Pathogenic Factors Associated With Osgood-Schlatter Disease in Adolescent Male Soccer Players

Download as pdf or txt
Download as pdf or txt
You are on page 1of 8

Original Research

Pathogenic Factors Associated


With Osgood-Schlatter Disease
in Adolescent Male Soccer Players
A Prospective Cohort Study
Hiroyuki Watanabe,*† PhD, PT, Meguru Fujii,‡ MS, PT, Masumi Yoshimoto,§ MS, PT,
Hiroshi Abe,|| PhD, PT, Naruaki Toda,|| MS, PT, Reiji Higashiyama,{ MD,
and Naonobu Takahira,† MD
Investigation performed at Kitasato University, Sagamihara, Japan

Background: A previous cross-sectional study reported that pathogenic factors associated with Osgood-Schlatter disease (OSD)
in adolescent athletes include increased quadriceps muscle tightness, lower leg malalignment, and development of apophysitis in
the tibial tuberosity.
Purpose: To confirm these pathogenic factors associated with OSD in a longitudinal study with regard to physical function and
performance.
Study Design: Cohort study; Level of evidence, 2.
Methods: In this study, 37 boys (mean age, 10.2 ± 0.4 years) were recruited from 2 soccer teams at an elementary school. This
cohort study was conducted over an observation period of 1 year, with measurements recorded at baseline, followed by screening
for OSD every 6 months. Variables evaluated at baseline included physical function (morphometry, joint flexibility, and lower
extremity alignment), presence of Sever disease, and kicking motion.
Results: Pathogenic factors associated with OSD in the support leg of adolescent male soccer players included height, weight,
body mass index, quadriceps femoris muscle tightness in the kicking and support legs, and gastrocnemius muscle tightness,
soleus muscle tightness, and medial longitudinal arch in the support leg. Additional factors included a diagnosis of Sever disease
and distance from the lateral malleolus of the support leg’s fibula to the center of gravity during kicking.
Conclusion: The onset of OSD was found to be affected by many factors, including developmental stage, physical attributes, and
pre-existing apophysitis. In particular, a diagnosis of Sever disease and backward shifting of the center of gravity during kicking
increased the risk of the subsequent onset of OSD, suggesting that these factors are very important as a possible focus for
interventions.
Keywords: knee; pediatric; growth; ultrasonography; prevention

Soccer is a sport that is currently enjoyed worldwide and example, elbow joint injuries in baseball players and knee
can be played from childhood into adulthood. As such, soc- joint injuries in soccer players.19
cer is effective in increasing the activity of both children Osgood-Schlatter disease (OSD), named for the physi-
and elderly people. However, adolescent soccer players cians who first described it in 1903, is a type of osteochon-
exhibit many musculoskeletal disorders resulting from drosis. OSD is traction apophysitis resulting from the
repeated biomechanical stress.27 Children who are active repeated contraction of the quadriceps femoris muscle on
during a growth spurt may develop multiple sites of epiphy- the tibial tuberosity.13,22 The onset of OSD is related to
sitis, and many sport injuries in adolescent athletes are activities and performance specific to sports such as soc-
caused by the architectural fragility of the epiphysis, for cer, basketball, and volleyball. 31 In particular, OSD
accounts for the highest incidence of knee joint injuries
in adolescent male soccer players.24,30 To date, pathogenic
The Orthopaedic Journal of Sports Medicine, 6(8), 2325967118792192
factors reportedly associated with OSD in adolescent ath-
DOI: 10.1177/2325967118792192 letes include increased quadriceps muscle tightness, lower
ª The Author(s) 2018 leg malalignment, and development of apophysitis in the

This open-access article is published and distributed under the Creative Commons Attribution - NonCommercial - No Derivatives License (http://creativecommons.org/
licenses/by-nc-nd/4.0/), which permits the noncommercial use, distribution, and reproduction of the article in any medium, provided the original author and source are
credited. You may not alter, transform, or build upon this article without the permission of the Author(s). For article reuse guidelines, please visit SAGE’s website at
http://www.sagepub.com/journals-permissions.

