Plantar heel pain in adulthood is the most common problem of the foot, and can be provoked by bone, soft tissue, nerve, or systemic disease.1,2 Although accurate diagnosis and appropriate management are important, distinguishing the various causes of highly similar symptoms is difficult. Plantar heel pains from skeletal problems are caused by calcaneal stress fracture, apophysitis of the calcaneus (Sever's disease), osteomyelitis, or inflammatory arthropathy. Soft tissue pathology includes fat pad atrophy (FPA) or contusion, plantar fascia rupture and plantar fasciitis (PF). Heel pain may be induced by neural causes such as entrapment or compression of the first branch of the lateral plantar nerve (Baxter's nerve), medial calcaneal branch of posterior tibial nerve, or nerve to abductor digiti quinti muscle. Other neural causes include S1 radiculopathy, tarsal tunnel syndrome, and peripheral neuropathy.1,3

PF is reported to be the most common cause of plantar heel pain.1 The pathology is still unknown, but histopathologic examination of biopsy specimens from patients undergoing excessive extension or microinjuries of the plantar fascia shows secondary degenerative changes in the plantar fascia, with or without fibroblastic proliferation, and without acute inflammation.4 The peak age of incidence in the general population is between 40 and 60 years. The risk factors for PF include running excessively (or suddenly increasing running distance), occupations that involve long periods of standing, pes planus, limited ankle dorsiflexion, and obesity.1,3,5 FPA occurs after 40 years because of atrophy and thinning of the fat pad in the inferior heel, with loss of water, collagen, and elastic tissue, reducing shock absorbency and protection of the calcaneus.3

Differential diagnosis between PF and FPA is important for proper treatment. Baxter and Pfeffer6 determined differential diagnosis according to different tender sites that were closely related to the origins of heel pains. Therefore, we studied the variable causes of plantar heel pain and clinical characteristics of PF and FPA. We generated basic data for differential diagnosis using detailed history taking and thorough physical examination.

PF is reported to be the most common cause of pain in the inferior heel. It is estimated to account for 11-15% of all foot symptoms that require professional care among adults,10,11 and occurs in up to 10% of the US population.12 The incidence peaks between the age of 40 and 60 years in the general population.1,3 PF was the most common diagnosis in this study, occurring in 53.2% of patients with plantar heel pain. PF is caused by repetitive pronatory stress that increases tensile force on the plantar fascia, causing the plantar arch to lower. The pronatory effect increases with age, and is related to limited ankle dorsiflexion caused by decreased elasticity of the tendons, and the reduced range of motion that occurs with age. PF usually has diverse causes. We investigated variable causes of plantar heel pain and their incidence. Interestingly, the fourth most common was PFFPA. Aging caused physiological changes leading to PF, increasing stress on the calcaneus and plantar fascia because of loss of buffering tissue such as water and collagen of the fat pad. The fat pad atrophied and shock absorbency diminished in subjects that were older than 40 years. PF can be co-morbid with FPA, and this should be considered in designing treatment strategy. Our study had 38 people (15.2%) with pes cavus or pes planus and no structural abnormality of the heel. They had been misdiagnosed as having PF and treated with conservative therapy including local steroid injection. Because patients with pes cavus or pes planus might develop sufficient plantar pain to require professional care at a hospital, either condition should be considered in differential diagnosis. Our study had four patients with plantar fascia rupture (1.6%). One had heel pain after running on a treadmill, and the other three patients reported a past medical history of local steroid injection for heel pain. One of these three had two steroid injections and another developed pain during basketball game, 4 months after a steroid local injection. The other patient described an audible "pop" while walking 2 months after a local steroid injection.

The peak age of incidence of PF in the general population is between 40 and 60 years.1,3 In this study, the mean age of patients with PF was 44.7 years. PF patients under 40 years (42.9%) were obese, or had occupations and leisure activities that could lead to heel pain.1,3,5 Younger patients may also be more interested in quality of life and heel pain.

