. Sep;14(7):389-94. Fatty acid composition of normal and atrophied heel fat pad. Foot Ankle. 199369. Pai S, Ledoux WR (2010) The compressive mechanical properties of diabetic and non-diabetic plantar soft tissue. J Biomech 43:1754–176070. Pai S, Ledoux WR (2011) The quasi-linear viscoelastic properties of diabetic and non-diabetic plantar soft tissue. Ann Biomed Eng 39:1517–152771. Buschmann WR, Jahss MH, Kummer F, Desal P, Gee RO, Ricci JL (1995) Histology and histomorphometric analysis of the normal and atrophic hell fat pad. Foot Ankle Int 16:254–25872. Rome et al., 2002. Rome K., Campbell R., Flint A., and Haslock I.: Heel pad thickness—A contributing factor associated with plantar heel pain in young adults. Foot Ankle Int 2002; 23: pp. 142-14773. Rolf C, Gunther P, Ericsater J, Turan I. Plantar fascia rupture: diagnosis and treatment. J Foot Ankle Surg 1997; 36:112-114.74. Leach R, Jones R, Silva T. Rupture of the plantar fascia in athletes. J Bone Joint Surg Am 1978; 60:537-53975. Christel P, Rigal S, Poux D, Roger B, Witvoët J. Traitement chirurgical des ruptures de l'aponévrose plantaire. Rev Chir Orthop Reparatrice Appar Mot 1993; 79:218-22576. Saxena A, Fullem B. Plantar fascia ruptures in athletes. Am J Sports Med.2004;32:662-66577. .Yu J.S.: Pathologic and post-operative conditions of the plantar fascia: review of MR imaging appearances. Skeletal Radiol 2000; 29: pp. 49178. .Acevedo J.I., and Beskin J.L.: Complications of plantar fascia rupture associated with corticosteroid injection. Foot Ankle Int 1998; 19: pp. 9179. Sellman JR. Plantar fascia rupture associated with corticosteroid injection. Foot Ankle 1994; 15:376-38180. DiMarcangelo MT, Yu TC. Diagnostic imaging of heel pain and plantar fasciitis. Clin Podiatr Med Surg 1997; 14:281-30181. Tsai WC1, Chiu MF, Wang CL, Tang FT, Wong MK. Ultrasound evaluation of plantar fasciitis. Scand J Rheumatol. 2000;29(4):255-9.82. Sutera R1, Iovane A, Sorrentino F, Candela F, Mularo V, La Tona G, Midiri M. Plantar fascia evaluation with a dedicated magnetic resonance scanner in weight-bearing position.. Radiol Med. 2010 Mar;115(2):246-60. doi: 10.1007/s11547-010-0534-z. Epub 2010 Feb 22.83. Mukai Chimutengwende-Gordon, MRCS, Paul O'Donnell, FRCR, Dishan Singh, FRCS(Orth)Magnetic Resonance Imaging in Plantar Heel Pain.84. Lee TH, Wapner KL, Hecht PJ. Plantar fibromatosis. J Bone Joint Surg Am 1993; 75:1080-108485. Gehrmann RM, Renard RL.. Current concepts review: stress fractures of the foot. Foot Ankle Int. 2006;27:750-75786. Kier R. Magnetic resonance imaging of plantar fasciitis and other causes of heel pain. Magn Reson Imaging Clin N Am 1994; 2:97-10787. Anderson EG: Fatigue fractures of the foot. Injury 1990;21(5):275–27988. Lee JK, Yao L. Stress fractures: MR imaging. Radiology 1988; 169:217-220.89. Anderson MW, Greenspan A. Stress fractures. Radiology 1996; 199:1-1290. Pfeffer G.B.: Plantar heel pain. In Baxter D E. (eds): The Foot and Ankle in Sport. St. Louis: Mosby, 1995. pp. 195-20691. Oztuna et al., 2002. Oztuna V., Ozge A., Eskandari M.M., Colak M., Golpinar A., and Kuyurtar F.: Nerve entrapment in painful heel syndrome. Foot and Ankle International 2002; 23: pp. 208-21192. Lau J.T., and Daniels T.R.: Tarsal tunnel syndrome: a review of the literature. Foot Ankle Int 1999; 20: pp. 201-20993. Daniels TR, Lau JT, Hearn TC: The effects of foot position and load on tibial nerve tension. Foot Ankle Int 1998;19(2):73–78.94. Rondhuis JJ, Huson A: The first branch of the lateral plantar nerve and heel pain. Acta Morphol Neerl Scand 1986;24(4):269–279.95. Recht MP, Grooff P, Ilaslan H, Recht HS, Sferra J, Donley BG: Selective atrophy of the abductor digiti quinti: An MRI study. AJR Am J Roentgenol 2007;189(3):W123-W12796. Baxter et al., 1989. Baxter D.E., Pfeffer G.B., and Thigpen M.: Chronic heel pain: treatment rationale. Orthopedic Clinics of North America 1989; 20: pp. 563-56997. Davidson and Copoloff, 1990. Davidson M.R., and Copoloff J.A.: Neuromas of the heel. Clinics in Podiatric Medicine and Surgery 1990; 7: pp. 271-28898. Berens DL. Roentgen features of ankylosing spondylitis. Clin Orthop. 1971;74:20–33.99. Bywater EL. Heel lesions of rheumatoid arthritis. Ann Rheum Dis. 1954;13:42–51.
100.Tozzi MA, Stamm R, Bigelli AJ, Hart DJ. Reiter's syndrome: a review and case report. J Am Podiatry Assoc. 1981;71:418–22