1
2 Watanabe et al The Orthopaedic Journal of Sports Medicine

tibial tuberosity.7,14,18,35 However, these reports are based


on the results of cross-sectional studies that indicate phys-
ical function and performance characteristics after the
onset of disease.
The onset of Sever disease, also known as calcaneal apo-
physitis, occurs at an earlier developmental stage than
OSD.16 One of the risk factors of apophysitis is increased
activity; thus, adolescent athletes with Sever disease may
be more likely to develop OSD. For this reason, confirming
the existence of Sever disease may be a risk factor for the
onset of OSD.
It has been reported that the magnitude of knee exten-
sion moment differs between the kicking and support legs
when a kicking motion is performed in soccer.21 Backward
shifting of the center of gravity (COG) during kicking
increases the knee extension moment of the support leg.
Because adolescent soccer players struggle to use their
right and left legs equally during kicking, this shifting of
the COG and increased extension moment of the support
leg may contribute to the onset of OSD. However, it Figure 1. Flowchart for procedure for dividing participants
remains unclear whether a backward-shifting COG during into 2 groups: control group and Osgood-Schlatter disease
kicking is a direct pathogenic factor in adolescent soccer (OSD) group. 3D, 3-dimensional.
players. The objective of this study was to examine the
pathogenic factors associated with OSD in a longitudinal Procedure
cohort study by assessing physical function, the influence of
Sever disease, and 3-dimensional (3D) biomechanical kick- This cohort study was conducted over an observation period
ing analysis results. of 1 year (April 2011 to April 2012). After performing base-
line measurements, evaluations were conducted approxi-
mately every 6 months for 1 year (Figure 1). At baseline,
METHODS 1 participant showed pre-existing symptoms of OSD and
was excluded from the study. Ultimately, 36 participants
Participants were included in the study.
The measures at baseline included a questionnaire,
A total of 37 boys were recruited from 2 soccer teams at an followed by a physical examination (assessing morphome-
elementary school (mean age, 10.2 ± 0.4 years; mean try, joint flexibility, muscle tightness, and lower leg align-
height, 139.0 ± 5.8 cm; mean weight, 33.0 ± 5.6 kg; ment) and screening for Sever disease. Next, participants
mean body mass index [BMI], 17.1 ± 2.0 kg/m2). The mean performed kicking motions that were filmed with high-
length of experience playing soccer was 46.3 ± 21.2 speed cameras using reflective markers. Only baseline
months at the commencement of this study. Participants measurements of kicking were taken. After baseline, OSD
were all Japanese male athletes from the same 2 teams diagnostic testing was carried out every 6 months.
and in the same grade at school. For participant selection,
the conditions were set as above to address inclusion bias
by examining teams belonging to different cities or teams Joint Flexibility Testing
with nearly equal competitive results. Exclusion criteria
included pre-existing sport injuries of the knee such as Several methods for measuring joint flexibility have been
OSD, Sinding-Larsen-Johansson syndrome, and patellar previously reported. The Beighton method measures the
tendinitis. 5 joints of the finger, elbow joint, knee joint, and trunk.2
Participants and their parents provided written Alternatively, general joint laxity tests can be conducted on
informed consent before participation, and the study proto- the 7 main joints in the body (wrist, elbow, shoulder, hip,
col was approved by the Kitasato University School of knee, ankle, and spinal column).12 Both methods are simi-
Allied Health Sciences. lar and are known to be highly reliable.

*Address correspondence to Hiroyuki Watanabe, PhD, PT, Department of Rehabilitation, School of Allied Health Sciences, Kitasato University, 1-15-1
Kitasato, Sagamihara, Kanagawa 252-0373, Japan (email: hw@ahs.kitasato-u.ac.jp).

Department of Rehabilitation, School of Allied Health Sciences, Kitasato University, Sagamihara, Japan.

Nishifuna Clinic, Funabashi Orthopedic Hospital, Funabashi, Japan.
§
Department of Physical Therapy, Faculty of Health and Medical Science, Teikyo Heisei University, Tokyo, Japan.
||
Department of Rehabilitation, Kitasato Institute Hospital, Kitasato University, Tokyo, Japan.
{
Department of Orthopedic Surgery, School of Medicine, Kitasato University, Sagamihara, Japan.
The authors declared that they have no conflicts of interest in the authorship and publication of this contribution.
Ethical approval for this study was obtained from the Kitasato University School of Allied Health Sciences Ethics Committee (2011-2018).
The Orthopaedic Journal of Sports Medicine Pathogenic Factors of Osgood-Schlatter Disease 3