Baxter and Pfeffer6 reported on 69 heels from 53 patients with chronic heel pain who had a surgical release of the first branch of the lateral plantar nerve. Postoperatively, 61 heels (89%) had good or excellent results. Entrapment of the first branch of the lateral plantar nerve (Baxter's nerve) was not determined in this study, but 12 patients (15.3%) with FPA and 3 (13.0%) with PFFPA had tingling, cold, or burning sensations. Tingling or burning symptoms may be the result of neural causes. Nerves are localized in superficial regions where they can be easily compressed after atrophy of the heel fat pad. This makes them vulnerable to contusion if shock absorbency is reduced. Entrapment of the Baxter nerve was difficult to be examined objectively, so this study did not confirm that diagnosis, although this may have occurred among the subjects.

Because PF and FPA may share very similar symptoms and are difficult to distinguish from one another, we performed multinomial logistic regression for statistical modeling and predicting specific diagnoses. When we compared PF with FPA, first-step pain in the morning and tenderness on the medial calcaneal tuberosity tended to indicate PF, and worsening pain during prolonged standing, pain at night, or bilateral pain were more likely to indicate FPA. However, 43.2% of FPA patients experienced first-step pain in the morning. Consequently, we should not make a diagnosis based on only one symptom, and should consider other symptoms, results of physical examinations, and radiologic evaluation. In case of mixed characteristics of PF and FPA (Table 5), PFFPA should be considered first and ultrasonography possibly used as an adjuvant diagnostic tool. Bilateral pain of PF patients was reported in 33% of patients with heel pain1, and this occurred in 23.3% of patients in this study, but unilateral pain was still dominant. Bilateral pain was seen in 78.4% of patients with FPA, and was significantly more likely to indicate FPA than PF (odds ratio=57.22).

Limited ankle dorsiflexion on the involved side significantly increased the risk of PF.5,13 Approximately 10 degrees of ankle dorsiflexion with the knee extended was required during a normal gait.14 If the Achilles tendon is shortened, limiting ankle dorsiflexion, excessive pronation of the foot may occur to compensate for this limitation. Excessive pronation of the foot increases tensile loads on the plantar aponeurosis. Because heel cord tightness of patients with PF was more frequently seen in patients with PF than in patients with FPA (p=0.049), the greater the limitation in ankle dorsiflexion, the more load on the plantar fascia. This provides a good target for treatment. Digiovanni et al.15 reported relief or absence of plantar heel pain in 52% of patients participating in exercises to stretch the plantar fascia, and 22% after stretching the Achilles tendon. Even though the pathophysiology of PF is different from that of FPA, Achilles tendon stretching can be suggested as a part of treatment. Studying the effect of exercise intervention to reduce risk and lower incidence would be worthwhile.

Relationship between heel spur and plantar heel pain has been controversial. Davies et al.16 and Williams et al.17 checked for heel spurs in more than 50% of patients with plantar heel pain. Dimarcangelo and Yu18 looked for it in 50% of patients with PF, and some asymptomatic subjects or subjects without PF. This study showed that 38.3% of patients with PF had spurs, compared with 13.5% of those with FPA (p=0.001). No significant differences between PF and heel spur by multinomial logistic regression were observed.

A limitation of this study is that treatment and evaluation of effects after treatment were not investigated. For example, inferior heel pain from PF can be relieved with a prefabricated insole or heel cushion cup to minimize extension of the plantar fascia. Stretching exercises of the plantar fascia and Achilles tendon cab also relieved pain. An alternative treatment may be steroid local injection, or extracorporeal shock wave therapy for intractable pain. Heel cushions, heel cups, or low-dye taping can be applied to relieve the pressure on the calcaneus of FPA patients.1-3

Accurate diagnosis is important to evaluate the response of treatment and prognosis of disease because treatment such as local steroid injection can cause the atrophied tissue to shrink further in FPA patients. This study determined the causes of plantar heel pain in 250 subjects and gathered basic data on the incidence of the causes of plantar heel pain, and clinical differences and differential diagnosis in 133 subjects with PF and 37 patients with FPA. In the future, we also plan to evaluate the response to treatment.

Plantar heel pain can be caused by not only PF or FPA, but various other causes as well. Patients with PF or FPA typically show different characteristics of clinical features about timing of pain, tender site, and bilaterality. Plantar heel pain requires differential diagnosis with consideration for appropriate management.