TABLE 1
ICCs From Muscle Tightness Testsa

Iliopsoas Quadriceps Hamstring Gastrocnemius

ICC (1,3) 0.89 0.96 0.95 0.93


95% CI 0.78-0.95 0.93-0.98 0.91-0.98 0.87-0.97
a
ICC (1,3) represents the mean reliability when a single
researcher is evaluated multiple times. ICC, intraclass correlation
coefficient.

tibia after the knee joint was maximally extended was mea-
sured as hamstring muscle tightness.
Figure 2. Positioning for measuring muscle tightness: (A) Gastrocnemius Muscle Tightness. To measure gastroc-
iliopsoas, (B) quadriceps, (C) hamstring, (D) gastrocnemius, nemius muscle tightness, the ankle joint dorsiflexion angle
and (E) soleus muscles. was measured when maximally dorsiflexed in the supine
position, with the knee extended and maintained in a neu-
We used general joint laxity tests in this study. The 7 con- tral position relative to the varus-valgus angle of the ankle.
ditions measured included thumb to forearm position, elbow Soleus Muscle Tightness. To measure soleus muscle
hyperextension of 15 , shoulder hyperrotation, hip hyper– tightness, the ankle joint dorsiflexion angle was measured
external rotation of 90 in the standing position, knee when maximally dorsiflexed in the prone position with the
hyperextension of 10 , ankle hyperdorsiflexion of 45 in knee at 90 of flexion.
knee flexion, and anteflexion of the trunk. Positive shoulder
hyperrotation was defined as when participants could clasp Lower Leg Alignment
their hands from both the cranial and caudal sections of their
back. Positive hip hyper–external rotation was defined as The Q-angle was measured with the participants in a
when participants could maintain their hips at 90 of external supine position. A protractor, remodeled for Q-angle mea-
rotation with both their lower legs in a neutral position. Pos- surement, was centered over the patella, with one limb over
itive forward flexion of the trunk was defined as when parti- the tibial tubercle and the other in line with the anterior
cipants could touch the floor with the bilateral palms of their superior iliac spine.
hands while maintaining their lower legs in an extended posi- For medial longitudinal arch (MLA) measurement, par-
tion. For each condition, 1 point was given when range of ticipants were asked to assume a relaxed standing position
motion reached or exceeded baseline. The wrist, elbow, shoul- on both legs, looking straight ahead with their arms by
der, knee, and ankle received half a point for each side. Total their sides. The MLA was measured as the ratio of the
scores were calculated, with a maximum total score of 7. length from the posterior heel to the first metatarsophalan-
geal joint and the height from the floor to the navicular
tubercle.28,29
Muscle Tightness Testing

Muscle tightness tests were performed on the iliopsoas, Diagnosis of OSD and Sever Disease
quadriceps femoris, hamstring, gastrocnemius, and soleus
muscles on both sides (Figure 2).32 All measurements of Examinations were conducted using M-Turbo (SonoSite)
muscle tightness were repeated twice by a single skilled and 13-MHz (6-13 MHz) linear probes (Figure 3). To meas-
physical therapist (H.W.) who demonstrated excellent ure the skeletal maturation of the distal attachment of the
intrarater reliability on all muscle tightness measures patellar tendon, participants were placed in a supine posi-
(Table 1). tion with the knees bent. Ultrasound was performed in the
Iliopsoas Muscle Tightness. The iliopsoas muscle mea- long axis view, focusing on the patellar tendon attach-
surement was performed by obtaining the angle of the hip ment.36 The bone growth stage of the tibial tuberosity on
joint when passively bending the opposite hip joint to the ultrasound was defined using the Ehrenborg classification
maximum in a supine position (Thomas test position). as cartilaginous, apophyseal, epiphyseal, or bony.9
Quadriceps Muscle Tightness. The quadriceps muscle All research in this study was conducted on the soccer
measurement was performed by bending the angle of the grounds or practice field; none was carried out at medical
knee joint in a prone position. Muscle tightness was estab- institutions. For this reason, it was impossible to use diag-
lished in the quadriceps femoris muscle if the participant’s nostic imaging (eg, radiography, computed tomography,
buttocks were lifted by muscle tension during the magnetic resonance imaging). Ultrasonography was also
measurement. used to detect pathological features and monitor the course
Hamstring Muscle Tightness. Hamstring muscle tight- of OSD. A diagnosis was made based on tenderness of the
ness was established from the measurement position of 90 tibial tuberosity, the presence or extent of irregular results
in the hip and knee joint in a supine position. The angle on imaging, and thickened cartilage of the tibial tuberosity
between the vertical line to the floor and the long axis of the visible on ultrasound.6
4 Watanabe et al The Orthopaedic Journal of Sports Medicine

Figure 3. Linear probe positioning on the patellar tendon attachment and Achilles tendon attachment as well as examples of typical
ultrasound images taken in the longitudinal axis to diagnose (A) Osgood-Schlatter disease and (B) Sever disease.

A diagnosis of Sever disease was based on long- and


short-axis images of the end plate of the calcaneus using
ultrasonography as well as confirmed fragmentation of the
secondary nucleus.17 We also identified any abnormal find-
ings during the physical examination, such as a positive
squeeze test result, which suggests that pain is produced
by medial and lateral compression of the heel.24

Biomechanical Analysis
Reflective markers with a diameter of 1 cm were fixed in
25 places across the body: top of the head, earlobe (occip-
ital), and superior border of the sternum; both acromia,
elbow joints, wrist joints, third metacarpophalangeal
joints, greater trochanters, knee joints, lateral malleoli,
toes, heels, and iliac crests; and on the spinous processes
of the eighth thoracic vertebra and the superior border of
the sacrum (Figure 4). The 3D coordinates of the markers
were calculated using a 3D video motion analysis system
(Frame-DIAS IV; DKH). Participants wore the black
spats and footwear typically used in practice and competi-
tions. Measurements of the COG were obtained according
to the method provided by Yokoi et al37 using body part
coefficients. A net was assembled 3 m away from the ball
and 1 m above the ground to measure kicking action (Fig-
ure 5). Four high-speed cameras (EXILIM EX-F1; Casio)
were arranged at intervals of 4.5 m at 60 , 150 , 210 , and
330 around the participant. Filming continued until the
ball hit the target 3 times.
Of the 3 filmed trials, the trial with the greatest ball
impact was used for analysis. Kicking measurements were
made based on the distance of the lateral malleolus of the Figure 4. Reflective marker placement on the body.
support leg’s fibula from the COG during the kicking phase level of significance was set to 5%, and a 2-tailed test (Stu-
(COG distance). The COG distance at foot contact and at dent t test) was performed. After selecting the presence of
ball impact were also calculated (Figure 6). OSD as the dependent variable, the odds ratio (OR) and
95% CI for each item were calculated using univariate anal-
Statistical Analysis ysis. The coefficient of determination (Nagelkerke R2) and
effect size (f 2) for logistic regression analysis were also
The data were analyzed with SPSS v 22.0 (IBM). Means calculated. When f 2 > 0.35, it represented a large effect;
and SDs were calculated from the baseline data and com- 0.35  f 2 > 0.02 represented a medium effect; and
pared between the OSD group and non-OSD group. The f 2  0.02 represented a small effect.5
The Orthopaedic Journal of Sports Medicine Pathogenic Factors of Osgood-Schlatter Disease 5

RESULTS
Table 2 shows the results of the physical examination and
3D biomechanical analysis for the 36 study participants.
OSD was found in the support leg of 12 participants (inci-
dence rate: 33.3%) but was not found in the kicking leg of
any participant during the observation period. At baseline,
13 participants were diagnosed with Sever disease (preva-
lence rate: 36.1%). We identified 48 knees in the cartilagi-
nous stage, 16 knees in the apophyseal stage, and 8 knees
in the epiphyseal stage according to the Ehrenborg 9
classification.
Of the variables investigated, height (OR, 1.31 [95% CI,
1.06-1.63]; P ¼ .015), weight (OR, 1.37 [95% CI, 1.10-1.71];
P ¼ .005), BMI (OR, 1.92 [95% CI, 1.18-3.12]; P ¼ .009),
quadriceps femoris muscle tightness in the kicking leg
(OR, 0.84 [95% CI, 0.74-0.96]; P ¼ .009), quadriceps femoris
muscle tightness in the support leg (OR, 0.87 [95% CI, 0.78-
0.97]; P ¼ .015), gastrocnemius muscle tightness in the
Figure 5. Typical view of kicking recordings. A net was set up support leg (OR, 0.85 [95% CI, 0.74-0.98]; P ¼ .026), soleus
3 m away from the ball with a target 1 m above the ground. muscle tightness in the support leg (OR, 0.89 [95%

Figure 6. Center of gravity (COG) distance was measured as the distance from the lateral malleolus of the support leg’s fibula to the
COG during the kicking phase: (A) foot contact and (B) ball impact.

TABLE 2
Results of Physical Examination and 3-Dimensional Biomechanical Analysis at Baselinea

Control Group OSD Group

Height, cm 137.0 ± 0.4 142.6 ± 4.1


Weight, kg 30.7 ± 4.3 36.9 ± 5.1
BMI, kg/m2 16.3 ± 1.4 18.1 ± 2.2
GJL, point 2.4 ± 1.4 1.8 ± 2.2

Kicking Leg Support Leg Kicking Leg Support Leg

MTT, deg
Iliopsoas 5.0 ± 3.7 4.2 ± 4.2 4.4 ± 3.3 3.8 ± 3.9
Quadriceps 37.5 ± 7.5 36.3 ± 7.7 45.0 ± 6.0 44.0 ± 7.1
Hamstring 42.5 ± 9.2 45.8 ± 11.2 39.8 ± 6.5 41.0 ± 7.9
Gastrocnemius 7.1 ± 5.4 7.9 ± 5.0 11.2 ± 6.7 12.8 ± 6.3
Soleus 21.3 ± 6.8 21.3 ± 6.8 27.8 ± 8.5 27.6 ± 8.8
Lower leg alignment
Q-angle, deg 12.8 ± 2.9 12.5 ± 2.6 12.1 ± 3.0 11.0 ± 3.4
MLA, % 22.0 ± 2.4 21.1 ± 2.2 20.3 ± 3.5 19.1 ± 3.2
COG distance, cm
Foot contact 74.5 ± 5.0 79.3 ± 2.8
Ball impact 64.8 ± 4.4 67.1 ± 3.6
a
Values are reported as mean ± SD. BMI, body mass index; COG, center of gravity; GJL, general joint laxity; MLA, medial longitudinal
arch; MTT, muscle tightness test; OSD, Osgood-Schlatter disease.
6 Watanabe et al The Orthopaedic Journal of Sports Medicine

TABLE 3
Findings of Univariate Analysis for Explored Intrinsic Factorsa

OR 95% CI P Value Nagelkerke R2 Effect Size (f 2)

Height 1.31 1.06-1.63 .015 0.361 0.150


Weight 1.37 1.10-1.71 .005 0.407 0.199
BMI 1.92 1.18-3.12 .009 0.279 0.084
MTT
Kicking leg quadriceps 0.84 0.74-0.96 .009 0.184 0.035
Support leg quadriceps 0.87 0.78-0.97 .015 0.106 0.011
Support leg gastrocnemius 0.85 0.74-0.98 .026 0.200 0.042
Support leg soleus 0.89 0.79-0.99 .033 0.129 0.017
Lower leg alignment: support leg MLA 1.35 1.02-1.80 .039 0.231 0.056
Sever disease diagnosis 5.25 1.28-21.57 .021 0.178 0.033
COG distance: foot contact 1.41 1.07-1.87 .016 0.262 0.073
a
BMI, body mass index; COG, center of gravity; MLA, medial longitudinal arch; MTT, muscle tightness test; OR, odds ratio.

CI, 0.79-0.99]; P ¼ .033), MLA of the support leg (OR, 1.35 support leg muscles (quadriceps femoris, gastrocnemius,
[95% CI, 1.02-1.80]; P ¼ .039), Sever disease diagnosis and soleus), MLA in the support leg, diagnosis of Sever
(OR, 5.25 [95% CI, 1.28-21.57]; P ¼ .021), and COG distance disease, and location of the COG shifting backward during
at foot contact (OR, 1.41 [95% CI, 1.07-1.87]; P ¼ .016) kicking.
were identified as pathogenic factors associated with OSD With regard to muscle tightness, previous studies have
(Table 3). The 12 participants diagnosed with OSD received demonstrated that greater tightness in the quadriceps
immediate medical follow-up. femoris, biceps femoris, gastrocnemius, and soleus muscles
is associated with the development of OSD.23,34 Because
adolescence is a developmental stage, growth along the lon-
DISCUSSION gitudinal axis of the body is extensive. 26 This growth
enhances muscle tightness and results in characteristically
In this study, the incidence rate of OSD was 33.3%. Previ- reduced muscle flexibility during adolescence. Certain fea-
ous studies on adolescents have reported OSD incidence tures of adolescent soccer players may further reduce mus-
rates ranging from 9.8% to 21%.7,20,23 There are 2 possible cle flexibility, increasing OSD susceptibility. In particular,
reasons why the incidence of OSD was higher in this study.
reduction of muscle tightness in the quadriceps increases
First, the longitudinal investigation of 10-year-old boys in
traction stress on the secondary ossification center of the
this study resulted in a higher percentage than the onset
tibial tuberosity.
rate found in adolescents in previous studies (maximum
Although the present findings indicate that the onset of
age range, 15-18 years). OSD is known to occur as a result
OSD is more likely to occur when the MLA is higher, a
of traction stress on the secondary ossification center of the
formative MLA is advantageous because it functions as a
tibial tuberosity by the patellar tendon. For this reason, the
shock absorber. The foot arch developed to enable bipedal
onset of OSD is strongly related to the growth process of
walking. The foot also changes with development, and suf-
the secondary ossification center of the tibial tuberosity.4
This growth process is classified into 4 stages: the cartilag- ficient foot development is necessary to ensure the shock-
inous stage (ages 0-11 years), the apophyseal stage (ages absorbing function. Because foot development peaks at
11-14 years), the epiphyseal stage (ages 14-18 years), and approximately 10 years old, the participants in this study
the bony stage (ages >18 years).8 It has been reported that were considered to have already reached peak develop-
the onset of OSD occurs more frequently in the apophyseal ment.15,33 The MLA may be associated with other develop-
stage of development.4 The mean age of the participants in mental factors such as height, weight, and BMI, which also
this study (10.2 ± 0.4 years) is close to the apophyseal stage. affect OSD onset. Thus, the MLA results in this study were
It seems that the peak age for the onset of OSD may occur interpreted to be a confounding factor rather than evidence
at younger than 15 to 18 years. The second possible reason of the influence of foot architecture.
is that in this study, the morphology of the tibial tuberosity The age of onset of Sever disease is from 8 to 10 years in
was assessed using ultrasonography. Ultrasonography is boys, which is younger than the age of onset of OSD.25 In
superior at observing the cartilage under the quadriceps the present study, a diagnosis of Sever disease had an OR of
femoris muscle attachment; thus, the diagnostic accuracy 5.25, which was very high compared with the other factors
of OSD in this study may be greater than that of previous identified. It has been reported that the incidence rate of
studies.4,11 Sever disease is higher in players of high-impact sports or
Based on the baseline data, pathogenic factors associated sports with high activity levels.1 Because the onset of OSD
with OSD in the support leg were identified as height, is also influenced by the level of activity, it appears that
weight, BMI, increased muscle tightness in the quadriceps OSD occurs after the onset of Sever disease. As the pres-
femoris of the kicking leg, increased muscle tightness of the ence of Sever disease makes the onset of OSD 5 times more
The Orthopaedic Journal of Sports Medicine Pathogenic Factors of Osgood-Schlatter Disease 7

likely, we consider that interventions are necessary for including the stage of development, physical function, the
those who have Sever disease to prevent the onset of OSD. onset of preceding apophysitis, and a backward-positioned
A characteristic of the kicking motion used in soccer is COG while kicking. To prevent OSD, it is necessary to
that the trunk is in an upright position when the soccer address each factor that may be related to its onset. In
player makes impact with the ball.10 However, when soccer particular, a diagnosis of Sever disease and a posterior
players intend to perform a strong kick, postures in which COG during kicking increased the risk of OSD, suggesting
the trunk is inclined backward are observed with high fre- that these may be important factors to consider when tak-
quency. A study by Blackburn and Padua3 reported that ing preventative measures.
quadriceps muscle activity decreased as the COG position
approached the knee joint after landing. It has been sug-
gested that kicking with the trunk inclined backward shifts REFERENCES
the COG posteriorly, increasing quadriceps muscle activity
1. Atanda A Jr, Shah SA, O’Brien K. Osteochondrosis: common causes
and the knee extension moment on the support leg. 21 of pain in growing bones. Am Fam Physician. 2011;83(3):285-291.
Accordingly, the results of this study demonstrate that par- 2. Beighton P, Solomon L, Soskolne CL. Articular mobility in an African
ticipants with an increased risk of OSD were found to have population. Ann Rheum Dis. 1973;32(5):413-418.
a posterior COG while kicking compared with those with a 3. Blackburn JT, Padua DA. Sagittal-plane trunk position, landing forces,
lower risk of OSD. For this reason, we infer that partici- and quadriceps electromyographic activity. J Athl Train. 2009;44(2):
pants with a high OSD risk utilize a posture that involves 174-179.
4. Blankstein A, Cohen I, Heim M, Diamant L, Salai M, Chechick A.
their trunk being tilted backward during kicking. The inci-
Ultrasonography as a diagnostic modality in Osgood-Schlatter dis-
dence rate of OSD increased 1.9 times with a 1-cm shift in ease. Arch Orthop Trauma Surg. 2001;121(9):536-539.
the COG backward. The trunk tilting backward during 5. Cohen J. A power primer. Psychol Bull. 1992;112(1):155-159.
kicking may also be a result of increased tightness in the 6. Czyrny Z. Osgood-Schlatter disease in ultrasound diagnostics: a pic-
gastrocnemius or soleus muscles of the support leg. 30 torial essay. Med Ultrason. 2010;12(4):323-335.
Increased tightness in the soleus muscle limits ankle joint 7. de Lucena GL, dos Santos Gomes C, Guerra RO. Prevalence and
associated factors of Osgood-Schlatter syndrome in a population-
dorsiflexion during kicking and reduces forward movement
based sample of Brazilian adolescents. Am J Sports Med. 2011;
of the COG. 39(2):415-420.
We conclude that a posterior shift in the COG during 8. Ducher G, Cook J, Lammers G, et al. The ultrasound appearance of
kicking increases the knee joint extension moment, which the patellar tendon attachment to the tibia in young athletes is condi-
in turn increases the risk of OSD. Therefore, we believe tional on gender and pubertal stage. J Sci Med Sport. 2010;13(1):
that coaches should offer preventative motion guidance to 20-23.
9. Ehrenborg G, Lagergren C. Roentgenologic changes in the Osgood-
adolescent soccer players whose COG shifts backward dur-
Schlatter lesion. Acta Chir Scand. 1961;121:315-327.
ing kicking. 10. El Rassi G, Takemitsu M, Woratanarat P, Shah SA. Lumbar spondy-
lolysis in pediatric and adolescent soccer players. Am J Sports Med.
Limitations 2005;33(11):1688-1693.
11. Flaviis LD, Nessi R, Scaglione P, et al. Skeletal radiology and Sinding-
The present research prospectively investigated OSD onset Larsen-Johansson diseases of the knee. Skeletal Radiol. 1989;18(3):
factors by conducting a yearlong cohort study measuring 193-197.
12. Fujitaka K, Taniguchi A, Isomoto S, et al. Pathogenesis of fifth meta-
physical and biomechanical characteristics in adolescent tarsal fractures in college soccer players. Orthop J Sports Med. 2015;
male soccer players. However, we only measured each 3(9):2325967115603654.
player once he was 10 years old; thus, we could not observe 13. Gholve PA, Scher DM, Khakharia S, Widmann RF, Green DW. Osgood
any changes in physical characteristics that occurred pre- Schlatter syndrome. Curr Opin Pediatr. 2007;19(1):44-50.
viously. In the 3D motion analysis, the experimental envi- 14. Gigante A, Bevilacqua C, Bonetti MG, Greco F. Increased external
ronment was each team’s playing ground, so we were tibial torsion in Osgood-Schlatter disease. Acta Orthop Scand. 2003;
74(4):431-436.
unable to use a floor gauge to measure ground-reaction
15. Grivas TB, Mihas C, Arapaki A, Vasiliadis E. Correlation of foot length
forces. As a result, it was not possible to calculate the exten- with height and weight in school age children. J Forensic Leg Med.
sion moment of the knee joint during kicking. In addition, 2008;15(2):89-95.
although this study collected data on many parameters, 16. Hendrix CL. Calcaneal apophysitis (Sever disease). Clin Podiatr Med
confounding factors could not be excluded because of the Surg. 2005;22(1):55-62.
small sample size. 17. Hoşgören B, Köktener A, Dilmen G. Ultrasonography of the calcaneus
in Sever’s disease. Indian Pediatr. 2005;42(8):801-803.
18. Kaya DO, Toprak U, Baltaci G, Yosmaoglu B, Ozer H. Long-term
functional and sonographic outcomes in Osgood-Schlatter disease.
CONCLUSION Knee Surg Sports Traumatol Arthrosc. 2013;21(5):1131-1139.
19. Kerssemakers SP, Fotiadou AN, De Jonge MC, Karantanas AH, Maas
Pathogenic factors associated with OSD in the support leg M. Sport injuries in the paediatric and adolescent patient: a growing
of adolescent male soccer players were identified as height, problem. Pediatr Radiol. 2009;39(5):471-484.
weight, BMI, tightness in the quadriceps femoris muscle of 20. Kujala UM, Kvist M, Heinonen O. Osgood-Schlatter’s disease in ado-
lescent athletes: retrospective study of incidence and duration. Am J
the kicking leg, tightness of the support leg muscles (quad- Sports Med. 1985;13(4):236-241.
riceps femoris, gastrocnemiuse, and soleus), MLA of the 21. Lees A, Asai T, Andersen TB, Nunome H, Sterzing T. The biome-
support leg, diagnosis of Sever disease, and COG distance. chanics of kicking in soccer: a review. J Sports Sci. 2010;28(8):
The onset of OSD seems to be affected by many factors, 805-817.
8 Watanabe et al The Orthopaedic Journal of Sports Medicine

22. Maher PJ, Ilgen JS. Osgood-Schlatter disease. BMJ Case Rep. 2013; 30. Šarčević Z. Limited ankle dorsiflexion: a predisposing factor to Mor-
2013:bcr2012007614. bus Osgood Schlatter? Knee Surg Sports Traumatol Arthrosc. 2008;
23. Nakase J, Goshima K, Numata H, Oshima T, Takata Y, Tsuchiya H. 16(8):726-728.
Precise risk factors for Osgood-Schlatter disease. Arch Orthop 31. Suzue N, Matsuura T, Iwame T, et al. State-of-the-art ultrasono-
Trauma Surg. 2015;135(9):1277-1281. graphic findings in lower extremity sports injuries. J Med Invest.
24. Perhamre S, Lundin F, Norlin R, Klässbo M. Sever’s injury: treat it with 2015;62(3-4):109-113.
a heel cup. A randomized, crossover study with two insole alterna- 32. Tojima M, Noma K, Torii S. Changes in serum creatine kinase, leg
tives. Scand J Med Sci Sports. 2011;21(6):e42-e47. muscle tightness, and delayed onset muscle soreness after a full
25. Rachel JN, Williams JB, Sawyer JR, Warner WC, Kelly DM. Is radio- marathon race. J Sports Med Phys Fitness. 2016;56(6):782-788.
graphic evaluation necessary in children with a clinical diagnosis of 33. Uden H, Scharfbillig R, Causby R. The typically developing paediatric
calcaneal apophysitis (Sever disease)? J Pediatr Orthop. 2011;31(5): foot: how flat should it be? A systematic review. J Foot Ankle Res.
548-550. 2017;10(1):1-17.
26. Rauch F, Bailey DA, Baxter-Jones A, Mirwald R, Faulkner R. The 34. Weiler R, Ingram M, Wolman R. 10-minute consultation: Osgood-
“muscle-bone unit” during the pubertal growth spurt. Bone. 2004; Schlatter disease. BMJ. 2011;343:D4534.
34(5):771-775. 35. Willner P. Osgood-Schlatter’s disease: etiology and treatment. Clin
27. Rössler R, Junge A, Chomiak J, Dvorak J, Faude O. Soccer injuries in Orthop Relat Res. 1969;62:178-179.
players aged 7 to 12 years. Am J Sports Med. 2016;44(2):309-317. 36. Yanagisawa S, Osawa T, Saito K, et al. Assessment of Osgood-
28. Roth S, Roth A, Jotanovic Z, Madarevic T. Navicular index for differ- Schlatter disease and the skeletal maturation of the distal attachment
entiation of flatfoot from normal foot. Int Orthop. 2013;37(6): of the patellar tendon in preadolescent males. Orthop J Sports Med.
1107-1112. 2014;2(7):2325967114542084.
29. Saltzman CL, Nawoczenski DA, Talbot KD. Measurement of the 37. Yokoi T, Shibukawa K, Ae M. Body segment parameters of Japanese
medial longitudinal arch. Arch Phys Med Rehabil. 1995;76(1):45-49. children. Jap J Phys Educ. 1986;31(1):53-66.

You might also like

pFad - Phonifier reborn

Pfad - The Proxy pFad of © 2024 Garber Painting. All rights reserved.

Note: This service is not intended for secure transactions such as banking, social media, email, or purchasing. Use at your own risk. We assume no liability whatsoever for broken pages.


Alternative Proxies:

Alternative Proxy

pFad Proxy

pFad v3 Proxy

pFad v4 Proxy